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12
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1.08k
cancer_type
stringclasses
3 values
gene
dict
cancer
dict
CGE
stringclasses
2 values
CCS
stringclasses
3 values
PT
stringclasses
3 values
IGE
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4 values
expression_change_keyword_1
dict
expression_change_keyword_2
dict
10945637.s12
Thus, FGF6 is increased in PIN and prostate cancer and can promote the proliferation of the transformed prostatic epithelial cells via paracrine and autocrine mechanisms.
prostate
{ "name": "FGF6", "pos": [ 6, 9 ] }
{ "name": "prostate cancer", "pos": [ 35, 49 ] }
increased
normalTOcancer
causality
unchanged
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "increased", "pos": [ 14, 22 ], "type": "Positive_regulation" }
11722842.s0
Isolation and characterization of the major form of human MUC18 cDNA gene and correlation of MUC18 over-expression in prostate cancer cell lines and tissues with malignant progression.
prostate
{ "name": "MUC18", "pos": [ 93, 97 ] }
{ "name": "prostate cancer", "pos": [ 118, 132 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "over-expression", "pos": [ 99, 113 ], "type": "Gene_expression" }
{ "name": "over-expression", "pos": [ 99, 113 ], "type": "Positive_regulation" }
11722842.s13
We therefore conclude that MUC18 expression is increased during prostate cancer initiation (high grade PIN) and progression to carcinoma, and in metastatic cell lines and metastatic carcinoma.
prostate
{ "name": "MUC18", "pos": [ 27, 31 ] }
{ "name": "prostate cancer", "pos": [ 64, 78 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "expression", "pos": [ 33, 42 ], "type": "Gene_expression" }
{ "name": "increased", "pos": [ 47, 55 ], "type": "Positive_regulation" }
11839683.s9
These results demonstrate that in a sequence-specific manner, RIalpha antisense, via efficient depletion of the growth stimulatory molecule RIalpha, induces growth inhibition, apoptosis, and phenotypic (cell morphology) changes, providing an innovative approach to combat hormone-insensitive prostate cancer cell growth.
prostate
{ "name": "growth stimulatory molecule RIalpha", "pos": [ 112, 146 ] }
{ "name": "prostate cancer", "pos": [ 292, 306 ] }
decreased
cancerTOnormal
causality
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "depletion", "pos": [ 95, 103 ], "type": "Negative_regulation" }
12006585.s2
We have found that Cdc6 expression is down-regulated in prostate cancer as detected by semiquantitative reverse transcriptase-PCR of prostate cell lines and laser-captured microdissected prostate tissues.
prostate
{ "name": "Cdc6", "pos": [ 19, 22 ] }
{ "name": "prostate cancer", "pos": [ 56, 70 ] }
decreased
normalTOcancer
observation
unchanged
{ "name": "expression", "pos": [ 24, 33 ], "type": "Gene_expression" }
{ "name": "down-regulated", "pos": [ 38, 51 ], "type": "Negative_regulation" }
12006585.s4
Furthermore, a 100-fold reduction in the transcription efficiency of the Cdc6 promoter-luciferase construct was noted in the metastatic PC3 cells compared with that in BPH-1 cells.
prostate
{ "name": "Cdc6 promoter-luciferase construct", "pos": [ 73, 106 ] }
{ "name": "PC3", "pos": [ 136, 138 ] }
decreased
normalTOcancer
observation
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "reduction", "pos": [ 24, 32 ], "type": "Negative_regulation" }
12409226.s7
Sustained increase of the c-myc gene product was detectable in PC-3 but not in DU-145 cells.
prostate
{ "name": "c-myc gene product", "pos": [ 26, 43 ] }
{ "name": "PC-3", "pos": [ 63, 66 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "increase", "pos": [ 10, 17 ], "type": "Positive_regulation" }
12409226.s8
Concurrently, we demonstrated BN-dependent activation of the transcription factor Elk-1 and significant increase of cell proliferation in both prostate cancer cell lines.
prostate
{ "name": "transcription factor Elk-1", "pos": [ 61, 86 ] }
{ "name": "prostate cancer", "pos": [ 143, 157 ] }
increased
normalTOcancer
observation
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "activation", "pos": [ 43, 52 ], "type": "Positive_regulation" }
12433721.s1
Electronic profiling of publicly available expressed sequence tag databases identified a gene, cysteine-rich secretoryprotein-3 (CRISP-3), that is up-regulated in prostate cancer, and of which the expression is relatively prostate-specific.
prostate
{ "name": "CRISP-3", "pos": [ 129, 135 ] }
{ "name": "prostate cancer", "pos": [ 163, 177 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "up-regulated", "pos": [ 147, 158 ], "type": "Positive_regulation" }
12569365.s4
Cdc25B is frequently overexpressed in human prostate cancer tissues (29 of 30; 97%).
prostate
{ "name": "Cdc25B", "pos": [ 0, 5 ] }
{ "name": "prostate cancer", "pos": [ 44, 58 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "overexpressed", "pos": [ 21, 33 ], "type": "Gene_expression" }
{ "name": "overexpressed", "pos": [ 21, 33 ], "type": "Positive_regulation" }
12598323.s1
PTOV1 was recently identified as a novel gene and protein during a differential display screening for genes overexpressed in prostate cancer.
prostate
{ "name": "PTOV1", "pos": [ 0, 4 ] }
{ "name": "prostate cancer", "pos": [ 125, 139 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "overexpressed", "pos": [ 108, 120 ], "type": "Gene_expression" }
{ "name": "overexpressed", "pos": [ 108, 120 ], "type": "Positive_regulation" }
12598323.s3
By immunohistochemical analysis, we have found that PTOV1 is overexpressed in 71% of 38 prostate carcinomas and in 80% of samples with prostate intraepithelial neoplasia.
prostate
{ "name": "PTOV1", "pos": [ 52, 56 ] }
{ "name": "prostate carcinomas", "pos": [ 88, 106 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "overexpressed", "pos": [ 61, 73 ], "type": "Gene_expression" }
{ "name": "overexpressed", "pos": [ 61, 73 ], "type": "Positive_regulation" }
12618764.s0
MEK5 overexpression is associated with metastatic prostate cancer, and stimulates proliferation, MMP-9 expression and invasion.
prostate
{ "name": "MEK5", "pos": [ 0, 3 ] }
{ "name": "prostate cancer", "pos": [ 50, 64 ] }
increased
normalTOcancer
causality
unchanged
{ "name": "overexpression", "pos": [ 5, 18 ], "type": "Gene_expression" }
{ "name": "overexpression", "pos": [ 5, 18 ], "type": "Positive_regulation" }
12875974.s2
The overexpression of Bax inhibitor-1 (BI-1) in prostate carcinoma and prostate cancer cell lines was confirmed by using Northern blot and Western blot analyses.
prostate
{ "name": "BI-1", "pos": [ 39, 42 ] }
{ "name": "prostate cancer", "pos": [ 71, 85 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "overexpression", "pos": [ 4, 17 ], "type": "Gene_expression" }
{ "name": "overexpression", "pos": [ 4, 17 ], "type": "Positive_regulation" }
12907652.s9
These observations suggest that U19 is growth inhibitory and tumor suppressive and that the disruption of androgen-dependent growth inhibition via U19 down-regulation is commonly associated with prostate cancer progression.
prostate
{ "name": "U19", "pos": [ 147, 149 ] }
{ "name": "prostate cancer", "pos": [ 195, 209 ] }
decreased
normalTOcancer
causality
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "down-regulation", "pos": [ 151, 165 ], "type": "Negative_regulation" }
14744752.s5
First, a comprehensive serial immunohistochemical analysis of primary and metastatic prostate cancer samples showed increased stage-specific expression of IL-11Ralpha during disease progression.
prostate
{ "name": "IL-11Ralpha", "pos": [ 155, 165 ] }
{ "name": "prostate cancer", "pos": [ 85, 99 ] }
increased
normalTOcancer
observation
unidentifiable
{ "name": "expression", "pos": [ 141, 150 ], "type": "Gene_expression" }
{ "name": "increased", "pos": [ 116, 124 ], "type": "Positive_regulation" }
14744778.s2
We have shown previously that although AP-2 is expressed highly in normal prostatic epithelium, its expression is lost in high-grade prostatic intraepithelial neoplasia and prostate cancer, suggesting that loss of AP-2 plays a role in prostate cancer development.
prostate
{ "name": "AP-2", "pos": [ 214, 217 ] }
{ "name": "prostate cancer", "pos": [ 173, 187 ] }
decreased
normalTOcancer
causality
unchanged
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "loss", "pos": [ 206, 209 ], "type": "Negative_regulation" }
14744778.s10
Elucidating the molecular events resulting from loss of AP-2 in the prostate epithelium has implications for the understanding and prevention of the onset of prostate cancer.
prostate
{ "name": "AP-2", "pos": [ 56, 59 ] }
{ "name": "prostate cancer", "pos": [ 158, 172 ] }
decreased
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "loss", "pos": [ 48, 51 ], "type": "Negative_regulation" }
14766760.s7
The interaction between FADD and caspase-8 was inhibited, but abrogation of JNK activity or HIPK3 expression was found to restore this interaction and increased the sensitivity of DU 145 cells to Fas receptor-mediated apoptosis.
prostate
{ "name": "HIPK3", "pos": [ 92, 96 ] }
{ "name": "DU 145", "pos": [ 180, 185 ] }
decreased
cancerTOnormal
causality
unidentifiable
{ "name": "expression", "pos": [ 98, 107 ], "type": "Gene_expression" }
{ "name": "abrogation", "pos": [ 62, 71 ], "type": "Negative_regulation" }
15026365.s14
In clinical prostate cancer specimens from patients with varying grades of disease, the stained tissue sections showed high levels of SREBP-1 protein compared with noncancerous prostate tissue.
prostate
{ "name": "SREBP-1 protein", "pos": [ 134, 148 ] }
{ "name": "prostate cancer", "pos": [ 12, 26 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "levels", "pos": [ 124, 129 ], "type": "Positive_regulation" }
15026365.s17
In summary, the LNCaP xenograft model of human prostate cancer as well as clinical specimens of prostate cancer demonstrated an up-regulation of SREBPs and their downstream effector genes during progression to androgen independence.
prostate
{ "name": "SREBPs", "pos": [ 145, 150 ] }
{ "name": "prostate cancer", "pos": [ 47, 61 ] }
increased
normalTOcancer
observation
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "up-regulation", "pos": [ 128, 140 ], "type": "Positive_regulation" }
15833840.s1
An increase in the activity of mitogen-activated protein kinase (MAPK) has been correlated with the progression of prostate cancer to advanced disease in humans.
prostate
{ "name": "mitogen-activated protein kinase", "pos": [ 31, 62 ] }
{ "name": "prostate cancer", "pos": [ 115, 129 ] }
increased
normalTOcancer
observation
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "increase", "pos": [ 3, 10 ], "type": "Positive_regulation" }
15833840.s3
Increasing RSK isoform 2 (RSK2) levels in the human prostate cancer line, LNCaP, enhanced prostate-specific antigen (PSA) expression, an important diagnostic marker for prostate cancer, whereas inhibiting RSK activity using a RSK-specific inhibitor, 3Ac-SL0101, decreased PSA expression.
prostate
{ "name": "PSA", "pos": [ 117, 119 ] }
{ "name": "prostate cancer", "pos": [ 52, 66 ] }
increased
normalTOcancer
observation
unidentifiable
{ "name": "expression", "pos": [ 122, 131 ], "type": "Gene_expression" }
{ "name": "enhanced", "pos": [ 81, 88 ], "type": "Positive_regulation" }
15833840.s3
Increasing RSK isoform 2 (RSK2) levels in the human prostate cancer line, LNCaP, enhanced prostate-specific antigen (PSA) expression, an important diagnostic marker for prostate cancer, whereas inhibiting RSK activity using a RSK-specific inhibitor, 3Ac-SL0101, decreased PSA expression.
prostate
{ "name": "PSA", "pos": [ 272, 274 ] }
{ "name": "prostate cancer", "pos": [ 52, 66 ] }
decreased
unidentifiable
{ "name": "expression", "pos": [ 276, 285 ], "type": "Gene_expression" }
{ "name": "decreased", "pos": [ 262, 270 ], "type": "Negative_regulation" }
15837784.s0
Down-regulation of ATM protein sensitizes human prostate cancer cells to radiation-induced apoptosis.
prostate
{ "name": "ATM protein", "pos": [ 19, 29 ] }
{ "name": "prostate cancer", "pos": [ 48, 62 ] }
decreased
cancerTOnormal
causality
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "Down-regulation", "pos": [ 0, 14 ], "type": "Negative_regulation" }
15897876.s7
CBX7 overexpression in LNCaP cells resulted in a slight growth advantage in both androgen-dependent and -independent conditions.
prostate
{ "name": "CBX7", "pos": [ 0, 3 ] }
{ "name": "LNCaP", "pos": [ 23, 27 ] }
increased
normalTOcancer
causality
unidentifiable
{ "name": "overexpression", "pos": [ 5, 18 ], "type": "Gene_expression" }
{ "name": "overexpression", "pos": [ 5, 18 ], "type": "Positive_regulation" }
16115918.s1
Cytochrome P450 1B1 (CYP1B1), a dioxin inducible member of the CYP supergene family, is overexpressed in various human malignancies including prostate cancer.
prostate
{ "name": "Cytochrome P450 1B1 (CYP1B1)", "pos": [ 0, 27 ] }
{ "name": "prostate cancer", "pos": [ 142, 156 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "overexpressed", "pos": [ 88, 100 ], "type": "Gene_expression" }
{ "name": "overexpressed", "pos": [ 88, 100 ], "type": "Positive_regulation" }
16424021.s0
Increased expression of osteopontin contributes to the progression of prostate cancer.
prostate
{ "name": "osteopontin", "pos": [ 24, 34 ] }
{ "name": "prostate cancer", "pos": [ 70, 84 ] }
increased
normalTOcancer
causality
unidentifiable
{ "name": "expression", "pos": [ 10, 19 ], "type": "Gene_expression" }
{ "name": "Increased", "pos": [ 0, 8 ], "type": "Positive_regulation" }
16601286.s0
Increased expression of type 2 3alpha-hydroxysteroid dehydrogenase/type 5 17beta-hydroxysteroid dehydrogenase (AKR1C3) and its relationship with androgen receptor in prostate carcinoma.
prostate
{ "name": "type 2 3alpha-hydroxysteroid dehydrogenase/type 5 17beta-hydroxysteroid dehydrogenase (AKR1C3)", "pos": [ 24, 117 ] }
{ "name": "prostate carcinoma", "pos": [ 166, 183 ] }
increased
unidentifiable
{ "name": "expression", "pos": [ 10, 19 ], "type": "Gene_expression" }
{ "name": "Increased", "pos": [ 0, 8 ], "type": "Positive_regulation" }
16601286.s13
We conclude that elevated expression of AKR1C3 is highly associated with prostate carcinoma.
prostate
{ "name": "AKR1C3", "pos": [ 40, 45 ] }
{ "name": "prostate carcinoma", "pos": [ 73, 90 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "expression", "pos": [ 26, 35 ], "type": "Gene_expression" }
{ "name": "elevated", "pos": [ 17, 24 ], "type": "Positive_regulation" }
16609016.s9
Kaplan-Meier survival analysis confirmed increased RPL19 expression to be highly predictive of shorter patient survival (P &lt; 0.05), revealing RPL19 to be a sensitive predictor of prostate cancer progression.
prostate
{ "name": "RPL19", "pos": [ 51, 55 ] }
{ "name": "prostate cancer", "pos": [ 182, 196 ] }
increased
unidentifiable
{ "name": "expression", "pos": [ 57, 66 ], "type": "Gene_expression" }
{ "name": "increased", "pos": [ 41, 49 ], "type": "Positive_regulation" }
16818616.s6
Transfection-mediated WWOX overexpression in DU145 cells suppressed colony growth (P = 0.0012), and WWOX overexpression by infection with Ad-WWOX virus induced apoptosis through a caspase-dependent mechanism and suppressed cell growth.
prostate
{ "name": "WWOX", "pos": [ 100, 103 ] }
{ "name": "DU145", "pos": [ 45, 49 ] }
increased
cancerTOnormal
causality
unidentifiable
{ "name": "overexpression", "pos": [ 105, 118 ], "type": "Gene_expression" }
{ "name": "overexpression", "pos": [ 105, 118 ], "type": "Positive_regulation" }
17003780.s7
Together, our data suggest that strong Tiam1 overexpression relative to the corresponding benign epithelial cells is a new and independent predictor of decreased DFS for patients with prostate cancer.
prostate
{ "name": "Tiam1", "pos": [ 39, 43 ] }
{ "name": "prostate cancer", "pos": [ 184, 198 ] }
increased
unidentifiable
{ "name": "overexpression", "pos": [ 45, 58 ], "type": "Gene_expression" }
{ "name": "overexpression", "pos": [ 45, 58 ], "type": "Positive_regulation" }
17134822.s0
Polycomb-group oncogenes EZH2, BMI1, and RING1 are overexpressed in prostate cancer with adverse pathologic and clinical features.
prostate
{ "name": "Polycomb-group oncogenes EZH2", "pos": [ 0, 28 ] }
{ "name": "prostate cancer", "pos": [ 68, 82 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "overexpressed", "pos": [ 51, 63 ], "type": "Gene_expression" }
{ "name": "overexpressed", "pos": [ 51, 63 ], "type": "Positive_regulation" }
17481580.s4
Out of seven isoforms of gal8, the proto isoform gal8e and our newly discovered proto isoform gal8g were upregulated in LNCaP cells compared to PrEC, whereas the two tandem-repeat isoforms gal8a and gal8b were equally expressed in these cells.
prostate
{ "name": "gal8e", "pos": [ 49, 53 ] }
{ "name": "LNCaP", "pos": [ 120, 124 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "upregulated", "pos": [ 105, 115 ], "type": "Positive_regulation" }
17481580.s4
Out of seven isoforms of gal8, the proto isoform gal8e and our newly discovered proto isoform gal8g were upregulated in LNCaP cells compared to PrEC, whereas the two tandem-repeat isoforms gal8a and gal8b were equally expressed in these cells.
prostate
{ "name": "gal8g", "pos": [ 94, 98 ] }
{ "name": "LNCaP", "pos": [ 120, 124 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "upregulated", "pos": [ 105, 115 ], "type": "Positive_regulation" }
17513602.s0
Increased expression of cyclin B1 sensitizes prostate cancer cells to apoptosis induced by chemotherapy.
prostate
{ "name": "cyclin B1", "pos": [ 24, 32 ] }
{ "name": "prostate cancer", "pos": [ 45, 59 ] }
increased
cancerTOnormal
causality
unidentifiable
{ "name": "expression", "pos": [ 10, 19 ], "type": "Gene_expression" }
{ "name": "Increased", "pos": [ 0, 8 ], "type": "Positive_regulation" }
17875724.s7
We present here for the first time that signal transducers and activators of transcription 3 (Stat3), which is constitutively activated in a wide variety of human cancers, including prostate cancer, interacts with PKCepsilon.
prostate
{ "name": "signal transducers and activators of transcription 3", "pos": [ 40, 91 ] }
{ "name": "prostate cancer", "pos": [ 182, 196 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "activated", "pos": [ 126, 134 ], "type": "Positive_regulation" }
17908958.s0
Smad3 is overexpressed in advanced human prostate cancer and necessary for progressive growth of prostate cancer cells in nude mice.
prostate
{ "name": "Smad3", "pos": [ 0, 4 ] }
{ "name": "prostate cancer", "pos": [ 41, 55 ] }
increased
normalTOcancer
causality
unchanged
{ "name": "overexpressed", "pos": [ 9, 21 ], "type": "Gene_expression" }
{ "name": "overexpressed", "pos": [ 9, 21 ], "type": "Positive_regulation" }
18008330.s1
Clinical data showed that the levels of interleukin-4 (IL-4) are significantly elevated in serum of patients with ablation resistant prostate cancer.
prostate
{ "name": "interleukin-4", "pos": [ 40, 52 ] }
{ "name": "prostate cancer", "pos": [ 133, 147 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "levels", "pos": [ 30, 35 ], "type": "Gene_expression" }
{ "name": "elevated", "pos": [ 79, 86 ], "type": "Positive_regulation" }
18008330.s9
Overexpression of IL-4 increases the sensitivity of androgen-sensitive LNCaP prostate cancer cells in response to androgen stimulation and enhances the growth of LNCaP cells both in the presence and absence of androgen in vitro and in vivo.
prostate
{ "name": "IL-4", "pos": [ 18, 21 ] }
{ "name": "prostate cancer", "pos": [ 77, 91 ] }
increased
normalTOcancer
causality
unidentifiable
{ "name": "Overexpression", "pos": [ 0, 13 ], "type": "Gene_expression" }
{ "name": "Overexpression", "pos": [ 0, 13 ], "type": "Positive_regulation" }
18167127.s0
Loss of BRCA2 promotes prostate cancer cell invasion through up-regulation of matrix metalloproteinase-9.
prostate
{ "name": "BRCA2", "pos": [ 8, 12 ] }
{ "name": "prostate cancer", "pos": [ 23, 37 ] }
decreased
normalTOcancer
causality
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "Loss", "pos": [ 0, 3 ], "type": "Negative_regulation" }
18167127.s6
Consistently, PI3-kinase inhibition with a dominant-negative mutant or MAPK/ERK activation with a gain-of-function mutant reduced MMP-9 levels and prevented migration and invasion in wild-type PC-3 cells.
prostate
{ "name": "PI3-kinase", "pos": [ 14, 23 ] }
{ "name": "PC-3", "pos": [ 193, 196 ] }
decreased
cancerTOnormal
causality
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "inhibition", "pos": [ 25, 34 ], "type": "Negative_regulation" }
11431361.s0
Hyaluronan synthase 3 overexpression promotes the growth of TSU prostate cancer cells.
prostate
{ "name": "Hyaluronan synthase 3", "pos": [ 0, 20 ] }
{ "name": "prostate cancer", "pos": [ 64, 78 ] }
increased
normalTOcancer
causality
unidentifiable
{ "name": "overexpression", "pos": [ 22, 35 ], "type": "Gene_expression" }
{ "name": "overexpression", "pos": [ 22, 35 ], "type": "Positive_regulation" }
16491480.s2
We have previously described the increased expression of two prostate-specific G-protein coupled receptors (PSGR and PSGR2) in human prostate cancer.
prostate
{ "name": "PSGR", "pos": [ 108, 111 ] }
{ "name": "prostate cancer", "pos": [ 133, 147 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "expression", "pos": [ 43, 52 ], "type": "Gene_expression" }
{ "name": "increased", "pos": [ 33, 41 ], "type": "Positive_regulation" }
16491480.s2
We have previously described the increased expression of two prostate-specific G-protein coupled receptors (PSGR and PSGR2) in human prostate cancer.
prostate
{ "name": "PSGR2", "pos": [ 117, 121 ] }
{ "name": "prostate cancer", "pos": [ 133, 147 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "expression", "pos": [ 43, 52 ], "type": "Gene_expression" }
{ "name": "increased", "pos": [ 33, 41 ], "type": "Positive_regulation" }
16491480.s9
AMACR was the best single marker of prostate cancer but in 7 of the 59 total cases the expression of AMACR was not significantly elevated while PSGR and/or PSGR2 were substantially elevated.
prostate
{ "name": "PSGR", "pos": [ 144, 147 ] }
{ "name": "prostate cancer", "pos": [ 36, 50 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "elevated", "pos": [ 181, 188 ], "type": "Positive_regulation" }
17426117.s3
Reduction of AR expression in the two androgen-sensitive prostate cancer cell lines, LNCaP and LAPC4, significantly decreased AR-mediated transcription and cell growth.
prostate
{ "name": "AR", "pos": [ 13, 14 ] }
{ "name": "prostate cancer", "pos": [ 57, 71 ] }
decreased
cancerTOnormal
causality
unidentifiable
{ "name": "expression", "pos": [ 16, 25 ], "type": "Gene_expression" }
{ "name": "Reduction", "pos": [ 0, 8 ], "type": "Negative_regulation" }
8612685.s0
Downregulation of protein kinase C suppresses induction of apoptosis in human prostatic carcinoma cells.
prostate
{ "name": "protein kinase C", "pos": [ 18, 33 ] }
{ "name": "prostatic carcinoma", "pos": [ 78, 96 ] }
decreased
normalTOcancer
causality
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "Downregulation", "pos": [ 0, 13 ], "type": "Negative_regulation" }
8612685.s7
PKC isozyme analysis revealed that chronic PDBu treatment caused downregulation of PKC-alpha and -epsilon in DU-145 cells.
prostate
{ "name": "PKC-alpha and -epsilon", "pos": [ 83, 104 ] }
{ "name": "DU-145", "pos": [ 109, 114 ] }
decreased
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "downregulation", "pos": [ 65, 78 ], "type": "Negative_regulation" }
12544353.s7
Antisense bcl-2 oligodeoxynucleotides decreased Bcl-2 protein levels and significantly inhibited PC-3 cell growth in a dose dependent manner.
prostate
{ "name": "Bcl-2 protein", "pos": [ 48, 60 ] }
{ "name": "PC-3", "pos": [ 97, 100 ] }
decreased
cancerTOnormal
observation
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "decreased", "pos": [ 38, 46 ], "type": "Negative_regulation" }
16302272.s1
Experimental work in various prostate cancer models revealed that the androgen receptor is frequently upregulated and implicated in tumor progression.
prostate
{ "name": "androgen receptor", "pos": [ 70, 86 ] }
{ "name": "prostate cancer", "pos": [ 29, 43 ] }
increased
normalTOcancer
causality
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "upregulated", "pos": [ 102, 112 ], "type": "Positive_regulation" }
21320357.s4
EPCR expression is up-regulated both at the mRNA and protein levels in invasive prostate DU-145 and PC-3 cells in comparison to normal prostate epithelial cells (PrEC) and less-invasive LNCaP cells.
prostate
{ "name": "EPCR", "pos": [ 0, 3 ] }
{ "name": "DU-145", "pos": [ 89, 94 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "expression", "pos": [ 5, 14 ], "type": "Gene_expression" }
{ "name": "up-regulated", "pos": [ 19, 30 ], "type": "Positive_regulation" }
15638997.s4
Response to bicalutamide in LNCaP cells was represented by downregulation of androgen-regulated genes, activation of the p53 pathway and inhibition of telomerase, which was associated with downregulation of v-myc avian myelocytomatosis viral oncogene homologue (MYC) and telomerase reverse transcriptase subunit.
prostate
{ "name": "p53", "pos": [ 121, 123 ] }
{ "name": "LNCaP", "pos": [ 28, 32 ] }
increased
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "activation", "pos": [ 103, 112 ], "type": "Positive_regulation" }
15638997.s4
Response to bicalutamide in LNCaP cells was represented by downregulation of androgen-regulated genes, activation of the p53 pathway and inhibition of telomerase, which was associated with downregulation of v-myc avian myelocytomatosis viral oncogene homologue (MYC) and telomerase reverse transcriptase subunit.
prostate
{ "name": "MYC", "pos": [ 262, 264 ] }
{ "name": "LNCaP", "pos": [ 28, 32 ] }
decreased
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "downregulation", "pos": [ 189, 202 ], "type": "Negative_regulation" }
15638997.s4
Response to bicalutamide in LNCaP cells was represented by downregulation of androgen-regulated genes, activation of the p53 pathway and inhibition of telomerase, which was associated with downregulation of v-myc avian myelocytomatosis viral oncogene homologue (MYC) and telomerase reverse transcriptase subunit.
prostate
{ "name": "telomerase reverse transcriptase subunit", "pos": [ 271, 310 ] }
{ "name": "LNCaP", "pos": [ 28, 32 ] }
decreased
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "downregulation", "pos": [ 189, 202 ], "type": "Negative_regulation" }
15638997.s6
In conclusion, we provide an explanation for telomerase inhibition after androgen receptor blockade in LNCaP cells and we also report activation of the p53 pathway in LNCaP cells and in-vitro sensitivity to bicalutamide of low confluent androgen-insensitive DU145 cells.
prostate
{ "name": "p53", "pos": [ 152, 154 ] }
{ "name": "LNCaP", "pos": [ 103, 107 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "activation", "pos": [ 134, 143 ], "type": "Positive_regulation" }
15638997.s6
In conclusion, we provide an explanation for telomerase inhibition after androgen receptor blockade in LNCaP cells and we also report activation of the p53 pathway in LNCaP cells and in-vitro sensitivity to bicalutamide of low confluent androgen-insensitive DU145 cells.
prostate
{ "name": "androgen receptor", "pos": [ 73, 89 ] }
{ "name": "LNCaP", "pos": [ 103, 107 ] }
decreased
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "blockade", "pos": [ 91, 98 ], "type": "Negative_regulation" }
19584279.s0
Reactivation of androgen receptor-regulated TMPRSS2:ERG gene expression in castration-resistant prostate cancer.
prostate
{ "name": "androgen receptor-regulated TMPRSS2", "pos": [ 16, 50 ] }
{ "name": "prostate cancer", "pos": [ 96, 110 ] }
increased
normalTOcancer
observation
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "Reactivation", "pos": [ 0, 11 ], "type": "Positive_regulation" }
19584279.s0
Reactivation of androgen receptor-regulated TMPRSS2:ERG gene expression in castration-resistant prostate cancer.
prostate
{ "name": "ERG gene", "pos": [ 52, 59 ] }
{ "name": "prostate cancer", "pos": [ 96, 110 ] }
increased
normalTOcancer
observation
unidentifiable
{ "name": "expression", "pos": [ 61, 70 ], "type": "Gene_expression" }
{ "name": "Reactivation", "pos": [ 0, 11 ], "type": "Positive_regulation" }
19584279.s5
Moreover, as observed in the clinical samples, ERG expression was fully restored in the VCaP xenografts that relapsed after castration, coincident with AR reactivation.
prostate
{ "name": "ERG", "pos": [ 47, 49 ] }
{ "name": "VCaP", "pos": [ 88, 91 ] }
increased
normalTOcancer
observation
unidentifiable
{ "name": "expression", "pos": [ 51, 60 ], "type": "Gene_expression" }
{ "name": "restored", "pos": [ 72, 79 ], "type": "Positive_regulation" }
19584279.s5
Moreover, as observed in the clinical samples, ERG expression was fully restored in the VCaP xenografts that relapsed after castration, coincident with AR reactivation.
prostate
{ "name": "AR", "pos": [ 152, 153 ] }
{ "name": "VCaP", "pos": [ 88, 91 ] }
increased
normalTOcancer
observation
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "reactivation", "pos": [ 155, 166 ], "type": "Positive_regulation" }
18358509.s4
We observed that re-expression of AR in the AR-negative cells PC3 decreases anchorage-independent growth and Matrigel invasiveness of PC3-AR cells where plasma membrane interaction between AR and EGFR led to an interference with downstream signalling and internalization of activated EGFR.
prostate
{ "name": "EGFR", "pos": [ 284, 287 ] }
{ "name": "PC3", "pos": [ 62, 64 ] }
increased
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "activated", "pos": [ 274, 282 ], "type": "Positive_regulation" }
16427044.s4
M12 cells, like many other human cancer cells, contain constitutively activated signal transducer and activator of transcription 3 (STAT3).
prostate
{ "name": "STAT3", "pos": [ 132, 136 ] }
{ "name": "M12", "pos": [ 0, 2 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "activated", "pos": [ 70, 78 ], "type": "Positive_regulation" }
16427044.s6
Strikingly, IFN-gamma-induced apoptosis and growth inhibition of M12 cells were associated with persistent suppression of the constitutive tyrosine-phosphorylated STAT3 (pY-STAT3).
prostate
{ "name": "STAT3", "pos": [ 163, 167 ] }
{ "name": "M12", "pos": [ 65, 67 ] }
decreased
cancerTOnormal
observation
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "suppression", "pos": [ 107, 117 ], "type": "Negative_regulation" }
20336778.s3
In this study, while demonstrating suppressed levels of Tm1 in the prostate cancer cell lines LNCaP, PC3, and DU-145 compared to normal prostate epithelial cell primary isolates (PrEC), a novel splice variant of the TPM2 gene was identified.
prostate
{ "name": "Tm1", "pos": [ 56, 58 ] }
{ "name": "prostate cancer", "pos": [ 67, 81 ] }
decreased
normalTOcancer
observation
unchanged
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "suppressed", "pos": [ 35, 44 ], "type": "Negative_regulation" }
10931458.s14
These findings suggest that inhibition of COX-2 development may lead not only to inhibition of the proliferation and metastasis of prostate carcinoma but also to the inhibition of prostate carcinogenesis.
prostate
{ "name": "COX-2", "pos": [ 42, 46 ] }
{ "name": "prostate carcinoma", "pos": [ 131, 148 ] }
decreased
cancerTOnormal
causality
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "inhibition", "pos": [ 28, 37 ], "type": "Negative_regulation" }
18349265.s4
Prostate cancer bony metastases show increased expression of the PTH receptor (PTH-IR) and PTH promotes the growth and invasiveness of prostate cancer cells in bone.
prostate
{ "name": "PTH receptor", "pos": [ 65, 76 ] }
{ "name": "prostate cancer", "pos": [ 135, 149 ] }
increased
normalTOcancer
causality
unidentifiable
{ "name": "expression", "pos": [ 47, 56 ], "type": "Gene_expression" }
{ "name": "increased", "pos": [ 37, 45 ], "type": "Positive_regulation" }
18349265.s4
Prostate cancer bony metastases show increased expression of the PTH receptor (PTH-IR) and PTH promotes the growth and invasiveness of prostate cancer cells in bone.
prostate
{ "name": "PTH-IR", "pos": [ 79, 84 ] }
{ "name": "prostate cancer", "pos": [ 135, 149 ] }
increased
normalTOcancer
causality
unidentifiable
{ "name": "expression", "pos": [ 47, 56 ], "type": "Gene_expression" }
{ "name": "increased", "pos": [ 37, 45 ], "type": "Positive_regulation" }
18349265.s4
Prostate cancer bony metastases show increased expression of the PTH receptor (PTH-IR) and PTH promotes the growth and invasiveness of prostate cancer cells in bone.
prostate
{ "name": "PTH", "pos": [ 91, 93 ] }
{ "name": "prostate cancer", "pos": [ 135, 149 ] }
increased
normalTOcancer
causality
unidentifiable
{ "name": "expression", "pos": [ 47, 56 ], "type": "Gene_expression" }
{ "name": "increased", "pos": [ 37, 45 ], "type": "Positive_regulation" }
10216950.s8
A broad spectrum of tumor derived cell lines, from varied tissue sources and blood samples from patients having confirmed prostate carcinoma, all scored positive for expression of PTI-1, while corresponding normal tissues or blood samples were negative.
prostate
{ "name": "PTI-1", "pos": [ 180, 184 ] }
{ "name": "prostate carcinoma", "pos": [ 122, 139 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "expression", "pos": [ 166, 175 ], "type": "Gene_expression" }
{ "name": "positive", "pos": [ 153, 160 ], "type": "Positive_regulation" }
9586898.s11
A decrease in PSA level is associated with both survival and response in soft tissue lesions and should be incorporated into the response criteria and reporting of trials of cytotoxic agents in prostate cancer.
prostate
{ "name": "PSA", "pos": [ 14, 16 ] }
{ "name": "prostate cancer", "pos": [ 194, 208 ] }
decreased
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "decrease", "pos": [ 2, 9 ], "type": "Negative_regulation" }
21064106.s0
miR 488* inhibits androgen receptor expression in prostate carcinoma cells.
prostate
{ "name": "androgen receptor", "pos": [ 18, 34 ] }
{ "name": "prostate carcinoma", "pos": [ 50, 67 ] }
decreased
unidentifiable
{ "name": "expression", "pos": [ 36, 45 ], "type": "Gene_expression" }
{ "name": "inhibits", "pos": [ 9, 16 ], "type": "Negative_regulation" }
17409433.s3
NSAIDs exert their anti-inflammatory effects by inhibiting cyclooxygenase (COX) activity; however, evidence suggests that COX-independent mechanisms mediate decreased prostate cancer cell survival.
prostate
{ "name": "cyclooxygenase", "pos": [ 59, 72 ] }
{ "name": "prostate cancer", "pos": [ 167, 181 ] }
decreased
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "inhibiting", "pos": [ 48, 57 ], "type": "Negative_regulation" }
17409433.s3
NSAIDs exert their anti-inflammatory effects by inhibiting cyclooxygenase (COX) activity; however, evidence suggests that COX-independent mechanisms mediate decreased prostate cancer cell survival.
prostate
{ "name": "COX", "pos": [ 75, 77 ] }
{ "name": "prostate cancer", "pos": [ 167, 181 ] }
decreased
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "inhibiting", "pos": [ 48, 57 ], "type": "Negative_regulation" }
17409433.s10
Hence, R-flurbiprofen and ibuprofen selectively induce p75(NTR)-dependent decreased survival of prostate cancer cells independently of COX inhibition.
prostate
{ "name": "COX", "pos": [ 135, 137 ] }
{ "name": "prostate cancer", "pos": [ 96, 110 ] }
decreased
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "inhibition", "pos": [ 139, 148 ], "type": "Negative_regulation" }
11704864.s5
Here we show that an increase in the level of expression of Bcl-2 in the human prostate carcinoma cell line LNCaP observed in response to hormone withdrawal is further augmented by TNF-alpha treatment, and this effect is abated by inhibitors of NF-kappa B.
prostate
{ "name": "NF-kappa B", "pos": [ 245, 254 ] }
{ "name": "prostate carcinoma", "pos": [ 79, 96 ] }
decreased
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "inhibitors", "pos": [ 231, 240 ], "type": "Negative_regulation" }
11704864.s6
Concomitantly, bcl-2 p2 promoter studies in LNCaP cells show a 40-fold increase in promoter activity after stimulation with TNF-alpha in the absence of hormone.
prostate
{ "name": "TNF-alpha", "pos": [ 124, 132 ] }
{ "name": "LNCaP", "pos": [ 44, 48 ] }
increased
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "stimulation", "pos": [ 107, 117 ], "type": "Positive_regulation" }
11704864.s5
Here we show that an increase in the level of expression of Bcl-2 in the human prostate carcinoma cell line LNCaP observed in response to hormone withdrawal is further augmented by TNF-alpha treatment, and this effect is abated by inhibitors of NF-kappa B.
prostate
{ "name": "Bcl-2", "pos": [ 60, 64 ] }
{ "name": "prostate carcinoma", "pos": [ 79, 96 ] }
increased
unidentifiable
{ "name": "expression", "pos": [ 46, 55 ], "type": "Gene_expression" }
{ "name": "increase", "pos": [ 21, 28 ], "type": "Positive_regulation" }
19879420.s2
For example, some studies showed that CLU expression is increased in advanced stages of prostate cancer and that suppression of CLU expression sensitizes prostate cancer cells to chemotherapeutic drugs killing.
prostate
{ "name": "CLU", "pos": [ 128, 130 ] }
{ "name": "prostate cancer", "pos": [ 88, 102 ] }
decreased
cancerTOnormal
causality
up-regulated
{ "name": "expression", "pos": [ 132, 141 ], "type": "Gene_expression" }
{ "name": "suppression", "pos": [ 113, 123 ], "type": "Negative_regulation" }
19879420.s2
For example, some studies showed that CLU expression is increased in advanced stages of prostate cancer and that suppression of CLU expression sensitizes prostate cancer cells to chemotherapeutic drugs killing.
prostate
{ "name": "CLU", "pos": [ 38, 40 ] }
{ "name": "prostate cancer", "pos": [ 88, 102 ] }
increased
normalTOcancer
observation
unchanged
{ "name": "expression", "pos": [ 42, 51 ], "type": "Gene_expression" }
{ "name": "increased", "pos": [ 56, 64 ], "type": "Positive_regulation" }
19879420.s3
In contrast with the hypothesis that CLU is a positive modulator of prostate cancer, we and others have observed that CLU is downregulated during human prostate cancer progression.
prostate
{ "name": "CLU", "pos": [ 118, 120 ] }
{ "name": "prostate cancer", "pos": [ 68, 82 ] }
decreased
normalTOcancer
observation
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "downregulated", "pos": [ 125, 137 ], "type": "Negative_regulation" }
19879420.s4
Accordingly, a meta-analysis of available microarray data shows that CLU mRNA is significantly downregulated in prostate cancer tissue compared to normal prostate in 14 out of 15 independent studies.
prostate
{ "name": "CLU mRNA", "pos": [ 69, 76 ] }
{ "name": "prostate cancer", "pos": [ 112, 126 ] }
decreased
normalTOcancer
observation
unchanged
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "downregulated", "pos": [ 95, 107 ], "type": "Negative_regulation" }
19879420.s6
Consistently, CLU expression was found to be significantly reduced in untreated and hormone-refractory human prostate carcinomas.
prostate
{ "name": "CLU", "pos": [ 14, 16 ] }
{ "name": "prostate carcinomas", "pos": [ 109, 127 ] }
decreased
normalTOcancer
observation
unidentifiable
{ "name": "expression", "pos": [ 18, 27 ], "type": "Gene_expression" }
{ "name": "reduced", "pos": [ 59, 65 ], "type": "Negative_regulation" }
21479359.s10
In PC-3 cells, adhesion molecule expression, analyzed by immunoblotting, was unaffected by LA, while a down-regulation of c-met (up to 28%) was observed after 24 h of treatment but which did not hold up over time (48-144 h).
prostate
{ "name": "c-met", "pos": [ 122, 126 ] }
{ "name": "PC-3", "pos": [ 3, 6 ] }
decreased
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "down-regulation", "pos": [ 103, 117 ], "type": "Negative_regulation" }
21479359.s11
Our findings demonstrate the efficacy of LA in upregulating E-cadherin, β- and γ-catenin in LNCaP cells.
prostate
{ "name": "E-cadherin", "pos": [ 60, 69 ] }
{ "name": "LNCaP", "pos": [ 92, 96 ] }
increased
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "upregulating", "pos": [ 47, 58 ], "type": "Positive_regulation" }
21479359.s11
Our findings demonstrate the efficacy of LA in upregulating E-cadherin, β- and γ-catenin in LNCaP cells.
prostate
{ "name": "γ-catenin", "pos": [ 79, 87 ] }
{ "name": "LNCaP", "pos": [ 92, 96 ] }
increased
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "upregulating", "pos": [ 47, 58 ], "type": "Positive_regulation" }
12603425.s3
In BPH samples there was a significant correlation between CD38 loss (mean 21% of acini) and HLA-DR up-regulation (mean 20%; P &lt; 0.001).
prostate
{ "name": "HLA-DR", "pos": [ 93, 98 ] }
{ "name": "BPH", "pos": [ 3, 5 ] }
increased
normalTOcancer
observation
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "up-regulation", "pos": [ 100, 112 ], "type": "Positive_regulation" }
12603425.s4
Moreover, 76% of all CD38-negative acini in BPH had HLA-DR up-regulation in the same prostate epithelial cells, predominantly in atrophic and cystic glands, and in cells with retained secretions (74%).
prostate
{ "name": "HLA-DR", "pos": [ 52, 57 ] }
{ "name": "BPH", "pos": [ 44, 46 ] }
increased
normalTOcancer
observation
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "up-regulation", "pos": [ 59, 71 ], "type": "Positive_regulation" }
12603425.s8
The absence of CD38 and presence of HLA-DR expression in prostatic epithelium is consistent in BPH and tissue surrounding tumour, and strongly related to gland atrophy.
prostate
{ "name": "CD38", "pos": [ 15, 18 ] }
{ "name": "BPH", "pos": [ 95, 97 ] }
decreased
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "absence", "pos": [ 4, 10 ], "type": "Negative_regulation" }
14665875.s1
The prostate cancer detection rate in patients with elevated prostate specific antigen (PSA) increases with extended needle biopsy protocols.
prostate
{ "name": "prostate specific antigen", "pos": [ 61, 85 ] }
{ "name": "prostate cancer", "pos": [ 4, 18 ] }
increased
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "elevated", "pos": [ 52, 59 ], "type": "Positive_regulation" }
14665875.s1
The prostate cancer detection rate in patients with elevated prostate specific antigen (PSA) increases with extended needle biopsy protocols.
prostate
{ "name": "PSA", "pos": [ 88, 90 ] }
{ "name": "prostate cancer", "pos": [ 4, 18 ] }
increased
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "elevated", "pos": [ 52, 59 ], "type": "Positive_regulation" }
15193259.s1
R-etodolac, a nonsteroidal anti-inflammatory drug, inhibits the progression of CWRSA6 androgen-independent and LuCaP-35 androgen-dependent prostate cancer xenograft growth through downregulation of cyclin D1 expression via the PPARgamma pathway.
prostate
{ "name": "cyclin D1", "pos": [ 198, 206 ] }
{ "name": "prostate cancer", "pos": [ 139, 153 ] }
decreased
cancerTOnormal
causality
unidentifiable
{ "name": "expression", "pos": [ 208, 217 ], "type": "Gene_expression" }
{ "name": "downregulation", "pos": [ 180, 193 ], "type": "Negative_regulation" }
17143532.s0
Constitutive activation of MAPK/ERK inhibits prostate cancer cell proliferation through upregulation of BRCA2.
prostate
{ "name": "BRCA2", "pos": [ 104, 108 ] }
{ "name": "prostate cancer", "pos": [ 45, 59 ] }
increased
cancerTOnormal
causality
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "upregulation", "pos": [ 88, 99 ], "type": "Positive_regulation" }
19483721.s0
Overexpressing PKIB in prostate cancer promotes its aggressiveness by linking between PKA and Akt pathways.
prostate
{ "name": "PKIB", "pos": [ 15, 18 ] }
{ "name": "prostate cancer", "pos": [ 23, 37 ] }
increased
normalTOcancer
causality
unidentifiable
{ "name": "Overexpressing", "pos": [ 0, 13 ], "type": "Gene_expression" }
{ "name": "Overexpressing", "pos": [ 0, 13 ], "type": "Positive_regulation" }
15647840.s8
DHT-induced E2F-1 protein and mRNA expressions was also inhibited by BMP-2, suggesting that BMP-2 inhibits DHT-induced growth of LNCaP cells through a decrease in E2F protein expression and suppression of E2F activity by hypophosphorylation of Rb.
prostate
{ "name": "E2F", "pos": [ 205, 207 ] }
{ "name": "LNCaP", "pos": [ 129, 133 ] }
decreased
cancerTOnormal
causality
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "suppression", "pos": [ 190, 200 ], "type": "Negative_regulation" }
15647840.s8
DHT-induced E2F-1 protein and mRNA expressions was also inhibited by BMP-2, suggesting that BMP-2 inhibits DHT-induced growth of LNCaP cells through a decrease in E2F protein expression and suppression of E2F activity by hypophosphorylation of Rb.
prostate
{ "name": "E2F protein", "pos": [ 163, 173 ] }
{ "name": "LNCaP", "pos": [ 129, 133 ] }
decreased
cancerTOnormal
causality
unidentifiable
{ "name": "expression", "pos": [ 175, 184 ], "type": "Gene_expression" }
{ "name": "decrease", "pos": [ 151, 158 ], "type": "Negative_regulation" }
15647840.s8
DHT-induced E2F-1 protein and mRNA expressions was also inhibited by BMP-2, suggesting that BMP-2 inhibits DHT-induced growth of LNCaP cells through a decrease in E2F protein expression and suppression of E2F activity by hypophosphorylation of Rb.
prostate
{ "name": "E2F-1 protein", "pos": [ 12, 24 ] }
{ "name": "LNCaP", "pos": [ 129, 133 ] }
decreased
cancerTOnormal
causality
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "inhibited", "pos": [ 56, 64 ], "type": "Negative_regulation" }
21789713.s0
Dual blockade of PKA and NF-κB inhibits H2 relaxin-mediated castrate-resistant growth of prostate cancer sublines and induces apoptosis.
prostate
{ "name": "PKA", "pos": [ 17, 19 ] }
{ "name": "prostate cancer", "pos": [ 89, 103 ] }
decreased
cancerTOnormal
observation
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "blockade", "pos": [ 5, 12 ], "type": "Negative_regulation" }
21789713.s0
Dual blockade of PKA and NF-κB inhibits H2 relaxin-mediated castrate-resistant growth of prostate cancer sublines and induces apoptosis.
prostate
{ "name": "NF-κB", "pos": [ 25, 29 ] }
{ "name": "prostate cancer", "pos": [ 89, 103 ] }
decreased
cancerTOnormal
observation
unidentifiable
{ "name": "\nNone\n", "pos": null, "type": null }
{ "name": "blockade", "pos": [ 5, 12 ], "type": "Negative_regulation" }

Dataset Card for CoMAGC

Dataset Summary

CoMAGC Dataset Summary:

CoMAGC is a corpus with multi-faceted annotations of gene-cancer relations. CoMAGC consists of 821 sentences collected from MEDLINE abstracts, and the sentences are about three different types of cancers, or prostate, breast and ovarian cancers. In CoMAGC, a piece of annotation is composed of four semantically orthogonal concepts that together express 1) how a gene changes, 2) how a cancer changes and 3) the causality between the gene and the cancer. The four concepts that constitute the multi-faceted annotation scheme are Change in Gene Expression (CGE), Change in Cell State (CCS), Proposition Type (PT) and Initial Gene Expression level (IGE).

  • CGE captures whether the expression level of a gene is increased or decreased in a cell
  • CCS captures the way how the cell changes together with a gene expression level change
    • normalTOnormal: The cell or tissue remains as normal after the change in the gene’s expression level.
    • normalTOcancer: The cell or tissue acquires cancerous properties as the gene expression level changes; some cancerous properties are strengthened.
    • cancerTOcancer: There's no change in the cancerous properties of the cell or tissue despite the change in the expression level of the gene.
    • cancerTOnormal: The cell or tissue loses some cancerous properties as the gene expression level changes; some cancerous properties are weakened.
    • unidentifiable: The information about whether or not the gene expression level change accompanies cell or tissue state change is not provided.
  • PT captures whether the causality between the gene expression change and the cell property change
    • observation: Cell or tissue change accompanied by the gene expression level change is reported as observed but the causality between the two is not claimed. |
    • causality: The causality between the gene expression level change and the cell or tissue change is claimed.
  • IGE captures the initial expression level of a gene before the change in its expression level
    • up-regulated: The initial gene expression level is higher than the expression level of the gene in the normal state.
    • down-regulated: The initial gene expression level is lower than the expression level of the gene in the normal state.
    • unchanged: The initial gene expression level is comparable to the expression level of the gene in the normal state.
    • unidentifiable: The information about the initial gene expression level is not provided. |

The original dataset in XML format is available here: http://biopathway.org/CoMAGC/

We converted the dataset to a JSONL format before pushing the data to the hub.

Languages

The language in the dataset is English.

Dataset Structure

Dataset Instances

An example of 'train' looks as follows:

{
  "pmid": "11722842.s0",
  "sentence": "Isolation and characterization of the major form of human MUC18 cDNA gene and correlation of MUC18 over-expression in prostate cancer cell lines and tissues with malignant progression.",
  "cancer_type": "prostate",
  "gene": {
    "name": "MUC18",
    "pos": [93, 97]
  },
  "cancer": {
    "name": "prostate cancer",
    "pos": [118, 132]
  },
  "CGE": "increased",
  "CCS": "normalTOcancer",
  "PT": "observation",
  "IGE": "unchanged",
  "expression_change_keyword_1": {
    "name": "over-expression",
    "pos": [99, 113],
    "type": "Gene_expression"
  },
  "expression_change_keyword_2": {
    "name": "over-expression",
    "pos": [99, 113],
    "type": "Positive_regulation"
  }
}

Data Fields

  • pmid: the id of this sentence, a string feature.
  • sentence: the text of this sentence, a string feature.
  • cancer_type: the type of cancer in this sentence, a string feature.
  • gene: gene entity
    • pos: character offsets of the gene entity, a list of int32 features.
    • name: gene entity text, a string feature.
  • cancer: cancer entity
    • pos: character offsets of the cancer entity, a list of int32 features.
    • name: cancer entity text, a string feature.
  • CGE: change in gene expression, a string feature.
  • CCS: change in cell state, a string feature.
  • PT: proposition type, a string feature.
  • IGE: initial gene expression, a string feature.
  • expression_change_keyword_1: a dict
    • name: keyword text, a string feature.
    • pos: character offsets of the keyword, a list of int32 features.
    • type: type of the expression change keyword, a string feature.
  • expression_change_keyword_2: a dict
    • name: keyword text, a string feature.
    • pos: character offsets of the keyword, a list of int32 features.
    • type: type of the expression change keyword, a string feature.

Citation

BibTeX:

@article{lee2013comagc,
  title={CoMAGC: a corpus with multi-faceted annotations of gene-cancer relations},
  author={Lee, Hee-Jin and Shim, Sang-Hyung and Song, Mi-Ryoung and Lee, Hyunju and Park, Jong C},
  journal={BMC bioinformatics},
  volume={14},
  pages={1--17},
  year={2013},
  publisher={Springer}
}

APA:

  • Lee, H. J., Shim, S. H., Song, M. R., Lee, H., & Park, J. C. (2013). CoMAGC: a corpus with multi-faceted annotations of gene-cancer relations. BMC bioinformatics, 14, 1-17.

Dataset Card Authors

@phucdev

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