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HoC167 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: The anti-breast cancer drug tamoxifen has recently been shown to cause an increase in intracellular free-Ca(2+) concentrations ( [ Ca(2+)](i) ) in renal tubular cells , breast cells and bladder cells . Because tamoxifen is known to alter ovary function in human patients and in rats , the present study was aimed at exploring whether tamoxifen could alter Ca(2+) movement in Chinese hamster ovary ( CHO-K1 ) cells . Cytosolic free-Ca(2+) levels in populations of cells have been explored by using fura-2 as a fluorescent Ca(2+) indicator . Tamoxifen at concentrations above 1 micro M increased [ Ca(2+)](i) in a concentration-dependent manner with an EC(50) value of 8 micro M. The Ca(2+) signal was reduced by removing extracellular Ca(2+) , but was not affected by nifedipine , verapamil , diltiazem or ICI 182,780 ( an estrogen receptor antagonist ) . Pretreatment with 1 micro M thapsigargin ( an endoplasmic reticulum Ca(2+) pump inhibitor ) to deplete the endoplasmic reticulum Ca(2+) abolished 10 micro M tamoxifen-induced Ca(2+) release . Neither inhibition of phospholipase C with 2 micro M U73122 nor depletion of ryanodine-sensitive Ca(2+) stores with 50 micro M ryanodine affected tamoxifen-induced Ca(2+) release . Cell proliferation assays using ELISA revealed that overnight incubation with 5-10 micro M tamoxifen inhibited cell proliferation by 20% , and 20 micro M tamoxifen killed all cells . Together , the results suggest that , in CHO-K1 cells , tamoxifen induced a [ Ca(2+)](i) increase by causing store-Ca(2+) release from the endoplasmic reticulum in an phospholipase C-independent manner , and by inducing Ca(2+) influx . The action of tamoxifen appears to be dissociated from estrogen receptor activation . Longer incubation with tamoxifen ( >5 micro M ) was cytotoxic .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "sustaining proliferative signaling"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: The anti-breast cancer drug tamoxifen has recently been shown to cause an increase in intracellular free-Ca(2+) concentrations ( [ Ca(2+)](i) ) in renal tubular cells , breast cells and bladder cells . Because tamoxifen is known to alter ovary function in human patients and in rats , the present study was aimed at exploring whether tamoxifen could alter Ca(2+) movement in Chinese hamster ovary ( CHO-K1 ) cells . Cytosolic free-Ca(2+) levels in populations of cells have been explored by using fura-2 as a fluorescent Ca(2+) indicator . Tamoxifen at concentrations above 1 micro M increased [ Ca(2+)](i) in a concentration-dependent manner with an EC(50) value of 8 micro M. The Ca(2+) signal was reduced by removing extracellular Ca(2+) , but was not affected by nifedipine , verapamil , diltiazem or ICI 182,780 ( an estrogen receptor antagonist ) . Pretreatment with 1 micro M thapsigargin ( an endoplasmic reticulum Ca(2+) pump inhibitor ) to deplete the endoplasmic reticulum Ca(2+) abolished 10 micro M tamoxifen-induced Ca(2+) release . Neither inhibition of phospholipase C with 2 micro M U73122 nor depletion of ryanodine-sensitive Ca(2+) stores with 50 micro M ryanodine affected tamoxifen-induced Ca(2+) release . Cell proliferation assays using ELISA revealed that overnight incubation with 5-10 micro M tamoxifen inhibited cell proliferation by 20% , and 20 micro M tamoxifen killed all cells . Together , the results suggest that , in CHO-K1 cells , tamoxifen induced a [ Ca(2+)](i) increase by causing store-Ca(2+) release from the endoplasmic reticulum in an phospholipase C-independent manner , and by inducing Ca(2+) influx . The action of tamoxifen appears to be dissociated from estrogen receptor activation . Longer incubation with tamoxifen ( >5 micro M ) was cytotoxic .
OUTPUT:
|
HoC23 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: Notch signaling controls cell fate decisions of hematopoietic progenitors by inhibiting certain steps of differentiation and inducing either self-renewal or differentiation toward lymphoid or myeloid lineages . In addition , truncated Notch1 alleles could be associated with 10% of all cases of human T lymphoblastic leukemia and , when introduced into mouse bone marrow stem cells , cause T-cell neoplasms . However , functional links between the abundant expression of intact Notch1 and oncogenesis are still lacking . Here we show that Notch1 is highly expressed in B- and T-cell-derived tumor cells of Hodgkin and anaplastic large cell lymphoma . We demonstrate a novel mechanism for the oncogenic capacity of Notch1 by showing that the interaction between intact Notch1 on tumor cells and its ligand Jagged1 dramatically induces proliferation and inhibition of apoptosis in vitro . We further provide evidence that in Hodgkin and anaplastic large cell lymphoma , Jagged1 is expressed in malignant and in bystander cells colocalizing with Notch1-positive tumor cells . Notch1 signaling may therefore be activated in tumor cells by Jagged1 through homotypic or heterotypic cell-cell interactions , and it seems likely that these interactions contribute to lymphomagenesis in vivo . Thus , our data suggest that activated Notch1 signaling plays an important role in the pathobiology of Hodgkin and anaplastic large cell lymphoma and that it might be a potential new target for treatment .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "resisting cell death;sustaining proliferative signaling"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: Notch signaling controls cell fate decisions of hematopoietic progenitors by inhibiting certain steps of differentiation and inducing either self-renewal or differentiation toward lymphoid or myeloid lineages . In addition , truncated Notch1 alleles could be associated with 10% of all cases of human T lymphoblastic leukemia and , when introduced into mouse bone marrow stem cells , cause T-cell neoplasms . However , functional links between the abundant expression of intact Notch1 and oncogenesis are still lacking . Here we show that Notch1 is highly expressed in B- and T-cell-derived tumor cells of Hodgkin and anaplastic large cell lymphoma . We demonstrate a novel mechanism for the oncogenic capacity of Notch1 by showing that the interaction between intact Notch1 on tumor cells and its ligand Jagged1 dramatically induces proliferation and inhibition of apoptosis in vitro . We further provide evidence that in Hodgkin and anaplastic large cell lymphoma , Jagged1 is expressed in malignant and in bystander cells colocalizing with Notch1-positive tumor cells . Notch1 signaling may therefore be activated in tumor cells by Jagged1 through homotypic or heterotypic cell-cell interactions , and it seems likely that these interactions contribute to lymphomagenesis in vivo . Thus , our data suggest that activated Notch1 signaling plays an important role in the pathobiology of Hodgkin and anaplastic large cell lymphoma and that it might be a potential new target for treatment .
OUTPUT:
|
HoC1043 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: Retinoic acid ( RA ) has been believed to be an anticancer drug for a long history . However , the molecular mechanisms of RA actions on cancer cells remain diverse . In this study , the dose-dependent inhibition of RA on DU145 cell proliferation was identified . Interestingly , RA treatment triggered p35 cleavage ( p25 formation ) and Cdk5 overactivation , and all could be blocked by Calpain inhibitor , Calpeptin ( CP ) . Subsequently , RA-triggered DU145 apoptosis detected by sub-G1 phase accumulation and Annexin V staining could also be blocked by CP treatment . Furthermore , RA-triggered caspase 3 activation and following Cdk5 over-activation were destroyed by treatments of both CP and Cdk5 knockdown . In conclusion , we report a new mechanism in which RA could cause apoptosis of androgen-independent prostate cancer cells through p35 cleavage and Cdk5 over-activation . This finding may contribute to constructing a clearer image of RA function and bring RA as a valuable chemoprevention agent for prostate cancer patients .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "resisting cell death"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: Retinoic acid ( RA ) has been believed to be an anticancer drug for a long history . However , the molecular mechanisms of RA actions on cancer cells remain diverse . In this study , the dose-dependent inhibition of RA on DU145 cell proliferation was identified . Interestingly , RA treatment triggered p35 cleavage ( p25 formation ) and Cdk5 overactivation , and all could be blocked by Calpain inhibitor , Calpeptin ( CP ) . Subsequently , RA-triggered DU145 apoptosis detected by sub-G1 phase accumulation and Annexin V staining could also be blocked by CP treatment . Furthermore , RA-triggered caspase 3 activation and following Cdk5 over-activation were destroyed by treatments of both CP and Cdk5 knockdown . In conclusion , we report a new mechanism in which RA could cause apoptosis of androgen-independent prostate cancer cells through p35 cleavage and Cdk5 over-activation . This finding may contribute to constructing a clearer image of RA function and bring RA as a valuable chemoprevention agent for prostate cancer patients .
OUTPUT:
|
HoC811 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: It is known that sperm samples from recurrent pregnancy loss ( RPL ) couples have an increase in their sperm DNA fragmentation ( SDF ) , but no studies have been performed in order to identify differences between single stranded SDF ( ssSDF ) and double stranded SDF ( dsSDF ) in these patients . This could be relevant because the type of DNA damage could have different effects . Semen samples were classified attending their clinical status : 25 fertile donors and 20 RPL patients with at least two unexplained first trimester miscarriages . SDF was analysed using alkaline and neutral Comet assay , SCD test and pulsed-field gel electrophoresis ( PFGE ) , and ROC analysis including data from 105 more infertile patients ( n = 150 ) was performed to establish predictive threshold values . SDF for alkaline and neutral Comet , and the SCD test was analysed in these categories of individuals . Data revealed the presence of two subgroups within fertile donors . The values obtained were 21.10±9.13 , 23.35±10.45 and 12.31±4.31 , respectively , for fertile donors with low values for both ssSDF and dsSDF ; 27.86±12.64 , 80.69±12.67 and 12.43±5.22 , for fertile donors with low ssSDF and high dsSDF ; and 33.61±15.50 , 84.64±11.28 and 19.28±6.05 , for unexplained RPL patients , also showing a low ssSDF and high dsSDF profile . This latter profile was seen in 85% of unexplained RPL and 33% of fertile donors , suggesting that it may be associated to a male risk factor for undergoing RPL . ROC analysis regarding recurrent miscarriage set the cut-off value at 77.50% of dsDNA SDF . PFGE for low ssSDF and high dsSDF profile samples and positive controls treated with DNase , to induce dsDNA breaks , showed a more intense band of about 48 kb , which fits the toroid model of DNA compaction in sperm , pointing out that some nuclease activity may be affecting their sperm DNA in RPL patients . This work identifies a very specific SDF profile related to the paternal risk of having RPL .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "genomic instability and mutation"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: It is known that sperm samples from recurrent pregnancy loss ( RPL ) couples have an increase in their sperm DNA fragmentation ( SDF ) , but no studies have been performed in order to identify differences between single stranded SDF ( ssSDF ) and double stranded SDF ( dsSDF ) in these patients . This could be relevant because the type of DNA damage could have different effects . Semen samples were classified attending their clinical status : 25 fertile donors and 20 RPL patients with at least two unexplained first trimester miscarriages . SDF was analysed using alkaline and neutral Comet assay , SCD test and pulsed-field gel electrophoresis ( PFGE ) , and ROC analysis including data from 105 more infertile patients ( n = 150 ) was performed to establish predictive threshold values . SDF for alkaline and neutral Comet , and the SCD test was analysed in these categories of individuals . Data revealed the presence of two subgroups within fertile donors . The values obtained were 21.10±9.13 , 23.35±10.45 and 12.31±4.31 , respectively , for fertile donors with low values for both ssSDF and dsSDF ; 27.86±12.64 , 80.69±12.67 and 12.43±5.22 , for fertile donors with low ssSDF and high dsSDF ; and 33.61±15.50 , 84.64±11.28 and 19.28±6.05 , for unexplained RPL patients , also showing a low ssSDF and high dsSDF profile . This latter profile was seen in 85% of unexplained RPL and 33% of fertile donors , suggesting that it may be associated to a male risk factor for undergoing RPL . ROC analysis regarding recurrent miscarriage set the cut-off value at 77.50% of dsDNA SDF . PFGE for low ssSDF and high dsSDF profile samples and positive controls treated with DNase , to induce dsDNA breaks , showed a more intense band of about 48 kb , which fits the toroid model of DNA compaction in sperm , pointing out that some nuclease activity may be affecting their sperm DNA in RPL patients . This work identifies a very specific SDF profile related to the paternal risk of having RPL .
OUTPUT:
|
HoC294 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: Novel photosensitizers Hypocrellin A ( HA ) and Hypocrellin B ( HB ) , lipid soluble perylquinone derivatives of the genus Hypericum have a strong photodynamic effect on tumors and viruses . However , the mechanisms of tumor cell death induced by HA and HB are still unclear . In this study , we attempt to elucidate the photodynamic effects of HA and HB compounds in poorly differentiated ( CNE2 ) and moderately differentiated ( TW0-1 ) human nasopharyngeal carcinoma ( NPC ) cells as well as human mucosal colon ( CCL-220.1 ) and bladder ( SD ) cells . Using these cell lines we investigated few hall marks of apoptotic commitments in a drug and light dose dependent manner . Tumor cells photoactivated with HA and HB showed cell size shrinkage and an increase in the sub-diploid DNA content . A loss of membrane phospholipid asymmetry associated with apoptosis was induced by all tumor cell lines as evidenced by the externalization of phosphatidylserine . Western blot analysis of poly ( ADP-ribose ) polymerase , a caspases substrate , showed the classical cleavage pattern ( 116 to 85kDa ) associated with apoptosis in HA and HB-treated cell lysates . In addition , PARP cleavage was blocked by using tetrapepdide caspases inhibitors such as DEVD or z-VAD . These results demonstrate that tumor cell death induced by HB and HA is mediated by caspase proteases . This study also identifies both colon and bladder cells were more sensitive cell lines than NPC ( CNE2 and TWO-1 ) cell lines .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "resisting cell death"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: Novel photosensitizers Hypocrellin A ( HA ) and Hypocrellin B ( HB ) , lipid soluble perylquinone derivatives of the genus Hypericum have a strong photodynamic effect on tumors and viruses . However , the mechanisms of tumor cell death induced by HA and HB are still unclear . In this study , we attempt to elucidate the photodynamic effects of HA and HB compounds in poorly differentiated ( CNE2 ) and moderately differentiated ( TW0-1 ) human nasopharyngeal carcinoma ( NPC ) cells as well as human mucosal colon ( CCL-220.1 ) and bladder ( SD ) cells . Using these cell lines we investigated few hall marks of apoptotic commitments in a drug and light dose dependent manner . Tumor cells photoactivated with HA and HB showed cell size shrinkage and an increase in the sub-diploid DNA content . A loss of membrane phospholipid asymmetry associated with apoptosis was induced by all tumor cell lines as evidenced by the externalization of phosphatidylserine . Western blot analysis of poly ( ADP-ribose ) polymerase , a caspases substrate , showed the classical cleavage pattern ( 116 to 85kDa ) associated with apoptosis in HA and HB-treated cell lysates . In addition , PARP cleavage was blocked by using tetrapepdide caspases inhibitors such as DEVD or z-VAD . These results demonstrate that tumor cell death induced by HB and HA is mediated by caspase proteases . This study also identifies both colon and bladder cells were more sensitive cell lines than NPC ( CNE2 and TWO-1 ) cell lines .
OUTPUT:
|
HoC915 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: Oxaliplatin is included in a number of effective combination regimens used as first and subsequent lines of therapy for metastatic colorectal cancer . Accumulating evidence indicates that autophagy plays a significant role in response to cancer therapy . However , the role of autophagy in oxaliplatin-induced cell death remains to be clarified . In this study , we showed that oxaliplatin induced cell death and autophagy in Caco-2 colorectal cancer cells . The suppression of autophagy using either pharmacologic inhibitors ( 3-methyladenine , bafilomycin A1 ) or RNA interference in essential autophagy genes ( ATG5 or Beclin1 ) enhanced the cell death and reactive oxygen species ( ROS ) production induced by oxaliplatin in Caco-2 cells . Blocking oxaliplatin-induced ROS production by using ROS scavengers ( NAC or Tiron ) decreased autophagy . Furthermore , numerous dilated endoplasmic reticula ( ER ) were present in oxaliplatin-treated Caco-2 cells , and blocking ER stress by RNA interference against candidate of metastasis-1 ( P8 ) and C/EBP-homologous protein ( CHOP ) decreased autophagy and ROS production . Taken together , these data indicate that oxaliplatin activates autophagy as a cytoprotective response via ER stress and ROS in human colorectal cancer cells .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "resisting cell death;tumor promoting inflammation"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: Oxaliplatin is included in a number of effective combination regimens used as first and subsequent lines of therapy for metastatic colorectal cancer . Accumulating evidence indicates that autophagy plays a significant role in response to cancer therapy . However , the role of autophagy in oxaliplatin-induced cell death remains to be clarified . In this study , we showed that oxaliplatin induced cell death and autophagy in Caco-2 colorectal cancer cells . The suppression of autophagy using either pharmacologic inhibitors ( 3-methyladenine , bafilomycin A1 ) or RNA interference in essential autophagy genes ( ATG5 or Beclin1 ) enhanced the cell death and reactive oxygen species ( ROS ) production induced by oxaliplatin in Caco-2 cells . Blocking oxaliplatin-induced ROS production by using ROS scavengers ( NAC or Tiron ) decreased autophagy . Furthermore , numerous dilated endoplasmic reticula ( ER ) were present in oxaliplatin-treated Caco-2 cells , and blocking ER stress by RNA interference against candidate of metastasis-1 ( P8 ) and C/EBP-homologous protein ( CHOP ) decreased autophagy and ROS production . Taken together , these data indicate that oxaliplatin activates autophagy as a cytoprotective response via ER stress and ROS in human colorectal cancer cells .
OUTPUT:
|
HoC464 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: OBJECTIVES Oxidative stress and pro-inflammatory mediators have been implicated in breast carcinogenesis . We attempted to evaluate the markers of oxidative stress , antioxidant mechanism and the inflammatory pathway in patients with breast cancer . METHODS This study was carried out in departments of Biochemistry and Surgery , Maulana Azad Medical College and associated Hospitals , New Delhi , India . A total of 60 cases of carcinoma of the breast and 60 healthy controls were included in the study . The parameters that were assayed include markers of oxidative stress-conjugated dienes , thiobarbitone reactive substances ( TBARS ) , antioxidants-superoxide dismutase ( SOD ) , catalase ( CAT ) , glutathione peroxidase ( GPx ) , glutathione ( GSH ) and markers of inflammation-interleukin-6(IL-6) and ferritin . RESULTS There was a significant decline in the antioxidant levels and a significant rise in oxidant levels in patients with carcinoma of the breast , compared to controls . The inflammatory markers-IL-6 and ferritin-were also significantly higher in patients with breast cancer . A significantly positive correlation was observed between the IL-6 levels and conjugated dienes with the stage of breast carcinoma ; whilst a significantly negative correlation was observed between the levels of conjugated dienes and superoxide dismutase and superoxide dismutase levels with the disease staging . CONCLUSIONS This study underlines the interplay between inflammatory pathways and oxidative stress in the pathogenesis of breast cancer . MINI ABSTRACT : An intense research is underway to identify the possible risk factors and the molecular mechanisms involved in pathogenesis of breast cancer . Inflammation and oxidative stress are two such etiologies investigated in our study .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "tumor promoting inflammation"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: OBJECTIVES Oxidative stress and pro-inflammatory mediators have been implicated in breast carcinogenesis . We attempted to evaluate the markers of oxidative stress , antioxidant mechanism and the inflammatory pathway in patients with breast cancer . METHODS This study was carried out in departments of Biochemistry and Surgery , Maulana Azad Medical College and associated Hospitals , New Delhi , India . A total of 60 cases of carcinoma of the breast and 60 healthy controls were included in the study . The parameters that were assayed include markers of oxidative stress-conjugated dienes , thiobarbitone reactive substances ( TBARS ) , antioxidants-superoxide dismutase ( SOD ) , catalase ( CAT ) , glutathione peroxidase ( GPx ) , glutathione ( GSH ) and markers of inflammation-interleukin-6(IL-6) and ferritin . RESULTS There was a significant decline in the antioxidant levels and a significant rise in oxidant levels in patients with carcinoma of the breast , compared to controls . The inflammatory markers-IL-6 and ferritin-were also significantly higher in patients with breast cancer . A significantly positive correlation was observed between the IL-6 levels and conjugated dienes with the stage of breast carcinoma ; whilst a significantly negative correlation was observed between the levels of conjugated dienes and superoxide dismutase and superoxide dismutase levels with the disease staging . CONCLUSIONS This study underlines the interplay between inflammatory pathways and oxidative stress in the pathogenesis of breast cancer . MINI ABSTRACT : An intense research is underway to identify the possible risk factors and the molecular mechanisms involved in pathogenesis of breast cancer . Inflammation and oxidative stress are two such etiologies investigated in our study .
OUTPUT:
|
HoC244 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: Using monolayer cultures of clonally isolated C3 and T5 rat prostate cancer cells , we determined that acidic ( aFGF ) and basic ( bFGF ) fibroblast growth factors profoundly enhanced T5 cell thymidine incorporation with half-maximum stimulation at 0.53 and 0.35 ng/ml , respectively . In contrast , aFGF or bFGF enhancement of C3 cell thymidine incorporation was about 5% of that of T5 cells , and effects were principally mitogen concentration independent . Saturation analyses and cross-linking studies established that both C3 and T5 cells contained high-affinity FGF receptors of 120 and 145 kilodaltons and that receptor content and Kd of C3 and T5 cells were comparable. aFGF or bFGF stimulation of T5 cell thymidine incorporation profoundly decreased as cell plating density was reduced from 1.5 x 10(5) to 1.0 x 10(4) cells/well . The modest response of C3 cells to either aFGF or bFGF also decreased as cell plating density was reduced . Because heparin preserves FGF biological activity and enhances bFGF binding to high-affinity FGF receptors , we examined the effect of heparin on FGF stimulation of C3 cell thymidine incorporation . We found that changes in cell plating density and/or medium heparin concentration had variable , inconsistent effects . These were C3 cell plating density associated and included inhibition or modest enhancement of FGF effects . Binding analyses established that high-affinity bFGF binding of C3 and T5 cells immediately prior to assessing FGF-stimulated thymidine incorporation was comparable and independent of cell plating density , implying that C3 cell FGF insensitivity was not attributable to differences in C3 and T5 cell FGF receptor content at the time of mitogen stimulation.(ABSTRACT TRUNCATED AT 250 WORDS )\n OUTPUT:\n"
},
{
"from": "agent",
"value": "sustaining proliferative signaling"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: Using monolayer cultures of clonally isolated C3 and T5 rat prostate cancer cells , we determined that acidic ( aFGF ) and basic ( bFGF ) fibroblast growth factors profoundly enhanced T5 cell thymidine incorporation with half-maximum stimulation at 0.53 and 0.35 ng/ml , respectively . In contrast , aFGF or bFGF enhancement of C3 cell thymidine incorporation was about 5% of that of T5 cells , and effects were principally mitogen concentration independent . Saturation analyses and cross-linking studies established that both C3 and T5 cells contained high-affinity FGF receptors of 120 and 145 kilodaltons and that receptor content and Kd of C3 and T5 cells were comparable. aFGF or bFGF stimulation of T5 cell thymidine incorporation profoundly decreased as cell plating density was reduced from 1.5 x 10(5) to 1.0 x 10(4) cells/well . The modest response of C3 cells to either aFGF or bFGF also decreased as cell plating density was reduced . Because heparin preserves FGF biological activity and enhances bFGF binding to high-affinity FGF receptors , we examined the effect of heparin on FGF stimulation of C3 cell thymidine incorporation . We found that changes in cell plating density and/or medium heparin concentration had variable , inconsistent effects . These were C3 cell plating density associated and included inhibition or modest enhancement of FGF effects . Binding analyses established that high-affinity bFGF binding of C3 and T5 cells immediately prior to assessing FGF-stimulated thymidine incorporation was comparable and independent of cell plating density , implying that C3 cell FGF insensitivity was not attributable to differences in C3 and T5 cell FGF receptor content at the time of mitogen stimulation.(ABSTRACT TRUNCATED AT 250 WORDS )
OUTPUT:
|
HoC881 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: A key requirement for the development of cancer immunotherapy is the identification of tumour-associated antigens that are differentially or exclusively expressed on the tumour and recognized by the host immune system . However , immune responses to such antigens are often muted or lacking due to the antigens being recognized as \" self \" , and further complicated by the tumour environment and regulation of immune cells within . In an effort to circumvent the lack of immune responses to tumour antigens , we have devised a strategy to develop potential synthetic immunogens . The strategy , termed mirror image phage display , is based on the concept of molecular mimicry as demonstrated by the idiotype/anti-idiotype paradigm in the immune system . Here as ' proof of principle ' we have selected molecular mimics of the well-characterised tumour associated antigen , the human mucin1 protein ( MUC1 ) from two different peptide phage display libraries . The putative mimics were compared in structure and function to that of the native antigen . Our results demonstrate that several of the mimic peptides display T-cell stimulation activity in vitro when presented by matured dendritic cells . The mimic peptides and the native MUC1 antigenic epitopes can cross-stimulate T-cells . The data also indicate that sequence homology and/or chemical properties to the original epitope are not the sole determining factors for the observed immunostimulatory activity of the mimic peptides .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "avoiding immune destruction"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: A key requirement for the development of cancer immunotherapy is the identification of tumour-associated antigens that are differentially or exclusively expressed on the tumour and recognized by the host immune system . However , immune responses to such antigens are often muted or lacking due to the antigens being recognized as " self " , and further complicated by the tumour environment and regulation of immune cells within . In an effort to circumvent the lack of immune responses to tumour antigens , we have devised a strategy to develop potential synthetic immunogens . The strategy , termed mirror image phage display , is based on the concept of molecular mimicry as demonstrated by the idiotype/anti-idiotype paradigm in the immune system . Here as ' proof of principle ' we have selected molecular mimics of the well-characterised tumour associated antigen , the human mucin1 protein ( MUC1 ) from two different peptide phage display libraries . The putative mimics were compared in structure and function to that of the native antigen . Our results demonstrate that several of the mimic peptides display T-cell stimulation activity in vitro when presented by matured dendritic cells . The mimic peptides and the native MUC1 antigenic epitopes can cross-stimulate T-cells . The data also indicate that sequence homology and/or chemical properties to the original epitope are not the sole determining factors for the observed immunostimulatory activity of the mimic peptides .
OUTPUT:
|
HoC554 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: Hepatocellular carcinoma ( HCC ) remains a common malignant cancer worldwide . There is an urgent need to identify new molecular targets for the development of novel therapeutic approaches . Herein , we review the structure , function and biology of glypican-3 ( GPC3 ) and its role in human cancer with a focus on its potential as a therapeutic target for immunotherapy . GPC3 is a cell-surface protein that is over-expressed in HCC . Loss-of-function mutations of GPC3 cause Simpson-Golabi-Behmel syndrome ( SGBS ) , a rare X-linked overgrowth condition . GPC3 binds Wnt and Hedgehog ( Hh ) signalling proteins . GPC3 is also able to bind basic growth factors such as fibroblast growth factor 2 through its heparan sulphate glycan chains . GPC3 is a promising candidate for liver cancer therapy given that it shows high expression in HCC . An anti-GPC3 monoclonal antibody has shown anti-cancer activity in mice and its humanised IgG molecule is currently undergoing clinical evaluation in patients with HCC . There is also evidence that soluble GPC3 may be a useful serum biomarker for HCC .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "sustaining proliferative signaling"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: Hepatocellular carcinoma ( HCC ) remains a common malignant cancer worldwide . There is an urgent need to identify new molecular targets for the development of novel therapeutic approaches . Herein , we review the structure , function and biology of glypican-3 ( GPC3 ) and its role in human cancer with a focus on its potential as a therapeutic target for immunotherapy . GPC3 is a cell-surface protein that is over-expressed in HCC . Loss-of-function mutations of GPC3 cause Simpson-Golabi-Behmel syndrome ( SGBS ) , a rare X-linked overgrowth condition . GPC3 binds Wnt and Hedgehog ( Hh ) signalling proteins . GPC3 is also able to bind basic growth factors such as fibroblast growth factor 2 through its heparan sulphate glycan chains . GPC3 is a promising candidate for liver cancer therapy given that it shows high expression in HCC . An anti-GPC3 monoclonal antibody has shown anti-cancer activity in mice and its humanised IgG molecule is currently undergoing clinical evaluation in patients with HCC . There is also evidence that soluble GPC3 may be a useful serum biomarker for HCC .
OUTPUT:
|
HoC908 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: The potential of cytologically reconstructed barley line D-2946 to cope with the major lesions that hamper genome integrity , namely DNA single- and double-strand breaks was investigated . Strand breaks induced by γ-rays and Li ions were assessed by neutral and alkaline comet assay . Repair capacity after bleomycin treatment was evaluated by agarose gel electrophoresis under neutral and alkaline conditions . Frequencies of radiation-induced chromosome aberrations were also determined . Results indicate that radiation-mediated constitutive rearrangement of the chromosome complement has led to a substantial modulation of the sensitivity of barley genome towards DNA strand breaks , produced by ionising radiation , Li ion implantation and bleomycin in an agent-specific manner , as well as of the clastogenic response to γ-rays . Based on these findings , reconstructed barley karyotype D-2946 can be considered a candidate radio-sensitive line with reduced ability to maintain genome integrity with respect to both DNA and chromosomal damage .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "genomic instability and mutation"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: The potential of cytologically reconstructed barley line D-2946 to cope with the major lesions that hamper genome integrity , namely DNA single- and double-strand breaks was investigated . Strand breaks induced by γ-rays and Li ions were assessed by neutral and alkaline comet assay . Repair capacity after bleomycin treatment was evaluated by agarose gel electrophoresis under neutral and alkaline conditions . Frequencies of radiation-induced chromosome aberrations were also determined . Results indicate that radiation-mediated constitutive rearrangement of the chromosome complement has led to a substantial modulation of the sensitivity of barley genome towards DNA strand breaks , produced by ionising radiation , Li ion implantation and bleomycin in an agent-specific manner , as well as of the clastogenic response to γ-rays . Based on these findings , reconstructed barley karyotype D-2946 can be considered a candidate radio-sensitive line with reduced ability to maintain genome integrity with respect to both DNA and chromosomal damage .
OUTPUT:
|
HoC550 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: Multiple myeloma is characterized by the clonal expansion of malignant plasma cells ( multiple myeloma cells [ MMCs] ) , in the bone marrow . Osteolytic bone lesions are detected in 80% of patients because of increased osteoclastic bone resorption and reduced osteoblastic bone formation . MMCs are found closely associated with sites of increased bone resorption . Osteoclasts strongly support MMC survival in vitro . To further elucidate the mechanisms involved in osteoclast/MMC interaction , we have identified 552 genes overexpressed in osteoclasts compared with other bone marrow cell subpopulations . Osteoclasts express specifically genes coding for 4 CCR2-targeting chemokines and genes coding for MMC growth factors . An anti-CCR2 monoclonal antibody blocked osteoclast chemoattractant activity for MMC , and CCR2 chemokines are also MMC growth factors , promoting mitogen-activated protein kinase activation in MMC . An anti-insulin growth factor-1 receptor monoclonal antibody completely blocked the osteoclast-induced survival of MMC suppressing both osteoclast and MMC survival . Specific a proliferation-inducing ligand or IL-6 inhibitors partially blocked osteoclast-induced MMC survival . These data may explain why newly diagnosed patients whose MMC express high levels of CCR2 present numerous bone lesions . This study displays additional mechanisms involved in osteoclast/MMC interaction and suggests using CCR2 and/or insulin growth factor-1 targeting strategies to block this interaction and prevent drug resistance .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "sustaining proliferative signaling"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: Multiple myeloma is characterized by the clonal expansion of malignant plasma cells ( multiple myeloma cells [ MMCs] ) , in the bone marrow . Osteolytic bone lesions are detected in 80% of patients because of increased osteoclastic bone resorption and reduced osteoblastic bone formation . MMCs are found closely associated with sites of increased bone resorption . Osteoclasts strongly support MMC survival in vitro . To further elucidate the mechanisms involved in osteoclast/MMC interaction , we have identified 552 genes overexpressed in osteoclasts compared with other bone marrow cell subpopulations . Osteoclasts express specifically genes coding for 4 CCR2-targeting chemokines and genes coding for MMC growth factors . An anti-CCR2 monoclonal antibody blocked osteoclast chemoattractant activity for MMC , and CCR2 chemokines are also MMC growth factors , promoting mitogen-activated protein kinase activation in MMC . An anti-insulin growth factor-1 receptor monoclonal antibody completely blocked the osteoclast-induced survival of MMC suppressing both osteoclast and MMC survival . Specific a proliferation-inducing ligand or IL-6 inhibitors partially blocked osteoclast-induced MMC survival . These data may explain why newly diagnosed patients whose MMC express high levels of CCR2 present numerous bone lesions . This study displays additional mechanisms involved in osteoclast/MMC interaction and suggests using CCR2 and/or insulin growth factor-1 targeting strategies to block this interaction and prevent drug resistance .
OUTPUT:
|
HoC1080 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: As a member of peroxiredoxin ( Prx ) family , PrxIII is predominantly located in mitochondria and plays an important role as a scavenger of reactive oxygen species ( ROS ) . Since previous reports demonstrated over-expression of PrxIII in cervical cancer , we conducted the present study to investigate the significance of PrxIII in cervical cancer development and/or progression . Cervical cancer cells were cultured from tissues derived from cervical cancer patients . After successful knockdown of PrxIII expression by small interfering RNA , we evaluated ROS level , viable cell number , and apoptosis of cervical cancer cells along with the culture time . The production of ROS was increased in cervical cancer cells as compared with normal cervical epithelia . Knockdown of PrxIII expression induced up-regulation of other Prx members including PrxI , PrxII , and PrxV . ROS level was higher in down-regulated cervical cancer cells than in controls and the difference was increasing with culture time . We also observed increased apoptosis and decreased viable cell number in down-regulated cervical cancer cells . Our results suggest that PrxIII is an indispensable ROS scavenger , which protects tumor cells against oxidative damage and subsequent apoptosis .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "tumor promoting inflammation;resisting cell death"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: As a member of peroxiredoxin ( Prx ) family , PrxIII is predominantly located in mitochondria and plays an important role as a scavenger of reactive oxygen species ( ROS ) . Since previous reports demonstrated over-expression of PrxIII in cervical cancer , we conducted the present study to investigate the significance of PrxIII in cervical cancer development and/or progression . Cervical cancer cells were cultured from tissues derived from cervical cancer patients . After successful knockdown of PrxIII expression by small interfering RNA , we evaluated ROS level , viable cell number , and apoptosis of cervical cancer cells along with the culture time . The production of ROS was increased in cervical cancer cells as compared with normal cervical epithelia . Knockdown of PrxIII expression induced up-regulation of other Prx members including PrxI , PrxII , and PrxV . ROS level was higher in down-regulated cervical cancer cells than in controls and the difference was increasing with culture time . We also observed increased apoptosis and decreased viable cell number in down-regulated cervical cancer cells . Our results suggest that PrxIII is an indispensable ROS scavenger , which protects tumor cells against oxidative damage and subsequent apoptosis .
OUTPUT:
|
HoC417 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: BACKGROUND Paclitaxel and pirarubicin exhibit cytotoxic and antitumor activities . However , little is known about the apoptosis-inducing effects of paclitaxel and pirarubicin on human osteosarcoma MG-63 cells . METHODS The effects of paclitaxel and pirarubicin on cell cycle arrest and apoptosis were studied in MG-63 cells using flow cytometry . PCNA , Bcl-2 , Bax , cyclin D1 and cyclin E expression was assessed by Western blotting . RESULTS Paclitaxel and pirarubicin caused G2/M and G0/G1 cell cycle arrest in MG-63 cells , respectively . Apoptosis of MG-63 cells mediated by paclitaxel was dependent on treatment duration . Interestingly , in cells treated with pirarubicin , apoptosis was related to treatment duration at concentrations of 10(2)-10(3) nM , whereas the effect of treatment duration was less marked at concentrations >10(4)-10(5) nM . Furthermore , paclitaxel and pirarubicin suppressed the expression of PCNA , cyclin D1 , cyclin E and Bcl-2 , and increased Bax expression . CONCLUSION These results suggest that the G2/M or G0/G1 cell cycle arrest and apoptosis induced by paclitaxel and pirarubicin are Bcl-2/Bax dependent , suggesting favorable effects of combination therapy with paclitaxel and pirarubicin in the treatment of osteosarcoma .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "evading growth suppressors;sustaining proliferative signaling;resisting cell death"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: BACKGROUND Paclitaxel and pirarubicin exhibit cytotoxic and antitumor activities . However , little is known about the apoptosis-inducing effects of paclitaxel and pirarubicin on human osteosarcoma MG-63 cells . METHODS The effects of paclitaxel and pirarubicin on cell cycle arrest and apoptosis were studied in MG-63 cells using flow cytometry . PCNA , Bcl-2 , Bax , cyclin D1 and cyclin E expression was assessed by Western blotting . RESULTS Paclitaxel and pirarubicin caused G2/M and G0/G1 cell cycle arrest in MG-63 cells , respectively . Apoptosis of MG-63 cells mediated by paclitaxel was dependent on treatment duration . Interestingly , in cells treated with pirarubicin , apoptosis was related to treatment duration at concentrations of 10(2)-10(3) nM , whereas the effect of treatment duration was less marked at concentrations >10(4)-10(5) nM . Furthermore , paclitaxel and pirarubicin suppressed the expression of PCNA , cyclin D1 , cyclin E and Bcl-2 , and increased Bax expression . CONCLUSION These results suggest that the G2/M or G0/G1 cell cycle arrest and apoptosis induced by paclitaxel and pirarubicin are Bcl-2/Bax dependent , suggesting favorable effects of combination therapy with paclitaxel and pirarubicin in the treatment of osteosarcoma .
OUTPUT:
|
HoC204 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: Epidermal growth factor ( EGF ) and transforming growth factor alpha ( TGF alpha ) content was measured in normal ovaries and benign ovarian tumours . Epidermal growth factor was present in 12.7% of normal ovaries , with a range 0.030-0.533 ng/mg DNA , and in 31.8% of benign ovarian tumours , with a range 0.1335-2.080 ng/ml DNA . TGF alpha was present in 84.5% of normal ovaries , with a range of values from 0.037-18.2 ng/mg DNA , and in 84.1% of benign ovarian tumours , with a range of 0.083-195 ng/mg DNA . The TGF alpha content in post menopausal benign ovarian tumours was significantly higher ( P < ; 0.0001 ) than TGF alpha in the pre-menopausal normal ovarian group . The frequency of detection and levels of TGF alpha measured were significantly higher than those of EGF in the normal ovary group ( P < ; 0.001 ) and also in the benign ovarian group ( P < ; 0.005 ) . We conclude that TGF alpha is the predominant growth factor present in normal ovaries and benign ovarian tumours .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "sustaining proliferative signaling"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: Epidermal growth factor ( EGF ) and transforming growth factor alpha ( TGF alpha ) content was measured in normal ovaries and benign ovarian tumours . Epidermal growth factor was present in 12.7% of normal ovaries , with a range 0.030-0.533 ng/mg DNA , and in 31.8% of benign ovarian tumours , with a range 0.1335-2.080 ng/ml DNA . TGF alpha was present in 84.5% of normal ovaries , with a range of values from 0.037-18.2 ng/mg DNA , and in 84.1% of benign ovarian tumours , with a range of 0.083-195 ng/mg DNA . The TGF alpha content in post menopausal benign ovarian tumours was significantly higher ( P < ; 0.0001 ) than TGF alpha in the pre-menopausal normal ovarian group . The frequency of detection and levels of TGF alpha measured were significantly higher than those of EGF in the normal ovary group ( P < ; 0.001 ) and also in the benign ovarian group ( P < ; 0.005 ) . We conclude that TGF alpha is the predominant growth factor present in normal ovaries and benign ovarian tumours .
OUTPUT:
|
HoC1098 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: In normal tissues , strict control of tissue size is achieved by regulating cell numbers . The mechanism that controls total cell number is known as contact inhibition of growth and it depends on the NF2/Merlin pathway . Negative regulation of this pathway by deleterious mutations or by oncogenes results in cell transformation and tumor progression . Here we provide evidence that the CD43 sialomucin cooperates with oncogenic signals to promote cell transformation by abrogating the contact inhibition of growth through a molecular mechanism that involves AKT-dependent Merlin phosphorylation and degradation . Accordingly , inhibition of endogenous CD43 expression by RNA interference in lung , cervix and colon human cancer cells impaired tumor growth in vivo . These data underscore a previously unidentified role for CD43 in non-hematopoietic tumor progression .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "evading growth suppressors"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: In normal tissues , strict control of tissue size is achieved by regulating cell numbers . The mechanism that controls total cell number is known as contact inhibition of growth and it depends on the NF2/Merlin pathway . Negative regulation of this pathway by deleterious mutations or by oncogenes results in cell transformation and tumor progression . Here we provide evidence that the CD43 sialomucin cooperates with oncogenic signals to promote cell transformation by abrogating the contact inhibition of growth through a molecular mechanism that involves AKT-dependent Merlin phosphorylation and degradation . Accordingly , inhibition of endogenous CD43 expression by RNA interference in lung , cervix and colon human cancer cells impaired tumor growth in vivo . These data underscore a previously unidentified role for CD43 in non-hematopoietic tumor progression .
OUTPUT:
|
HoC885 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: Necrotic cells are known to activate the innate immune system and trigger inflammation by releasing damage associated molecular patterns ( DAMPs ) . However , how necrotic cells influence the induction of antigen-specific CD8(+) T cell-mediated adaptive immune responses under sterile conditions , in the absence of pathogen associated molecular patterns ( PAMPs ) , remains poorly understood . Here , we examined antigen-specific CD8(+) T-cell responses to primary sterile necrotic tumor cells both in vitro and in vivo . We found that primary necrotic cells alone fail to generate CD8(+) T cell-dependent immune responses toward cell-associated antigens . We show that necrotic cells trigger CD8(+) T-cell immunity only in the presence of PAMPs or analogs , such as p(dI-dC) and/or unmethylated CpG DNA . The electroporation of tumor cells with these PAMPs prior to necrosis induction triggered antigen-specific CD8(+) T-cell responses through a TLR9/MyD88-dependent pathway . In addition , we found that necrotic cells contain factors that can block the cross-priming of CD8(+) T cells even under non-sterile conditions and can serve as a possible mechanism of immunosuppression . These results suggest that antigen-specific CD8(+) T-cell responses to primary necrotic tumor cells can be induced in the presence of PAMPs and thus have a substantial impact on the development of antitumor vaccination strategies .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "resisting cell death;tumor promoting inflammation;avoiding immune destruction"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: Necrotic cells are known to activate the innate immune system and trigger inflammation by releasing damage associated molecular patterns ( DAMPs ) . However , how necrotic cells influence the induction of antigen-specific CD8(+) T cell-mediated adaptive immune responses under sterile conditions , in the absence of pathogen associated molecular patterns ( PAMPs ) , remains poorly understood . Here , we examined antigen-specific CD8(+) T-cell responses to primary sterile necrotic tumor cells both in vitro and in vivo . We found that primary necrotic cells alone fail to generate CD8(+) T cell-dependent immune responses toward cell-associated antigens . We show that necrotic cells trigger CD8(+) T-cell immunity only in the presence of PAMPs or analogs , such as p(dI-dC) and/or unmethylated CpG DNA . The electroporation of tumor cells with these PAMPs prior to necrosis induction triggered antigen-specific CD8(+) T-cell responses through a TLR9/MyD88-dependent pathway . In addition , we found that necrotic cells contain factors that can block the cross-priming of CD8(+) T cells even under non-sterile conditions and can serve as a possible mechanism of immunosuppression . These results suggest that antigen-specific CD8(+) T-cell responses to primary necrotic tumor cells can be induced in the presence of PAMPs and thus have a substantial impact on the development of antitumor vaccination strategies .
OUTPUT:
|
HoC491 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: The main objective of the present investigation was to study the urinary neopterin excretion in the context of the activation of the adaptive cellular immune system at the tumor site . For this purpose , we compared pre-treatment urinary neopterin levels measured in 92 ovarian cancer patients , with intratumoral levels of mRNA transcripts from factors either involved in the adaptive antitumor immune defense ( CD3 , IFN-γ , IRF-1 , IRF-2 , SOCS1 and iNOS ) or immune tolerance ( FoxP3 ) . This study did not reveal an association between urinary neopterin and one of these investigated \" on tumor site transcripts \" . From all the factors reflecting the magnitude of the local adaptive antitumor response , intratumoral IRF-1 expression above the edge of the 25th percentile was found to predict most reliably favorable progression-free ( median 34 months vs. 10 months ; p < ; 0.001 ) and overall ( median 52 months vs. 16 months ; p < ; 0.001 ) survival . In contrast , pre-treatment urinary neopterin excretion above 275 μmol/mol creatinine , which indicates an unspecific activation of the innate immune system , was associated with a very poor overall survival with a median of only 11 months when compared with a median overall survival of 40 months in patients with lower urinary neopterin excretion ( p = 0.021 ) . Interestingly , the considerable survival benefit in patients with high IRF-1-expressing cancers was completely abrogated as well for progression-free as for overall survival when urinary neopterin concentrations were found to be concomitantly elevated . These findings demonstrate that in ovarian carcinomas the unspecific \" cancer-related inflammation \" contributes to a significant subversion of the adaptive antitumor immune defense mounted at the tumor site .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "tumor promoting inflammation"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: The main objective of the present investigation was to study the urinary neopterin excretion in the context of the activation of the adaptive cellular immune system at the tumor site . For this purpose , we compared pre-treatment urinary neopterin levels measured in 92 ovarian cancer patients , with intratumoral levels of mRNA transcripts from factors either involved in the adaptive antitumor immune defense ( CD3 , IFN-γ , IRF-1 , IRF-2 , SOCS1 and iNOS ) or immune tolerance ( FoxP3 ) . This study did not reveal an association between urinary neopterin and one of these investigated " on tumor site transcripts " . From all the factors reflecting the magnitude of the local adaptive antitumor response , intratumoral IRF-1 expression above the edge of the 25th percentile was found to predict most reliably favorable progression-free ( median 34 months vs. 10 months ; p < ; 0.001 ) and overall ( median 52 months vs. 16 months ; p < ; 0.001 ) survival . In contrast , pre-treatment urinary neopterin excretion above 275 μmol/mol creatinine , which indicates an unspecific activation of the innate immune system , was associated with a very poor overall survival with a median of only 11 months when compared with a median overall survival of 40 months in patients with lower urinary neopterin excretion ( p = 0.021 ) . Interestingly , the considerable survival benefit in patients with high IRF-1-expressing cancers was completely abrogated as well for progression-free as for overall survival when urinary neopterin concentrations were found to be concomitantly elevated . These findings demonstrate that in ovarian carcinomas the unspecific " cancer-related inflammation " contributes to a significant subversion of the adaptive antitumor immune defense mounted at the tumor site .
OUTPUT:
|
HoC893 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: There are contradictory observations about the different radiosensitivities of cancer stem cells and cancer non-stem cells . To resolve these contradictory observations , we studied radiosensitivities by employing breast cancer stem cell ( CSC)-like MDA-MB231 and MDA-MB453 cells as well as their corresponding non-stem cells . CSC-like cells proliferate without differentiating and have characteristics of tumor-initiating cells [ 1 ] . These cells were exposed to γ-rays ( 1.25-8.75 Gy ) and survival curves were determined by colony formation . A final slope , D(0) , of the survival curve for each cell line was determined to measure radiosensitivity . The D(0) of CSC-like and non-stem MDA-MB-453 cells were 1.16 Gy and 1.55 Gy , respectively . Similar results were observed in MDA-MB-231 cells ( 0.94 Gy vs. 1.56 Gy ) . After determination of radiosensitivity , we investigated intrinsic cellular determinants which influence radiosensitivity including cell cycle distribution , free-radical scavengers and DNA repair . We observed that even though cell cycle status and antioxidant content may contribute to differential radiosensitivity , differential DNA repair capacity may be a greater determinant of radiosensitivity . Unlike non-stem cells , CSC-like cells have little/no sublethal damage repair , a low intracellular level of ataxia telangiectasia mutated ( ATM ) and delay of γ-H2AX foci removal ( DNA strand break repair ) . These results suggest that low DNA repair capacity is responsible for the high radiosensitivity of these CSC-like cells .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "genomic instability and mutation"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: There are contradictory observations about the different radiosensitivities of cancer stem cells and cancer non-stem cells . To resolve these contradictory observations , we studied radiosensitivities by employing breast cancer stem cell ( CSC)-like MDA-MB231 and MDA-MB453 cells as well as their corresponding non-stem cells . CSC-like cells proliferate without differentiating and have characteristics of tumor-initiating cells [ 1 ] . These cells were exposed to γ-rays ( 1.25-8.75 Gy ) and survival curves were determined by colony formation . A final slope , D(0) , of the survival curve for each cell line was determined to measure radiosensitivity . The D(0) of CSC-like and non-stem MDA-MB-453 cells were 1.16 Gy and 1.55 Gy , respectively . Similar results were observed in MDA-MB-231 cells ( 0.94 Gy vs. 1.56 Gy ) . After determination of radiosensitivity , we investigated intrinsic cellular determinants which influence radiosensitivity including cell cycle distribution , free-radical scavengers and DNA repair . We observed that even though cell cycle status and antioxidant content may contribute to differential radiosensitivity , differential DNA repair capacity may be a greater determinant of radiosensitivity . Unlike non-stem cells , CSC-like cells have little/no sublethal damage repair , a low intracellular level of ataxia telangiectasia mutated ( ATM ) and delay of γ-H2AX foci removal ( DNA strand break repair ) . These results suggest that low DNA repair capacity is responsible for the high radiosensitivity of these CSC-like cells .
OUTPUT:
|
HoC977 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: There are many growth factors influencing the expansion of multiple myeloma ( MM ) . Angiogenesis is a process that may enhance MM growth , in various manners . Among them , insulin-like growth factor-1 ( IGF-1 ) is a major factor , acting in many levels . The aim of the study was to measure serum levels of IGF-1 in newly diagnosed MM patients and to correlate them with clinical stage of the disease and with markers of angiogenesis , such as vascular endothelial growth factor ( VEGF ) , hepatocyte growth factor ( HGF ) , and interleukin-6 and 15 ( IL-6 and IL-15 ) . Serum levels of the above factors were measured , by ELISA , in 57 newly diagnosed MM patients and in 20 healthy controls . There was no difference in serum levels of IGF-1 in MM patients and in controls , contrary to angiogenic factors , which were higher in MM patients ( p < ; 0.001 ) . Similarly , IGF-1 did not correlate with clinical stage of the disease nor the other angiogenic factors , which also correlated with each other ( p < ; 0.001 ) . Serum IGF-1 concentrations are not influenced in MM patients . Therefore , although it is a proliferation cytokine , it cannot be used as marker of disease activity .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "inducing angiogenesis"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: There are many growth factors influencing the expansion of multiple myeloma ( MM ) . Angiogenesis is a process that may enhance MM growth , in various manners . Among them , insulin-like growth factor-1 ( IGF-1 ) is a major factor , acting in many levels . The aim of the study was to measure serum levels of IGF-1 in newly diagnosed MM patients and to correlate them with clinical stage of the disease and with markers of angiogenesis , such as vascular endothelial growth factor ( VEGF ) , hepatocyte growth factor ( HGF ) , and interleukin-6 and 15 ( IL-6 and IL-15 ) . Serum levels of the above factors were measured , by ELISA , in 57 newly diagnosed MM patients and in 20 healthy controls . There was no difference in serum levels of IGF-1 in MM patients and in controls , contrary to angiogenic factors , which were higher in MM patients ( p < ; 0.001 ) . Similarly , IGF-1 did not correlate with clinical stage of the disease nor the other angiogenic factors , which also correlated with each other ( p < ; 0.001 ) . Serum IGF-1 concentrations are not influenced in MM patients . Therefore , although it is a proliferation cytokine , it cannot be used as marker of disease activity .
OUTPUT:
|
HoC966 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: Breast cancer constitutes a major health problem for women worldwide . However , its incidence varies between populations and geographical locations . These variations could be diet-related , since there are several carcinogenic compounds in the modern diet , while natural products contain various anti-cancer elements . Several lines of evidence indicate that , in addition to their clear preventive effect , these compounds could also be used as therapeutic agents . In the present report we have shown that oleuropein , a pharmacologically safe natural product of olive leaf , has potent anti-breast cancer properties . Indeed , oleuropein exhibits specific cytotoxicity against breast cancer cells , with higher effect on the basal-like MDA-MB-231 cells than on the luminal MCF-7 cells . This effect is mediated through the induction of apoptosis via the mitochondrial pathway . Moreover , oleuropein inhibits cell proliferation by delaying the cell cycle at S phase and up-regulated the cyclin-dependent inhibitor p21 . Furthermore , oleuropein inhibited the anti-apoptosis and pro-proliferation protein NF-κB and its main oncogenic target cyclin D1 . This inhibition could explain the great effect of oleuropein on cell proliferation and cell death of breast cancer cells . Therefore , oleuropein warrants further investigations to prove its utility in preventing/treating breast cancer , especially the less-responsive basal-like type .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "resisting cell death;evading growth suppressors;sustaining proliferative signaling"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: Breast cancer constitutes a major health problem for women worldwide . However , its incidence varies between populations and geographical locations . These variations could be diet-related , since there are several carcinogenic compounds in the modern diet , while natural products contain various anti-cancer elements . Several lines of evidence indicate that , in addition to their clear preventive effect , these compounds could also be used as therapeutic agents . In the present report we have shown that oleuropein , a pharmacologically safe natural product of olive leaf , has potent anti-breast cancer properties . Indeed , oleuropein exhibits specific cytotoxicity against breast cancer cells , with higher effect on the basal-like MDA-MB-231 cells than on the luminal MCF-7 cells . This effect is mediated through the induction of apoptosis via the mitochondrial pathway . Moreover , oleuropein inhibits cell proliferation by delaying the cell cycle at S phase and up-regulated the cyclin-dependent inhibitor p21 . Furthermore , oleuropein inhibited the anti-apoptosis and pro-proliferation protein NF-κB and its main oncogenic target cyclin D1 . This inhibition could explain the great effect of oleuropein on cell proliferation and cell death of breast cancer cells . Therefore , oleuropein warrants further investigations to prove its utility in preventing/treating breast cancer , especially the less-responsive basal-like type .
OUTPUT:
|
HoC634 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: Cancer cells preferentially metabolize glucose through aerobic glycolysis . This phenomenon , known as the Warburg effect , is an anomalous characteristic of glucose metabolism in cancer cells . Chronic inflammation is a key promoting factor of tumourigenesis . It remains , however , largely unexplored whether and how pro-tumourigenic inflammation regulates glucose metabolism in cancer cells . Here , we show that pro-inflammatory cytokines promote glycolysis in breast cancer cells , and that the inflammation-induced miR-155 functions as an important mediator in this process . We further show that miR-155 acts to upregulate hexokinase 2 ( hk2 ) , through two distinct mechanisms . First , miR-155 promotes hk2 transcription by activation of signal transducer and activator of transcription 3 ( STAT3 ) , a transcriptional activator for hk2 . Second , via targeting C/EBPβ ( a transcriptional activator for mir-143 ) , miR-155 represses mir-143 , a negative regulator of hk2 , thus resulting in upregulation of hk2 expression at the post-transcriptional level . The miR-155-mediated hk2 upregulation also appears to operate in other types of cancer cells examined . We suggest that the miR-155/miR-143/HK2 axis may represent a common mechanism linking inflammation to the altered metabolism in cancer cells .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "cellular energetics;tumor promoting inflammation"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: Cancer cells preferentially metabolize glucose through aerobic glycolysis . This phenomenon , known as the Warburg effect , is an anomalous characteristic of glucose metabolism in cancer cells . Chronic inflammation is a key promoting factor of tumourigenesis . It remains , however , largely unexplored whether and how pro-tumourigenic inflammation regulates glucose metabolism in cancer cells . Here , we show that pro-inflammatory cytokines promote glycolysis in breast cancer cells , and that the inflammation-induced miR-155 functions as an important mediator in this process . We further show that miR-155 acts to upregulate hexokinase 2 ( hk2 ) , through two distinct mechanisms . First , miR-155 promotes hk2 transcription by activation of signal transducer and activator of transcription 3 ( STAT3 ) , a transcriptional activator for hk2 . Second , via targeting C/EBPβ ( a transcriptional activator for mir-143 ) , miR-155 represses mir-143 , a negative regulator of hk2 , thus resulting in upregulation of hk2 expression at the post-transcriptional level . The miR-155-mediated hk2 upregulation also appears to operate in other types of cancer cells examined . We suggest that the miR-155/miR-143/HK2 axis may represent a common mechanism linking inflammation to the altered metabolism in cancer cells .
OUTPUT:
|
HoC851 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: Glioblastoma multiforme ( GBM ) and oxidative stress are closely linked . Oxidative stress affects many signaling pathways and may cause the induction of autophagy . The NF-E2-related factor 2 ( Nrf2)/Kelch-like ECH-associated protein 1 ( Keap1 ) signaling pathway is the main pathway responsible for cell defense against oxidative stress and Nrf2 is a critical transcription factor related with cancer multidrug resistance . However , the relation between Nrf2 and regulation of autophagy is not well understood . In this study , we used temozolomide ( TMZ ) , which inhibited the viability of GBM cells mainly by inducing autophagic cell death and explored the role of Nrf2 downregulation on autophagy induced by TMZ in GBM cells . In U251-Si-Nrf2 48h after transfection the protein levels of Nrf2 were significantly downregulated , while the protein levels of LC3B-II increased by western blot analysis . Knockdown of Nrf2 also led to a significant increase of autophagic vacuoles and acidic vesicular organelles ( AVOs ) , revealed by trans-mission electron microscopy ( TEM ) and acridine orange ( AO ) staining using flow cytometry . Collectively , these findings demonstrate that knockdown of Nrf2 can enhance the basal level of autophagy in the U251 glioma cell line . Furthermore , after the treatment with TMZ ( 100µM ) for 3 days , the U251-Si-Nrf2 transfected cells showed less viability rate by cell counting kit-8 ( CCK-8 ) assay and the levels of autophagy increased obviously through analysis of western blot and AO staining using flow cytometry . Taken together , our results suggest that knockdown of Nrf2 may enhance autophagy induced by TMZ in the U251 glioma cell line , which should be further evaluated for novel anticancer activity .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "resisting cell death"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: Glioblastoma multiforme ( GBM ) and oxidative stress are closely linked . Oxidative stress affects many signaling pathways and may cause the induction of autophagy . The NF-E2-related factor 2 ( Nrf2)/Kelch-like ECH-associated protein 1 ( Keap1 ) signaling pathway is the main pathway responsible for cell defense against oxidative stress and Nrf2 is a critical transcription factor related with cancer multidrug resistance . However , the relation between Nrf2 and regulation of autophagy is not well understood . In this study , we used temozolomide ( TMZ ) , which inhibited the viability of GBM cells mainly by inducing autophagic cell death and explored the role of Nrf2 downregulation on autophagy induced by TMZ in GBM cells . In U251-Si-Nrf2 48h after transfection the protein levels of Nrf2 were significantly downregulated , while the protein levels of LC3B-II increased by western blot analysis . Knockdown of Nrf2 also led to a significant increase of autophagic vacuoles and acidic vesicular organelles ( AVOs ) , revealed by trans-mission electron microscopy ( TEM ) and acridine orange ( AO ) staining using flow cytometry . Collectively , these findings demonstrate that knockdown of Nrf2 can enhance the basal level of autophagy in the U251 glioma cell line . Furthermore , after the treatment with TMZ ( 100µM ) for 3 days , the U251-Si-Nrf2 transfected cells showed less viability rate by cell counting kit-8 ( CCK-8 ) assay and the levels of autophagy increased obviously through analysis of western blot and AO staining using flow cytometry . Taken together , our results suggest that knockdown of Nrf2 may enhance autophagy induced by TMZ in the U251 glioma cell line , which should be further evaluated for novel anticancer activity .
OUTPUT:
|
HoC516 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: Autophagy is one of the survival processes of cancer cells , especially in stressful conditions such as starvation , hypoxia and chemotherapeutic agents . However , its roles in tumor survival have not yet been fully elucidated . Here , we found for the first time that JAK2/STAT3 was activated in HeLa cells when they were starved or treated with rapamycin . STAT3 activation was associated with autophagic processes , because it was completely inhibited by 3-methyladenine , partially inhibited by knockdown of molecules associated with autophagic processes and blocked by antioxidants , DPI , a Nox inhibitor and knockdown of p22 phox , indicating that ROS generated by Nox that was activated during autophagic processes activated JAK2/STAT3 pathway . Activated STAT3 directly bound to IL6 promoter and increased IL6 mRNA and protein secretion . Finally , the conditioned media , which included IL6 , from starved HeLa cells promoted cancer cell survival in both normal and starved conditions , confirmed by clonogenic , proliferation and cell death assays . These data together indicate that the autophagic process in cancer cells can contribute to their survival by JAk2/STAT3 activation and subsequent secretion of growth factors .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "resisting cell death;sustaining proliferative signaling"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: Autophagy is one of the survival processes of cancer cells , especially in stressful conditions such as starvation , hypoxia and chemotherapeutic agents . However , its roles in tumor survival have not yet been fully elucidated . Here , we found for the first time that JAK2/STAT3 was activated in HeLa cells when they were starved or treated with rapamycin . STAT3 activation was associated with autophagic processes , because it was completely inhibited by 3-methyladenine , partially inhibited by knockdown of molecules associated with autophagic processes and blocked by antioxidants , DPI , a Nox inhibitor and knockdown of p22 phox , indicating that ROS generated by Nox that was activated during autophagic processes activated JAK2/STAT3 pathway . Activated STAT3 directly bound to IL6 promoter and increased IL6 mRNA and protein secretion . Finally , the conditioned media , which included IL6 , from starved HeLa cells promoted cancer cell survival in both normal and starved conditions , confirmed by clonogenic , proliferation and cell death assays . These data together indicate that the autophagic process in cancer cells can contribute to their survival by JAk2/STAT3 activation and subsequent secretion of growth factors .
OUTPUT:
|
HoC455 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: The Ras-assocation domain family ( RASSF ) of tumor suppressor proteins until recently contained six proteins named RASSF1-6 . Recently , four novel family members , RASSF7-10 , have been identified by homology searches for RA-domain-containing proteins . These additional RASSF members are divergent and structurally distinct from RASSF1-6 , containing an N-terminal RA domain and lacking the Sav/RASSF/Hpo ( SARAH ) domain . Here , we show that RASSF8 is ubiquitously expressed throughout the murine embryo and in normal human adult tissues . Functionally , RNAi-mediated knockdown of RASSF8 in non-small-cell lung cancer ( NSCLC ) cell lines , increased anchorage-independent growth in soft agar and enhanced tumor growth in severe combined immunodeficiency ( SCID ) mice . Furthermore , EdU staining of RASSF8-depleted cells showed growth suppression in a manner dependent on contact inhibition . We show that endogenous RASSF8 is not only found in the nucleus , but is also membrane associated at sites of cell-cell adhesion , co-localizing with the adherens junction ( AJ ) component beta-catenin and binding to E-cadherin . Following RASSF8 depletion in two different lung cancer cell lines using alternative small interfering RNA ( siRNA ) sequences , we show that AJs are destabilized and E-cadherin is lost from the cell membrane . The AJ components beta-catenin and p65 are also lost from sites of cell-cell contact and are relocalized to the nucleus with a concomitant increase in beta-catenin-dependent and nuclear factor-kappaB ( NF-kappaB)-dependent signaling following RASSF8 depletion . RASSF8 may also be required to maintain actin -cytoskeletal organization since immunofluorescence analysis shows a striking disorganization of the actin- cytoskeleton following RASSF8 depletion . Accordingly , scratch wound healing studies show increased cellular migration in RASSF8-deficient cells . These results implicate RASSF8 as a tumor suppressor gene that is essential for maintaining AJs function in epithelial cells and have a role in epithelial cell migration .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "evading growth suppressors"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: The Ras-assocation domain family ( RASSF ) of tumor suppressor proteins until recently contained six proteins named RASSF1-6 . Recently , four novel family members , RASSF7-10 , have been identified by homology searches for RA-domain-containing proteins . These additional RASSF members are divergent and structurally distinct from RASSF1-6 , containing an N-terminal RA domain and lacking the Sav/RASSF/Hpo ( SARAH ) domain . Here , we show that RASSF8 is ubiquitously expressed throughout the murine embryo and in normal human adult tissues . Functionally , RNAi-mediated knockdown of RASSF8 in non-small-cell lung cancer ( NSCLC ) cell lines , increased anchorage-independent growth in soft agar and enhanced tumor growth in severe combined immunodeficiency ( SCID ) mice . Furthermore , EdU staining of RASSF8-depleted cells showed growth suppression in a manner dependent on contact inhibition . We show that endogenous RASSF8 is not only found in the nucleus , but is also membrane associated at sites of cell-cell adhesion , co-localizing with the adherens junction ( AJ ) component beta-catenin and binding to E-cadherin . Following RASSF8 depletion in two different lung cancer cell lines using alternative small interfering RNA ( siRNA ) sequences , we show that AJs are destabilized and E-cadherin is lost from the cell membrane . The AJ components beta-catenin and p65 are also lost from sites of cell-cell contact and are relocalized to the nucleus with a concomitant increase in beta-catenin-dependent and nuclear factor-kappaB ( NF-kappaB)-dependent signaling following RASSF8 depletion . RASSF8 may also be required to maintain actin -cytoskeletal organization since immunofluorescence analysis shows a striking disorganization of the actin- cytoskeleton following RASSF8 depletion . Accordingly , scratch wound healing studies show increased cellular migration in RASSF8-deficient cells . These results implicate RASSF8 as a tumor suppressor gene that is essential for maintaining AJs function in epithelial cells and have a role in epithelial cell migration .
OUTPUT:
|
HoC826 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: This study examined the possible role of p120ctn in the pathogenesis and development of pancreatic cancer . PANC-1 cells , a kind of human pancreatic carcinoma cell line , were cultured in this study. p120ctn was immunocytochemically detected in PANC-1 cells . The recombinant lentivirus vector was constructed to knock down the p120ctn expression of PANC-1 cells . Real-time quantitative PCR ( RQ-PCR ) and Western blotting were used to determine the expression of p120ctn and E-cadherin in PANC-1 cells after p120ctn knockdown . The adhesion , invasion and migration capacity of PANC-1 cells after p120ctn knockdown was detected by cell adhesion , invasion and migration assays . Cell growth was measured by the MTT method . Cell cycle and apoptosis were analyzed by fluorescence-activated cell sorting . The results showed that p120ctn knockdown led to significantly down-regulated E-cadherin and a reduced cell-to-cell adhesion ability in PANC-1 cells. shRNA-mediated knockdown of p120ctn reduced invasion and migration capacity of PANC-1 cells , inhibited cell growth , caused a significant decrease in the percentage of cells in G(1) , an increase in S , and promoted apoptosis of PANC-1 cells . It was concluded that p120ctn plays a pivotal role in the proliferation and metastasis of pancreatic carcinoma , suggesting that p120ctn is a novel target for pancreatic carcinoma treatment .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "activating invasion and metastasis"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: This study examined the possible role of p120ctn in the pathogenesis and development of pancreatic cancer . PANC-1 cells , a kind of human pancreatic carcinoma cell line , were cultured in this study. p120ctn was immunocytochemically detected in PANC-1 cells . The recombinant lentivirus vector was constructed to knock down the p120ctn expression of PANC-1 cells . Real-time quantitative PCR ( RQ-PCR ) and Western blotting were used to determine the expression of p120ctn and E-cadherin in PANC-1 cells after p120ctn knockdown . The adhesion , invasion and migration capacity of PANC-1 cells after p120ctn knockdown was detected by cell adhesion , invasion and migration assays . Cell growth was measured by the MTT method . Cell cycle and apoptosis were analyzed by fluorescence-activated cell sorting . The results showed that p120ctn knockdown led to significantly down-regulated E-cadherin and a reduced cell-to-cell adhesion ability in PANC-1 cells. shRNA-mediated knockdown of p120ctn reduced invasion and migration capacity of PANC-1 cells , inhibited cell growth , caused a significant decrease in the percentage of cells in G(1) , an increase in S , and promoted apoptosis of PANC-1 cells . It was concluded that p120ctn plays a pivotal role in the proliferation and metastasis of pancreatic carcinoma , suggesting that p120ctn is a novel target for pancreatic carcinoma treatment .
OUTPUT:
|
HoC1049 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: Family with sequence similarity 189 , member B ( FAM189B ) , alias COTE1 , a putative oncogene selected by microarray , for the first time was here found to be significantly up-regulated in hepatocellular carcinoma ( HCC ) specimens and HCC cell lines. mRNA expression of COTE1 in HCC samples and cell lines was detected by reverse transcription-polymerase chain reaction ( RT-PCR ) and real-time PCR , while protein expression of COTE1 in HCC tissues was assessed by immunohistochemistry . In addition , invasion of HCC cells was observed after overexpressing or silencing COTE1 . In the total of 48 paired HCC specimens , compared with the adjacent non-cancer tissues , the expression of COTE1 was up-regulated in 31 ( p<0.01 ) . In HCC cell lines , COTE1 expression was significantly higher than in normal human adult liver ( p<0.01 ) . Overexpression of COTE1 enhanced HCC-derived LM6 and MHCC-L cellular invasion in vitro . In contrast , COTE1 knockdown via RNAi markedly suppressed these phenotypes , as documented in LM3 and MHCC-H HCC cells . Mechanistic analyses indicated that COTE1 could physically associate with WW domain oxidoreductase ( WWOX ) , a tumor suppressor . COTE1 may be closely correlated with invasion of hepatocellular carcinoma ( HCC ) cells and thus may serve as an effective target for gene therapy .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "activating invasion and metastasis"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: Family with sequence similarity 189 , member B ( FAM189B ) , alias COTE1 , a putative oncogene selected by microarray , for the first time was here found to be significantly up-regulated in hepatocellular carcinoma ( HCC ) specimens and HCC cell lines. mRNA expression of COTE1 in HCC samples and cell lines was detected by reverse transcription-polymerase chain reaction ( RT-PCR ) and real-time PCR , while protein expression of COTE1 in HCC tissues was assessed by immunohistochemistry . In addition , invasion of HCC cells was observed after overexpressing or silencing COTE1 . In the total of 48 paired HCC specimens , compared with the adjacent non-cancer tissues , the expression of COTE1 was up-regulated in 31 ( p<0.01 ) . In HCC cell lines , COTE1 expression was significantly higher than in normal human adult liver ( p<0.01 ) . Overexpression of COTE1 enhanced HCC-derived LM6 and MHCC-L cellular invasion in vitro . In contrast , COTE1 knockdown via RNAi markedly suppressed these phenotypes , as documented in LM3 and MHCC-H HCC cells . Mechanistic analyses indicated that COTE1 could physically associate with WW domain oxidoreductase ( WWOX ) , a tumor suppressor . COTE1 may be closely correlated with invasion of hepatocellular carcinoma ( HCC ) cells and thus may serve as an effective target for gene therapy .
OUTPUT:
|
HoC453 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: Hepatocellular carcinoma ( HCC ) , one of the most frequent and deadliest cancers , has been increasing considerably in the United States . In the absence of a proven effective therapy for HCC , novel chemopreventive strategies are urgently needed to lower the current morbidity and mortality of HCC . Recently , we have reported that resveratrol , a compound present in grapes and red wine , significantly prevents diethylnitrosamine ( DENA)-induced liver tumorigenesis in rats , although the mechanism of action is not completely understood . In the present study , we have examined the underlying mechanisms of resveratrol chemoprevention of hepatocarcinogenesis by investigating the effects of resveratrol on oxidative damage and inflammatory markers during DENA-initiated rat liver carcinogenesis . There was a significant increase in hepatic lipid peroxidation and protein oxidation in carcinogen control animals compared with their normal counterparts at the end of the study ( 20 weeks ) . Elevated expressions of inducible nitric oxide synthase and 3-nitrotyrosine were noticed in the livers of the same animals . Dietary resveratrol ( 50-300 mg/kg ) administered throughout the study reversed all the aforementioned markers in a dose-responsive fashion in rats challenged with DENA . Resveratrol also elevated the protein and mRNA expression of hepatic nuclear factor E2-related factor 2 ( Nrf2 ) . Results of the present investigation provide evidence that attenuation of oxidative stress and suppression of inflammatory response mediated by Nrf2 could be implicated , at least in part , in the chemopreventive effects of this dietary agent against chemically induced hepatic tumorigenesis in rats . The outcome of this study may benefit the development of resveratrol in the prevention and intervention of human HCC .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "tumor promoting inflammation"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: Hepatocellular carcinoma ( HCC ) , one of the most frequent and deadliest cancers , has been increasing considerably in the United States . In the absence of a proven effective therapy for HCC , novel chemopreventive strategies are urgently needed to lower the current morbidity and mortality of HCC . Recently , we have reported that resveratrol , a compound present in grapes and red wine , significantly prevents diethylnitrosamine ( DENA)-induced liver tumorigenesis in rats , although the mechanism of action is not completely understood . In the present study , we have examined the underlying mechanisms of resveratrol chemoprevention of hepatocarcinogenesis by investigating the effects of resveratrol on oxidative damage and inflammatory markers during DENA-initiated rat liver carcinogenesis . There was a significant increase in hepatic lipid peroxidation and protein oxidation in carcinogen control animals compared with their normal counterparts at the end of the study ( 20 weeks ) . Elevated expressions of inducible nitric oxide synthase and 3-nitrotyrosine were noticed in the livers of the same animals . Dietary resveratrol ( 50-300 mg/kg ) administered throughout the study reversed all the aforementioned markers in a dose-responsive fashion in rats challenged with DENA . Resveratrol also elevated the protein and mRNA expression of hepatic nuclear factor E2-related factor 2 ( Nrf2 ) . Results of the present investigation provide evidence that attenuation of oxidative stress and suppression of inflammatory response mediated by Nrf2 could be implicated , at least in part , in the chemopreventive effects of this dietary agent against chemically induced hepatic tumorigenesis in rats . The outcome of this study may benefit the development of resveratrol in the prevention and intervention of human HCC .
OUTPUT:
|
HoC565 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: SWAP-70 , a phosphatidylinositol trisphosphate ( PtdIns(3,4,5)P(3) ) binding protein , has been suggested to be involved in transformation of mouse embryo fibroblasts ( MEFs ) as well as membrane ruffling after growth factor stimulation of the cells . A mutant , SWAP-70-374 , was found to be able to bind to F-actin in vitro , whereas wild-type SWAP-70 failed to do so . This mutant was present at the plasma membrane without any stimulation while the wild-type protein was present only in the cytosol unless cells were stimulated with EGF . Expression of this mutant in MEFs resulted in morphologic transformation , fast growth , and loss of contact inhibition , suggesting that SWAP-70 with this mutation can transform the cells . ERK1/2 was activated in SWAP-70-374-transformed cells . Use of MEK inhibitors revealed that the ERK1/2 pathway does not affect the cell growth of MEFs but is responsible for loss of contact inhibition . To investigate the function of SWAP-70 further , drugs that can inhibit SWAP-70-dependent cell responses were screened . Among various drugs , sanguinarine was found to inhibit transformation of MEFs by SWAP-70-374 . This drug was able to inhibit SWAP-70-mediated membrane ruffling as well , suggesting that its effect was closely related to the SWAP-70 signaling pathway . These results suggest that SWAP-70-374 can activate some signaling pathways , including the ERK1/2 pathway , to transform MEFs .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "evading growth suppressors"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: SWAP-70 , a phosphatidylinositol trisphosphate ( PtdIns(3,4,5)P(3) ) binding protein , has been suggested to be involved in transformation of mouse embryo fibroblasts ( MEFs ) as well as membrane ruffling after growth factor stimulation of the cells . A mutant , SWAP-70-374 , was found to be able to bind to F-actin in vitro , whereas wild-type SWAP-70 failed to do so . This mutant was present at the plasma membrane without any stimulation while the wild-type protein was present only in the cytosol unless cells were stimulated with EGF . Expression of this mutant in MEFs resulted in morphologic transformation , fast growth , and loss of contact inhibition , suggesting that SWAP-70 with this mutation can transform the cells . ERK1/2 was activated in SWAP-70-374-transformed cells . Use of MEK inhibitors revealed that the ERK1/2 pathway does not affect the cell growth of MEFs but is responsible for loss of contact inhibition . To investigate the function of SWAP-70 further , drugs that can inhibit SWAP-70-dependent cell responses were screened . Among various drugs , sanguinarine was found to inhibit transformation of MEFs by SWAP-70-374 . This drug was able to inhibit SWAP-70-mediated membrane ruffling as well , suggesting that its effect was closely related to the SWAP-70 signaling pathway . These results suggest that SWAP-70-374 can activate some signaling pathways , including the ERK1/2 pathway , to transform MEFs .
OUTPUT:
|
HoC1035 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: OBJECTIVE In addition to its effects on cholesterol levels , apoE3 has lipid-independent effects that contribute to cardiovascular protection ; one of these effects is the ability to inhibit cell cycling in VSMCs . The goal of this study was to identify and characterize cell cycle-regulatory mechanisms responsible for the anti-mitogenic effect of apoE . METHODS AND RESULTS Primary VSMCs were stimulated with serum in the absence or presence of apoE3. apoE3 upregulated expression of the cdk inhibitor , p27(kip1) , in primary VSMCs , and this effect required Cox2 and activation of PGI(2)-IP signaling . The microRNA family , miR221/222 has recently been identified as a post-translational regulator of p27 , and apoE3 inhibited miR221/222 expression in a Cox2- and PGI(2)/IP-dependent manner . Moreover , reconstituted miR222 expression was sufficient to override the effects of apoE on p27 expression and S phase entry . The ability to repress expression of miR221/222 is shared by apoE3-containing HDL but is absent from apoA-1 , LDL and apoE-depleted HDL . All three apoE isoforms regulate miR221/222 , and the effect is independent of the C-terminal lipid-binding domain. miR221/222 levels are increased in the aortae of apoE3-null mice and reduced when apoE3 expression is reconstituted by adeno-associated virus infection . Thus , regulation of miR221/222 by apoE3 occurs invivo as well as invitro . CONCLUSIONS ApoE inhibits VSMC proliferation by regulating p27 through miR221/222 . Control of cell cycle-regulatory microRNAs adds a new dimension to the spectrum of cardiovascular protective effects afforded by apoE and apoE-HDL .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "evading growth suppressors"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: OBJECTIVE In addition to its effects on cholesterol levels , apoE3 has lipid-independent effects that contribute to cardiovascular protection ; one of these effects is the ability to inhibit cell cycling in VSMCs . The goal of this study was to identify and characterize cell cycle-regulatory mechanisms responsible for the anti-mitogenic effect of apoE . METHODS AND RESULTS Primary VSMCs were stimulated with serum in the absence or presence of apoE3. apoE3 upregulated expression of the cdk inhibitor , p27(kip1) , in primary VSMCs , and this effect required Cox2 and activation of PGI(2)-IP signaling . The microRNA family , miR221/222 has recently been identified as a post-translational regulator of p27 , and apoE3 inhibited miR221/222 expression in a Cox2- and PGI(2)/IP-dependent manner . Moreover , reconstituted miR222 expression was sufficient to override the effects of apoE on p27 expression and S phase entry . The ability to repress expression of miR221/222 is shared by apoE3-containing HDL but is absent from apoA-1 , LDL and apoE-depleted HDL . All three apoE isoforms regulate miR221/222 , and the effect is independent of the C-terminal lipid-binding domain. miR221/222 levels are increased in the aortae of apoE3-null mice and reduced when apoE3 expression is reconstituted by adeno-associated virus infection . Thus , regulation of miR221/222 by apoE3 occurs invivo as well as invitro . CONCLUSIONS ApoE inhibits VSMC proliferation by regulating p27 through miR221/222 . Control of cell cycle-regulatory microRNAs adds a new dimension to the spectrum of cardiovascular protective effects afforded by apoE and apoE-HDL .
OUTPUT:
|
HoC229 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: A new cell line , CB109 , has been established from a human glioblastoma multiforme . The cytoskeleton was positive for glial fibrillary acidic protein , vimentin and fibronectin . Hyaluronan ( HA ) and the HA-binding protein hyaluronectin ( HN ) were expressed in the cell cytoplasm and in the extracellular matrix of spheroids and plated cells . Hyaluronidase did not prevent spheroid formation suggesting that HA was not involved in the cell-cell adhesion . HA precoating prevented cell adherence to the plates and favoured spheroid formation . HA was secreted in relatively large amounts into the culture medium . High performance liquid chromatography demonstrated that HA was in the high molecular weight form . The rate of HN secretion by cells was very low . Basic fibroblast growth factor significantly increased the proliferation in vitro and tumour growth after grafting into nude mice . The epidermal growth factor receptor was not expressed on cultivated CB109 cells . Cytogenetic analysis showed polysomy 7 , structural rearrangement of chromosome 10 short arm and a translocation 13q13-q14 without detectable alteration of the RB gene .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "sustaining proliferative signaling"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: A new cell line , CB109 , has been established from a human glioblastoma multiforme . The cytoskeleton was positive for glial fibrillary acidic protein , vimentin and fibronectin . Hyaluronan ( HA ) and the HA-binding protein hyaluronectin ( HN ) were expressed in the cell cytoplasm and in the extracellular matrix of spheroids and plated cells . Hyaluronidase did not prevent spheroid formation suggesting that HA was not involved in the cell-cell adhesion . HA precoating prevented cell adherence to the plates and favoured spheroid formation . HA was secreted in relatively large amounts into the culture medium . High performance liquid chromatography demonstrated that HA was in the high molecular weight form . The rate of HN secretion by cells was very low . Basic fibroblast growth factor significantly increased the proliferation in vitro and tumour growth after grafting into nude mice . The epidermal growth factor receptor was not expressed on cultivated CB109 cells . Cytogenetic analysis showed polysomy 7 , structural rearrangement of chromosome 10 short arm and a translocation 13q13-q14 without detectable alteration of the RB gene .
OUTPUT:
|
HoC1068 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: We recently reported that chronic myeloid leukaemia ( CML ) patients harbour high levels of STAT5 when they progress to advanced phases of disease . Advanced disease is characterized by an increased incidence of BCR-ABL1 mutations . We now describe a highly significant correlation between STAT5 expression and the incidence of BCR-ABL1 mutations in primary CML . Forced expression of STAT5 in murine BCR-ABL1 transformed cells sufficed to enhance the production of reactive oxygen species ( ROS ) and to trigger DNA damage . STAT5-mediated ROS production is independent of JAK2 but requires concomitant BCR-ABL1 signalling as forced STAT5 expression in untransformed BCR-ABL1 negative cells has no impact on ROS levels . Only within the context of a BCR-ABL1 positive cell does STAT5 transcriptionally regulate a target gene or set of genes that causes the enhanced ROS production . Our study suggests the existence of a feed-forward loop accelerating disease progression , in which BCR-ABL1 enhances its own mutation rate in a STAT5-ROS dependent manner . This model explains the increased occurrence of inhibitor-resistant BCR-ABL1 mutations in advanced disease stages driven and characterized by high STAT5 expression .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "genomic instability and mutation;tumor promoting inflammation"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: We recently reported that chronic myeloid leukaemia ( CML ) patients harbour high levels of STAT5 when they progress to advanced phases of disease . Advanced disease is characterized by an increased incidence of BCR-ABL1 mutations . We now describe a highly significant correlation between STAT5 expression and the incidence of BCR-ABL1 mutations in primary CML . Forced expression of STAT5 in murine BCR-ABL1 transformed cells sufficed to enhance the production of reactive oxygen species ( ROS ) and to trigger DNA damage . STAT5-mediated ROS production is independent of JAK2 but requires concomitant BCR-ABL1 signalling as forced STAT5 expression in untransformed BCR-ABL1 negative cells has no impact on ROS levels . Only within the context of a BCR-ABL1 positive cell does STAT5 transcriptionally regulate a target gene or set of genes that causes the enhanced ROS production . Our study suggests the existence of a feed-forward loop accelerating disease progression , in which BCR-ABL1 enhances its own mutation rate in a STAT5-ROS dependent manner . This model explains the increased occurrence of inhibitor-resistant BCR-ABL1 mutations in advanced disease stages driven and characterized by high STAT5 expression .
OUTPUT:
|
HoC83 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: The INK4a/ARF tumor suppressor locus is implicated in the senescence-like growth arrest provoked by oncogenic Ras in primary cells . INK4a and ARF are distinct proteins encoded by transcripts in which a shared exon is decoded in alternative reading frames . Here we analyze dermal fibroblasts ( designated Q34 ) from an individual carrying independent missense mutations in each copy of the common exon . Both mutations alter the amino acid sequence of INK4a and functionally impair the protein , although they do so to different degrees . Only one of the mutations affects the sequence of ARF , causing an apparently innocuous change near its carboxy terminus . Unlike normal human fibroblasts , Q34 cells are not permanently arrested by Ras or its downstream effectors Ets1 and Ets2 . Moreover , ectopic Ras enables the cells to grow as anchorage-independent colonies , and in relatively young Q34 cells anchorage independence can be achieved without addition of telomerase or perturbation of the p53 pathway . Whereas ARF plays the principal role in Ras-induced arrest of mouse fibroblasts , our data imply that INK4a assumes this role in human fibroblasts .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "genomic instability and mutation"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: The INK4a/ARF tumor suppressor locus is implicated in the senescence-like growth arrest provoked by oncogenic Ras in primary cells . INK4a and ARF are distinct proteins encoded by transcripts in which a shared exon is decoded in alternative reading frames . Here we analyze dermal fibroblasts ( designated Q34 ) from an individual carrying independent missense mutations in each copy of the common exon . Both mutations alter the amino acid sequence of INK4a and functionally impair the protein , although they do so to different degrees . Only one of the mutations affects the sequence of ARF , causing an apparently innocuous change near its carboxy terminus . Unlike normal human fibroblasts , Q34 cells are not permanently arrested by Ras or its downstream effectors Ets1 and Ets2 . Moreover , ectopic Ras enables the cells to grow as anchorage-independent colonies , and in relatively young Q34 cells anchorage independence can be achieved without addition of telomerase or perturbation of the p53 pathway . Whereas ARF plays the principal role in Ras-induced arrest of mouse fibroblasts , our data imply that INK4a assumes this role in human fibroblasts .
OUTPUT:
|
HoC778 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: The epidermal growth factor receptor ( EGFR ) is a member of the HER family receptors and its activation induced by its natural ligand EGF results in colon cancer growth and progression . Panitumumab ( pmAb ) is a fully human IgG2 anti-EGFR antibody that blocks the EGFR actions . In the present study , we evaluated the effects of pmAb on the EGF-mediated cellular responses in a panel of colon cancer cells ( HCT-8 , HT-29 , DLD-1 and HCT-116 ) . HCT-1116 and DLD-1 cells showed no significant EGF-dependent cell proliferation ; HT-29 and HCT-8 exhibited an EGF-dependent proliferation , with HCT-8 cells to be the most responsive with significant EGFR phosphorylation upon treatment with EGF . The effects of pmAb were then evaluated in the most EGF-responsive cells , HCT-8 . In that respect , pmAb impedes the signaling cascade mediated by EGFR intracellular phosphorylation and activity of focal adhesion kinase ( FAK ) as well as the EGF-induced invasive and migratory potential of colon cancer cells . At the level of matrix effectors implicated in colon cancer progression we report that pmAb is a potent inhibitor of constitute and EGF-mediated gene expression of certain matrix effectors , such as membrane-type 1 metalloproteinase ( MT1-MMP ) , extracellular metalloproteinases inducer ( EMMPRIN ) , urokinase plasminogen activator ( uPA ) and syndecan-4 . The obtained data demonstrated that pmAb is a specific blocker of EGF-mediated EGFR activation , resulting in a significant inhibition of colon cancer cell proliferation in early stages of growth , migration and invasiveness as well as of matrix effector implicated in cancer progression .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "sustaining proliferative signaling;activating invasion and metastasis"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: The epidermal growth factor receptor ( EGFR ) is a member of the HER family receptors and its activation induced by its natural ligand EGF results in colon cancer growth and progression . Panitumumab ( pmAb ) is a fully human IgG2 anti-EGFR antibody that blocks the EGFR actions . In the present study , we evaluated the effects of pmAb on the EGF-mediated cellular responses in a panel of colon cancer cells ( HCT-8 , HT-29 , DLD-1 and HCT-116 ) . HCT-1116 and DLD-1 cells showed no significant EGF-dependent cell proliferation ; HT-29 and HCT-8 exhibited an EGF-dependent proliferation , with HCT-8 cells to be the most responsive with significant EGFR phosphorylation upon treatment with EGF . The effects of pmAb were then evaluated in the most EGF-responsive cells , HCT-8 . In that respect , pmAb impedes the signaling cascade mediated by EGFR intracellular phosphorylation and activity of focal adhesion kinase ( FAK ) as well as the EGF-induced invasive and migratory potential of colon cancer cells . At the level of matrix effectors implicated in colon cancer progression we report that pmAb is a potent inhibitor of constitute and EGF-mediated gene expression of certain matrix effectors , such as membrane-type 1 metalloproteinase ( MT1-MMP ) , extracellular metalloproteinases inducer ( EMMPRIN ) , urokinase plasminogen activator ( uPA ) and syndecan-4 . The obtained data demonstrated that pmAb is a specific blocker of EGF-mediated EGFR activation , resulting in a significant inhibition of colon cancer cell proliferation in early stages of growth , migration and invasiveness as well as of matrix effector implicated in cancer progression .
OUTPUT:
|
HoC781 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: OBJECTIVE To investigate the relationship between lymphangiogenesis and lymphatic metastasis in cervical squamous carcinoma . METHODS Eighty cases of invasive cervical squamous cancer were selected as objects of our study . Double immunohistochemical staining with antibodies against lymphatic vessel endothelial hyaluronan receptor 1 and Ki-67 was used to label the lymphatic vessels and mark the proliferative lymphatic vessels in cervical squamous cancer . The peritumoral lymphatic vessel density and intratumoral lymphatic vessel density was assessed . The lymphatic vessels proliferation index was evaluated by calculating Ki-67 proliferation index ( PI ) to reflect the lymphangiogenesis of cervical squamous cancer . Then the correlation between lymphangiogenesis and clinicopathologic features of cervical squamous cancer was analyzed . RESULTS The LVD of cervical cancer ( 15.23 � 3.6 ) was clearly higher than that of the adjacent normal cervical subepithelial tissues ( 9.9 � 2.5 , P < ; 0.001 ) . The peritumoral lymphatic vessel density of cervical cancer ( 18.75 � 4.3 ) was significantly higher than the intratumoral lymphatic vessel density of cervical cancer ( 11.71 � 4.9 , P < ; 0.001 ) . Lymphatic PI ( LPI ) of cervical cancer ( 0.258 � 0.07 ) was higher than that of the adjacent normal cervical subepithelial tissues ( 0.068 � 0.08 , P < ; 0.001 ) . The peritumoral lymphatic vessel PI of cervical cancer ( 0.324 � 0.06 ) was notably higher than the intratumoral lymphatic vessel PI of cervical cancer ( 0.232 � 0.06 , P < ; 0.001 ) . Peritumoral lymphatic vessel density and peritumoral lymphatic vessel were clearly associated with the lymph node metastasis ( P = 0.001 and P = 0.002 , respectively ) and lymphovascular space invasion ( P = 0.024 and P = 0.01 , respectively ) . CONCLUSIONS The high density of peritumoral lymphatic vessels is a potential predictor of more aggressive phenotype of cervical squamous cancer .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "inducing angiogenesis;activating invasion and metastasis"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: OBJECTIVE To investigate the relationship between lymphangiogenesis and lymphatic metastasis in cervical squamous carcinoma . METHODS Eighty cases of invasive cervical squamous cancer were selected as objects of our study . Double immunohistochemical staining with antibodies against lymphatic vessel endothelial hyaluronan receptor 1 and Ki-67 was used to label the lymphatic vessels and mark the proliferative lymphatic vessels in cervical squamous cancer . The peritumoral lymphatic vessel density and intratumoral lymphatic vessel density was assessed . The lymphatic vessels proliferation index was evaluated by calculating Ki-67 proliferation index ( PI ) to reflect the lymphangiogenesis of cervical squamous cancer . Then the correlation between lymphangiogenesis and clinicopathologic features of cervical squamous cancer was analyzed . RESULTS The LVD of cervical cancer ( 15.23 � 3.6 ) was clearly higher than that of the adjacent normal cervical subepithelial tissues ( 9.9 � 2.5 , P < ; 0.001 ) . The peritumoral lymphatic vessel density of cervical cancer ( 18.75 � 4.3 ) was significantly higher than the intratumoral lymphatic vessel density of cervical cancer ( 11.71 � 4.9 , P < ; 0.001 ) . Lymphatic PI ( LPI ) of cervical cancer ( 0.258 � 0.07 ) was higher than that of the adjacent normal cervical subepithelial tissues ( 0.068 � 0.08 , P < ; 0.001 ) . The peritumoral lymphatic vessel PI of cervical cancer ( 0.324 � 0.06 ) was notably higher than the intratumoral lymphatic vessel PI of cervical cancer ( 0.232 � 0.06 , P < ; 0.001 ) . Peritumoral lymphatic vessel density and peritumoral lymphatic vessel were clearly associated with the lymph node metastasis ( P = 0.001 and P = 0.002 , respectively ) and lymphovascular space invasion ( P = 0.024 and P = 0.01 , respectively ) . CONCLUSIONS The high density of peritumoral lymphatic vessels is a potential predictor of more aggressive phenotype of cervical squamous cancer .
OUTPUT:
|
HoC564 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: BACKGROUND Epidemiologic data have shown that obesity independently increases colorectal cancer ( CRC ) risk , but the mechanisms are poorly understood . Obesity is an inflammatory state , and chronic colonic inflammation induces CRC . OBJECTIVE We conducted this proof-of-principle study to seek evidence of obesity-associated colorectal inflammation and to evaluate effects of diet-induced weight loss . DESIGN We measured inflammatory cytokines , gene arrays , and macrophage infiltration in rectosigmoid mucosal biopsies of 10 obese premenopausal women [ mean ± SD body mass index ( in kg/m(2) ) : 35 ± 3.5 ] before and after weight loss induced by a very-low-calorie diet . RESULTS Subjects lost a mean ( ±SD ) of 10.1 ± 1% of their initial weight . Weight loss significantly reduced fasting blood glucose , total cholesterol , triglycerides , LDL , tumor necrosis factor-α ( TNF-α ) , and interleukin ( IL)-8 concentrations ( P < ; 0.05 ) . After weight loss , rectosigmoid biopsies showed a 25-57% reduction in TNF-α , IL-1β , IL-8 , and monocyte chemotactic protein 1 concentrations ( P < ; 0.05 ) . T cell and macrophage counts decreased by 28% and 42% , respectively ( P < ; 0.05 ) . Gene arrays showed dramatic down-regulation of proinflammatory cytokine and chemokine pathways , prostaglandin metabolism , and the transcription factors STAT3 ( signal transducer and activator of transcription 3 ) and nuclear transcription factor κB . Weight loss reduced expression of FOS and JUN genes and down-regulated oxidative stress pathways and the transcription factors ATF ( activating transcription factor ) and CREB ( cyclic AMP response element-binding ) . CONCLUSIONS Our data show that diet-induced weight loss in obese individuals reduces colorectal inflammation and greatly modulates inflammatory and cancer-related gene pathways . These data imply that obesity is accompanied by inflammation in the colorectal mucosa and that diet-induced weight loss reduces this inflammatory state and may thereby lower CRC risk .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "tumor promoting inflammation"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: BACKGROUND Epidemiologic data have shown that obesity independently increases colorectal cancer ( CRC ) risk , but the mechanisms are poorly understood . Obesity is an inflammatory state , and chronic colonic inflammation induces CRC . OBJECTIVE We conducted this proof-of-principle study to seek evidence of obesity-associated colorectal inflammation and to evaluate effects of diet-induced weight loss . DESIGN We measured inflammatory cytokines , gene arrays , and macrophage infiltration in rectosigmoid mucosal biopsies of 10 obese premenopausal women [ mean ± SD body mass index ( in kg/m(2) ) : 35 ± 3.5 ] before and after weight loss induced by a very-low-calorie diet . RESULTS Subjects lost a mean ( ±SD ) of 10.1 ± 1% of their initial weight . Weight loss significantly reduced fasting blood glucose , total cholesterol , triglycerides , LDL , tumor necrosis factor-α ( TNF-α ) , and interleukin ( IL)-8 concentrations ( P < ; 0.05 ) . After weight loss , rectosigmoid biopsies showed a 25-57% reduction in TNF-α , IL-1β , IL-8 , and monocyte chemotactic protein 1 concentrations ( P < ; 0.05 ) . T cell and macrophage counts decreased by 28% and 42% , respectively ( P < ; 0.05 ) . Gene arrays showed dramatic down-regulation of proinflammatory cytokine and chemokine pathways , prostaglandin metabolism , and the transcription factors STAT3 ( signal transducer and activator of transcription 3 ) and nuclear transcription factor κB . Weight loss reduced expression of FOS and JUN genes and down-regulated oxidative stress pathways and the transcription factors ATF ( activating transcription factor ) and CREB ( cyclic AMP response element-binding ) . CONCLUSIONS Our data show that diet-induced weight loss in obese individuals reduces colorectal inflammation and greatly modulates inflammatory and cancer-related gene pathways . These data imply that obesity is accompanied by inflammation in the colorectal mucosa and that diet-induced weight loss reduces this inflammatory state and may thereby lower CRC risk .
OUTPUT:
|
HoC604 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: Estrogen receptor ( ER ) and NF-κB are transcription factors with profound effects on breast cancer cell proliferation and survival . While many studies demonstrate that ER and NF-κB can repress each other , we previously identified a gene signature that is synergistically upregulated by these two factors in more aggressive luminal B breast tumors . Herein , we examine a novel mechanism of cross talk between ER and NF-κB that results in the upregulation of the antiapoptotic gene BIRC3 ( also known as cIAP2 ) . We demonstrate that NF-κB , acting through two response elements , is required for ER recruitment to an adjacent estrogen response element ( ERE ) in the BIRC3 promoter . This effect is accompanied by a major increase in NF-κB-dependent histone acetylation around the ERE . Interestingly , CBP , a histone acetyltransferase previously implicated in repressive interactions between ER and NF-κB , plays a permissive role by promoting histone acetylation and ER recruitment , as well as enhanced expression of BIRC3 . These findings suggest a new gene regulatory mechanism by which inflammation and NF-κB activation can influence ER recruitment to inherently inactive ER binding sites . This fine-tuning mechanism may explain how two factors that generally repress each other's activity may work together on certain genes to promote breast cancer cell survival and tumor progression .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "sustaining proliferative signaling;tumor promoting inflammation"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: Estrogen receptor ( ER ) and NF-κB are transcription factors with profound effects on breast cancer cell proliferation and survival . While many studies demonstrate that ER and NF-κB can repress each other , we previously identified a gene signature that is synergistically upregulated by these two factors in more aggressive luminal B breast tumors . Herein , we examine a novel mechanism of cross talk between ER and NF-κB that results in the upregulation of the antiapoptotic gene BIRC3 ( also known as cIAP2 ) . We demonstrate that NF-κB , acting through two response elements , is required for ER recruitment to an adjacent estrogen response element ( ERE ) in the BIRC3 promoter . This effect is accompanied by a major increase in NF-κB-dependent histone acetylation around the ERE . Interestingly , CBP , a histone acetyltransferase previously implicated in repressive interactions between ER and NF-κB , plays a permissive role by promoting histone acetylation and ER recruitment , as well as enhanced expression of BIRC3 . These findings suggest a new gene regulatory mechanism by which inflammation and NF-κB activation can influence ER recruitment to inherently inactive ER binding sites . This fine-tuning mechanism may explain how two factors that generally repress each other's activity may work together on certain genes to promote breast cancer cell survival and tumor progression .
OUTPUT:
|
HoC266 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: The use of substrates containing well defined adducts at precise sites , is required to perform a careful analysis of the toxic and mutagenic potential of a lesion . As a first step in this direction the octamer 5'-d(CCGGCGGT) , containing the sequence of the codons 12 d(GGC) and 13 d(GGT) of the human H-ras gene , was reacted with the antitumoral drug cis-diamminedichloroplatinum(II) . The platinated products have been purified by HPLC . A first set of experiments , including enzymatic digestions with nuclease P1 followed by alkaline phosphatase and acid-catalysed hydrolysis , allowed us to determine which bases were engaged in the cis-DDP lesions . Our results indicate that only guanine residues were chelated with cisplatin to yield bifunctional adducts . Furthermore , by performing enzymatic digestions with phosphodiesterases , we have located the adducts with respect to the 5 ' end of the octamer . Among the purified and characterized platinated oligonucleotides , three present a particular interest , since we have shown here that the cis-d(GpG) adduct is precisely situated either at the d(GGC) or at the d(GGT) or at both sites of their sequence .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "genomic instability and mutation"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: The use of substrates containing well defined adducts at precise sites , is required to perform a careful analysis of the toxic and mutagenic potential of a lesion . As a first step in this direction the octamer 5'-d(CCGGCGGT) , containing the sequence of the codons 12 d(GGC) and 13 d(GGT) of the human H-ras gene , was reacted with the antitumoral drug cis-diamminedichloroplatinum(II) . The platinated products have been purified by HPLC . A first set of experiments , including enzymatic digestions with nuclease P1 followed by alkaline phosphatase and acid-catalysed hydrolysis , allowed us to determine which bases were engaged in the cis-DDP lesions . Our results indicate that only guanine residues were chelated with cisplatin to yield bifunctional adducts . Furthermore , by performing enzymatic digestions with phosphodiesterases , we have located the adducts with respect to the 5 ' end of the octamer . Among the purified and characterized platinated oligonucleotides , three present a particular interest , since we have shown here that the cis-d(GpG) adduct is precisely situated either at the d(GGC) or at the d(GGT) or at both sites of their sequence .
OUTPUT:
|
HoC314 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: OBJECTIVES Recently , it was revealed that carnosine inhibits growth of cells isolated from human malignant glioma . In order to understand how this effect is mediated , experiments were performed that addressed a possible influence of carnosine on energy metabolism . METHODS Cells from the glioma line T98G and primary cultured cells from human malignant glioma were cultivated in the presence of carnosine and inhibitors of cellular energy metabolism . As a specific inhibitor for anaerobic glycolysis , oxamate , and as an inhibitor for mitochondrial oxidative phosphorylation , potassium cyanide , were used , and the influence on ATP production was determined using cell-based assays . RESULTS The experiments identified glycolysis as crucial for ATP production in gliomas . In addition , ATP production by mitochondrial activity did not significantly contribute to ATP production and carnosine was identified to be an inhibitor of the vital anaerobic glycolysis . DISCUSSION Carnosine might be considered as a potential drug for the treatment of malignant glioma or other tumors since it inhibits the glycolytic energy metabolism that is crucial for cancer cells and malignant gliomas as shown in the current study . This is especially interesting since the dipeptide is a naturally occurring substance that should be well tolerated .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "cellular energetics"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: OBJECTIVES Recently , it was revealed that carnosine inhibits growth of cells isolated from human malignant glioma . In order to understand how this effect is mediated , experiments were performed that addressed a possible influence of carnosine on energy metabolism . METHODS Cells from the glioma line T98G and primary cultured cells from human malignant glioma were cultivated in the presence of carnosine and inhibitors of cellular energy metabolism . As a specific inhibitor for anaerobic glycolysis , oxamate , and as an inhibitor for mitochondrial oxidative phosphorylation , potassium cyanide , were used , and the influence on ATP production was determined using cell-based assays . RESULTS The experiments identified glycolysis as crucial for ATP production in gliomas . In addition , ATP production by mitochondrial activity did not significantly contribute to ATP production and carnosine was identified to be an inhibitor of the vital anaerobic glycolysis . DISCUSSION Carnosine might be considered as a potential drug for the treatment of malignant glioma or other tumors since it inhibits the glycolytic energy metabolism that is crucial for cancer cells and malignant gliomas as shown in the current study . This is especially interesting since the dipeptide is a naturally occurring substance that should be well tolerated .
OUTPUT:
|
HoC950 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: Lowering the threshold of cellular senescence , the process employed by cells to thwart abnormal cell proliferation , though inhibition of CDK2 or Skp2 ( regulator of CDK inhibitors ) has been recently suggested as a potential avenue for cancer treatment . In this study , we employ a published mathematical model of G1/S transition involving the DNA-damage signal transduction pathway to conduct carefully constructed computational experiments to highlight the effectiveness of manipulating cellular senescence in inhibiting damaged cell proliferation . We first demonstrate the suitability of the mathematical model to explore senescence by highlighting the overlap between senescence pathways and those involved in G1/S transition and DNA damage signal transduction . We then investigate the effect of CDK2 deficiency on senescence in healthy cells , followed by effectiveness of CDK2 deficiency in triggering senescence in DNA damaged cells . For this , we focus on the behaviour of CycE , whose peak response indicates G1/S transition , for several reduced CDK2 levels in healthy as well as two DNA-damage conditions to calculate the probability ( β ) or the percentage of CDK2 deficient cells passing G1/S checkpoint ( (1-β) indicates level of senescence ) . Results show that 50% CDK2 deficiency can cause senescence in all healthy cells in a fairly uniform cell population ; whereas , most healthy cells ( ≈67% ) in a heterogeneous population escape senescence . This finding is novel to our study . Under both low- and high-DNA damaged conditions , 50% CDK deficiency can cause 65% increase in senescence in a heterogeneous cell population . Furthermore , the model analyses the relationship between CDK2 and its CKIs ( p21 , p27 ) to help search for other effective ways to bring forward cellular senescence . Results show that the degradation rate of p21 and initial concentration of p27 are effective in lowering CDK2 levels to lower the senescence threshold . Specifically , CDK2 and p27 are the most effective in triggering senescence while p21 having a smaller influence . While receiving experimental support , these findings specify in detail the inhibitory effects of CKIs . However , simultaneous variation of CDK2 and CKIs produces a dramatic reduction of damage cells passing the G1/S with CDK2&p27 combination causing senescence in almost all damaged cells . This combined effect of CDK2&CKIs on senescence is a novel contribution in this study . A review of the crucial protein complexes revealed that the concentration of active CycE/CDK2-p that controls cell cycle arrest provides support for the above findings with CycE/CDK2-p undergoing the largest reduction ( over 100% ) under the combined CDK2&CKI conditions leading to the arrest of most of the damaged cells . Our study thus provides quantitative assessments for the previously published qualitative findings on senescence and highlights new avenues for bringing forward senescence bar .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "enabling replicative immortality;genomic instability and mutation;evading growth suppressors"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: Lowering the threshold of cellular senescence , the process employed by cells to thwart abnormal cell proliferation , though inhibition of CDK2 or Skp2 ( regulator of CDK inhibitors ) has been recently suggested as a potential avenue for cancer treatment . In this study , we employ a published mathematical model of G1/S transition involving the DNA-damage signal transduction pathway to conduct carefully constructed computational experiments to highlight the effectiveness of manipulating cellular senescence in inhibiting damaged cell proliferation . We first demonstrate the suitability of the mathematical model to explore senescence by highlighting the overlap between senescence pathways and those involved in G1/S transition and DNA damage signal transduction . We then investigate the effect of CDK2 deficiency on senescence in healthy cells , followed by effectiveness of CDK2 deficiency in triggering senescence in DNA damaged cells . For this , we focus on the behaviour of CycE , whose peak response indicates G1/S transition , for several reduced CDK2 levels in healthy as well as two DNA-damage conditions to calculate the probability ( β ) or the percentage of CDK2 deficient cells passing G1/S checkpoint ( (1-β) indicates level of senescence ) . Results show that 50% CDK2 deficiency can cause senescence in all healthy cells in a fairly uniform cell population ; whereas , most healthy cells ( ≈67% ) in a heterogeneous population escape senescence . This finding is novel to our study . Under both low- and high-DNA damaged conditions , 50% CDK deficiency can cause 65% increase in senescence in a heterogeneous cell population . Furthermore , the model analyses the relationship between CDK2 and its CKIs ( p21 , p27 ) to help search for other effective ways to bring forward cellular senescence . Results show that the degradation rate of p21 and initial concentration of p27 are effective in lowering CDK2 levels to lower the senescence threshold . Specifically , CDK2 and p27 are the most effective in triggering senescence while p21 having a smaller influence . While receiving experimental support , these findings specify in detail the inhibitory effects of CKIs . However , simultaneous variation of CDK2 and CKIs produces a dramatic reduction of damage cells passing the G1/S with CDK2&p27 combination causing senescence in almost all damaged cells . This combined effect of CDK2&CKIs on senescence is a novel contribution in this study . A review of the crucial protein complexes revealed that the concentration of active CycE/CDK2-p that controls cell cycle arrest provides support for the above findings with CycE/CDK2-p undergoing the largest reduction ( over 100% ) under the combined CDK2&CKI conditions leading to the arrest of most of the damaged cells . Our study thus provides quantitative assessments for the previously published qualitative findings on senescence and highlights new avenues for bringing forward senescence bar .
OUTPUT:
|
HoC921 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: SCOPE Glyceollins are a novel class of soybean phytoalexins with potential cancer-preventive and antiestrogenic effects . The angiogenic cascade during tumor development consists of the release of angiogenic factors and binding of angiogenic factors to receptors on endothelial cells to activate downstream signaling pathways . However , the potential medicinal value of glyceollins , especially in antiangiogenesis , remains unexplored . METHODS AND RESULTS Here , we investigated the antiangiogenic activity of glyceollins and their underlying mechanisms . Glyceollins inhibited vascular endothelial growth factor ( VEGF ) or basic fibroblast growth factor ( bFGF ) induced in vitro angiogenic activity . Glyceollins inhibited VEGF receptor-2 or FGF receptor-1 activity and their downstream signaling pathways such as extracellular regulated kinase 1/2 , c-Jun N-terminal kinase , as well as p38 mitogen-activated protein kinase and focal adhesion kinase induced by VEGF or bFGF . Glyceollins significantly suppressed VEGF receptor-2 kinase activity assayed by the ELISA . Glyceollins significantly attenuated in vivo and ex vivo microvessel development in a dose-dependent manner and tumor growth by suppressing microvessel density in Lewis lung carcinoma ( LLC ) mouse xenograft . CONCLUSION Thus , glyceollins , elicited ingredients of soy source , target the signaling pathways mediated by VEGF or bFGF , providing new perspectives into potential therapeutics for preventing and treating hypervascularized diseases including cancer .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "inducing angiogenesis"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: SCOPE Glyceollins are a novel class of soybean phytoalexins with potential cancer-preventive and antiestrogenic effects . The angiogenic cascade during tumor development consists of the release of angiogenic factors and binding of angiogenic factors to receptors on endothelial cells to activate downstream signaling pathways . However , the potential medicinal value of glyceollins , especially in antiangiogenesis , remains unexplored . METHODS AND RESULTS Here , we investigated the antiangiogenic activity of glyceollins and their underlying mechanisms . Glyceollins inhibited vascular endothelial growth factor ( VEGF ) or basic fibroblast growth factor ( bFGF ) induced in vitro angiogenic activity . Glyceollins inhibited VEGF receptor-2 or FGF receptor-1 activity and their downstream signaling pathways such as extracellular regulated kinase 1/2 , c-Jun N-terminal kinase , as well as p38 mitogen-activated protein kinase and focal adhesion kinase induced by VEGF or bFGF . Glyceollins significantly suppressed VEGF receptor-2 kinase activity assayed by the ELISA . Glyceollins significantly attenuated in vivo and ex vivo microvessel development in a dose-dependent manner and tumor growth by suppressing microvessel density in Lewis lung carcinoma ( LLC ) mouse xenograft . CONCLUSION Thus , glyceollins , elicited ingredients of soy source , target the signaling pathways mediated by VEGF or bFGF , providing new perspectives into potential therapeutics for preventing and treating hypervascularized diseases including cancer .
OUTPUT:
|
HoC1100 | [
{
"from": "human",
"value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: ANXA2 , a member of the annexin family , is overexpressed and plays important roles in tumor development . However , the significance of ANXA2 expression in gastric carcinoma has not been clarified.To elucidate its roles in growth of gastric cancer , ANXA2 expression in SGC-7901 cells was inhibited with a designated siRNA , then cell proliferation , cell cycling , apoptosis and motility were determined by MTT assay , flow cytometry , Hoechst 33342 staining and wound healing assay , respectively . To further assess the behavior of ANXA2 deleted SGC- 7901 cells , changes of microstructures were observed under fluorescence microscopy , laser scanning confocal microscopy and electron microscopy . We found that inhibition of ANXA2 expression caused cell proliferation to decrease significantly with G1 arrest , motility to be reduced with changes in pseudopodia/filopodia structure and F-actin and β-tubulin expression , and apoptosis to be enhanced albeit without significance . At the same time , ANXA2 deletion resulted in fewer pseudopodia/filopodia , non-stained areas were increased , contact inhibition among cells reappeared , and expression of F-actin and β-tubulin was decreased , with induction of polymerized disassembled forms . Taken together , these data suggest that ANXA2 overexpression is important to maintain the malignancy of cancer cells , and this member of the annexin family has potential to be considered as a target for the gene therapy of gastric carcinoma .\n OUTPUT:\n"
},
{
"from": "agent",
"value": "evading growth suppressors;resisting cell death;sustaining proliferative signaling"
}
] | The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
###
INPUT: ANXA2 , a member of the annexin family , is overexpressed and plays important roles in tumor development . However , the significance of ANXA2 expression in gastric carcinoma has not been clarified.To elucidate its roles in growth of gastric cancer , ANXA2 expression in SGC-7901 cells was inhibited with a designated siRNA , then cell proliferation , cell cycling , apoptosis and motility were determined by MTT assay , flow cytometry , Hoechst 33342 staining and wound healing assay , respectively . To further assess the behavior of ANXA2 deleted SGC- 7901 cells , changes of microstructures were observed under fluorescence microscopy , laser scanning confocal microscopy and electron microscopy . We found that inhibition of ANXA2 expression caused cell proliferation to decrease significantly with G1 arrest , motility to be reduced with changes in pseudopodia/filopodia structure and F-actin and β-tubulin expression , and apoptosis to be enhanced albeit without significance . At the same time , ANXA2 deletion resulted in fewer pseudopodia/filopodia , non-stained areas were increased , contact inhibition among cells reappeared , and expression of F-actin and β-tubulin was decreased , with induction of polymerized disassembled forms . Taken together , these data suggest that ANXA2 overexpression is important to maintain the malignancy of cancer cells , and this member of the annexin family has potential to be considered as a target for the gene therapy of gastric carcinoma .
OUTPUT:
|
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