bluuebunny/crossref_metadata_2025_split huggingface dataset:
Genes involved in tumor invasion and metastasis are differentially modulated by estradiol and progestin in human breast‐cancer cells
Authors: van den Brûle1 Frédéric A. , Engel Jason , Stetler‐Stevenson William G. , Liu Fu‐Tong , Sobel Mark E. , Castronovo Vincent 
Published: February 2007

AbstractInvasion of basement membranes by cancer cells is a critical step in metastasis, which requires the coordinated expression of specific genes such as laminin receptors and metalloproteinases. Estradiol and progesterone modulate the clinical progression of steroid‐sensitive breast cancers; however, little is known about the molecular regulation of the invasive phenotype by these hormones. We therefore examined the effects of 10 nM estradiol and/or 10 nM progestin R5020 on the expression of 2 non‐integrin laminin binding proteins, the 67‐kDa laminin receptor (67LR) and HLBP31 as well as the 72‐kDa type‐IV collagenase (MMP‐2) and its inhibitor, TIMP‐2, in steroid‐receptorpositive (T47D and MCF‐7) and ‐negative (MDA‐MB 231) human breast‐cancer cells. The relative steady‐state level of 67LR mRNA was increased 2‐ to 3‐fold by estradiol in both MCF‐7 (p < 0.001) and T47D (p < 0.001) cells, also by R5020, alone or in combination with estradiol, in T47D cells (p < 0.001) and to a much less extent in MCF‐7 cells. HLBP31 mRNA and protein levels were increased 2‐ to 3‐fold (p < 0.001) by R5020 alone or in combination with estradiol. but not by estradiol alone. None of the steroid treatments affected the expression or activity of MMP‐2. Interestingly, however, TIMP‐2 mRNA levels and protein expression in MCF‐7 and T47D cells were 50% down‐regulated (p < 0.001) by treatment with R5020 or R5020 plus estradiol, but not by treatment with estradiol alone. None of these genes were modulated in steroid‐independent MDA‐MB231 cells. The data suggest that estradiol and progesterone might act as coordinators regulating specific genes in the steroid‐sensitive breast‐cancer cell, leading to the acquisition of the metastatic phenotype. © 1992 Wiley‐Liss, Inc.
The presence of concanavalin‐a(C0N‐A)‐like molecules on natural‐killer (NK)‐Sensitive target cells: Their possible role in swainsonine‐augmented human NK cytotoxicity
Authors: Yagita Masato , Noda Ichiro , Maehara Masanori , Fujieda Shigeharu , Inoue Yoshiko , Hoshino Takashi , Saksela Eero 
Published: February 2007

AbstractIn the present study we examined the expression of concanavalin‐A(Con‐A)‐like molecules on natural‐killer (NK)‐sensitive target cells and investigated their possible role in the human NK‐cell phenomenon. The incubation of either peripheral‐blood lymphocytes (PBL) or large granular lymphocytes (LGL) with swainsonine (SW), an inhibitor of mannosidase II, resulted in the augmentation of cytotoxicity against K562 leukemia cells. The enhanced cytotoxicity was associated with increased binding of fluorescein isothiocyanate‐conjugated Con‐A to SW‐treated effector cells, and immunofluorescence staining of the target K562 cells using goat anti‐Con‐A antibody (Ab) showed a significant positive shift in the flow cytometric pattern. Electrophoretic separation and immunoblotting analysis revealed that 4 components with a molecular weight of approximately 95, 80, 60 and 50 kDa were recognized by anti‐Con‐Ab from the detergent‐extract of K562 cells. The addition of Con‐A during the antibody incubation step of the Western blotting abolished their expression, thus excluding non‐specific binding of the antibody. The addition of Con‐A also strongly inhibited the cytotoxicity of SW‐treated effector cells (PBL or LGL) against K562 cells, and this inhibition was abolished by 40 mM α‐methyl‐mannopyranoside (α‐MM), which binds to Con‐A. Furthermore, Con‐A increased the binding frequency of SW‐treated LGL to K562. in spite of the inhibited cytotoxicity, and this effect could be neutralized by the further addition of α‐MM. Our results suggest that Con A‐like molecules might play an important role in cell‐cell interactions between SW‐treated effector cells and NK target cells. © 1992 Wiley‐Liss, Inc.
Variations in the ganglioside profile of uveal melanoma correlate with cytologic heterogeneity
Authors: Kanda Shinji , Cochran Alistair J. , Lee William R. , Morton Donald L. , Irie Reiko F. 
Published: February 2007

AbstractGangliosides may play an important role in the proliferation and spread of human malignant melanoma. Because the frequency of metastases in uveal and cutaneous melanoma differs, it is possible that they may express different gangliosides. We analyzed the ganglioside profiles of primary uveal melanoma in 14 cases and of cutaneous melanoma metastasis in 19 cases. In cutaneous melanoma, GM3 ranged from 4.2% to 74.6% and GD3 from 22.1% to 91.8% of total lipid‐bound sialic acid. GM2 (found in 13 of 19 cases, ranging from 0.5% to 11.7%), GD2 (11/19, 0.5%–22.0%) and 9‐O‐acetyl‐GD3 (13/19, 0.5%‐12.6%) were also frequently observed. By contrast, in 11 cases of uveal melanoma, GM3 was >90%, GD3 was < 10%, GM2 was <1.1%; neither GD2 nor 9‐O‐acetyl‐GD3 were detected. The ganglioside profiles of these uveal melanomas were virtually identical to those of normal melanocytes obtained from foreskins. Histological examination of these 11 biopsies showed a monomorphous cell composition, but neither infiltration of lymphocytes or melanophages nor cell necrosis was observed. In 3 other cases, GD3 was increased to 19.5%‐46.0%. Histological examination of these 3 biopsy specimens showed at least 2 populations of tumor cells that were separable based on morphological grounds, and mononuclear inflammatory cells interspersed among the tumor cells. An increase in GD3 appears to be related to tumor polyclonality and infiltration of the tumor by lymphocytes and macrophages. These results suggest that ganglioside expression of uveal melanoma is associated with host immune responses to the tumor. Furthermore, the low metastatic capacity of uveal melanoma, in contrast to the high metastatic rate of cutaneous melanoma, may be a result of its differentiated ganglioside expression, which is strikingly similar to that of normal melanocytes. © 1992 Wiley‐Liss, Inc.
Expression of different tenascin isoforms in normal, hyperplastic and neoplastic human breast tissues
Authors: Borsi Laura , Carnemolla Barbara , Nicolò Guido , Spina Bruno , Tanara Giorgio , Zardi Luciano 
Published: February 2007

AbstractFunctionally different tenascin (TN) isoforms, containing varying numbers of a 91 amino‐acid motif resembling the fibronectin type‐III homology repeat, may be generated by alternative splicing of the TN primary transcript. In fact, only the TN isoform containing the alternatively spliced region can induce loss of focal adhesion in cultured cells and seems to be able to facilitate cell migration. We examined the patterns of alternative splicing of the TN primary transcript in normal, hyperplastic and neoplastic breast tissues, and found that, in all the invasive breast carcinomas analyzed, the relative amount of TN mRNA in which the alternatively spliced region was included was about 10 times higher than in RNA from normal breast tissues. A similar result was observed in phyllodes tumors and in those fibroadenomas which showed very high stromal cellularity. Western‐blot analysis using different monoclonal antibodies showed the same pattern as that seen in Northern blotting. The data reported here suggest that, in the breast, expression of the high‐molecular‐mass TN isoform is a marker of stromal element proliferation and that, in invasive breast carcinomas, this TN isoform could play a role in generating a permissive environment for proliferation, invasion and metastasis of neoplastic epithelial cells. © 1992 Wiley‐Liss, Inc.
Effect of DNA ploidy classification on prognosis in breast cancer
Authors: Joensuu Heikki , Alanen Kalle , Falkmer Ursula G. , Klemi Pekka , Nordling Stig , Remvikos Yorghos , Toikkanen Sakari 
Published: February 2007

AbstractA series of 327 breast cancers was analyzed for DNA ploidy by flow cytometry from paraffin‐embedded tissue, and the resulting DNA histograms were classified independently by 6 researchers in the field as DNA diploid (Di), aneuploid (An), tetraploid (Te), multiploid (Mu), or technically uninterpretable. The frequency of diploid, aneuploid, tetraploid and multiploid cancers varied from 28 to 41%, 33 to 49%, 8 to 21% and 2 to 6%. According to the scale Di‐An‐Te‐Mu, DNA ploidy was not significantly associated with breast‐cancer mortality by 2 classifiers, but if DNA euploid cancers (Di+Te) were tested against non‐euploid, or diploid cancers against non‐diploid, all classifiers found DNA euploid and diploid cancers to have better prognosis. Mortality associated with diploid or tetraploid cancers decreased with improving histogram quality and increasing uniformity of classification, whereas that associated with aneuploid cancers remained unaltered. Among the cases where all classifiers agreed on ploidy, tetraploid, diploid and aneuploid cancers were associated with 100%, 88% and 68% 5‐year survival rates. In this sub‐set the S‐phase fraction and possibly DNA ploidy were independent prognostic factors, together with histological grade, axillary node status, and primary tumor size. © 1992 Wiley‐Liss, Inc.
Correlation between the serum level of hepatitis C virus RNA and disease activities in acute and chronic hepatitis C
Authors: Gunji Toshiaki , Kato Nobuyuki , Mori Shigehisa , Ootsuyama Yuko , Hijikata Makoto , Imawari Michio , Shimotohno Kunitada 
Published: February 2007

AbstractThe influence of viremia on hepatic injury in patients infected with hepatitis C virus was examined by analysis of the relationship between alanine aminotransferase activity and the amount of hepatitis C virus RNA in sequential serum samples from 1 untreated patient with acute hepatitis C and 3 untreated patients with chronic hepatitis C. Semiquantitative analysis by the competitive‐reverse‐transcription/polymerase‐chain‐reaction method indicated that the quantity of hepatitis C virus RNA in the serum affected the disease activities of acute and chronic hepatitis C through their natural clinical courses in all these patients. The nucleotide sequence encoding the putative envelope region of the viral genome in the patient with acute hepatitis C was examined. Blood samples taken serially at 2 times of exacerbation of the hepatitis revealed 2 nucleotide mutations, resulting in changes of predicted amino acid residues. This finding suggests that nucleotide mutations in the envelope region of the viral genome may be responsible for the recurrent hepatic injury attributed to recurrence of viremia in patients with hepatitis C. From these aspects, the serial divergence of the virus genome in infected individuals, especially in the region encoding the viral envelope protein, may possibly play an important role in developing chronic infection of hepatitis C virus. © 1992 Wiley‐Liss, Inc.
Interaction of gangliosides with the methyltransferase‐I of microsomes from normal and neoplastic human mammary gland
Authors: Losa Gabriele A. , Graber Riccardo , Chigorno Vanna , Sonnino Sandro 
Published: February 2007

AbstractThe activity of the phospholipid methyltransferase‐1, which catalyzes the rapid transmethylation of phosphatidylethanolamine to phosphatidylcholine, was found to be about 6‐fold enhanced in microsomal membranes of breast cancer with respect to the level found in normal human mammary gland. Exogenous gangliosides GM1 and GM2 added to neoplastic breast microsomes induced progressive inhibition of the methyltransferase activity. In contrast, in microsomal membranes of non‐neoplastic breast tissue treated with these gangliosides, the methyltransferase activity was markedly increased. The addition of cholesterol to these microsomes led to complete inhibition of the GM1 ‐stimulated enzyme activity. The methyltransferase activity was not affected by GM3 alone in either type of tissue. Experiments carried out on non‐neoplastic microsomes revealed that the phospholipid methyltransferase‐1 was affected by that portion of gangliosides which remained stable associated to microsomal membranes. © 1992 Wiley‐Liss, Inc.
The causal link between human papillomavirus and invasive cervical cancer: A population‐based case‐control study in colombia and spain
Authors: Munoz N. , Bosch F. X. , de Sanjose S. , Tafur L. , Izarzugaza I. , Gili M. , Viladiu P. , Navarro C. , Martos C. , Ascunce N. , Gonzalez L. C. , Kaldor J. M. , Guerrero E. , Lorincz A. , Santamaria M. , De Ruiz P. Alonso , Aristizabal N. , Shah K. 
Published: February 2007

AbstractTo evaluate the association between human papillomavirus (HPV) and cervical cancer, we performed a population‐based case‐control study in Colombia and Spain, the former country having an incidence rate of cervical cancer about 8 times higher than the latter. It included 436 cases of histologically confirmed invasive cervical cancer and 387 randomly selected population controls. Information on demographic variables, sexual behaviour and other risk factors was obtained by interview. HPV‐DNA was measured in cervical‐swab specimens with 3 hybridization assays: ViraPap™, Southern hybridization (SH) and polymerase chain reaction (PCR). The presence of HPV‐DNA and detection of types 16, 18, 31, 33 and 35 were strongly associated with cervical cancer in each country regardless of the assay used. For both countries combined the adjusted odds ratios and 95% confidence intervals were: ViraPap OR = 25.9 (10.0–66.7); SH OR = 6.8 (3.4–13.4); and PCR OR = 28.8 (15.7–52.6). HPV‐16 was the most common type detected in both cases and controls. Our results indicate that there is a very strong association between HPV 16, 18, 31, 33 and 35 and invasive cervical cancer and that this association is probably causal. © 1992 Wiley‐Liss, Inc.
Risk factors for cervical cancer in Colombia and Spain
Authors: Bosch F. X. , Muñoz N. , de Sanjosé S. , Izarzugaza I. , Gili M. , Viladiu P. , Tormo M. J. , Moreo P. , Ascunce N. , Gonzalez L. C. , Tafur L. , Kaldor J. M. , Guerrero E. , Aristizabal N. , Santamaria M. , De Ruiz P. Alonso , Shah K. 
Published: February 2007

AbstractA population‐based case‐control study of cervical cancer was conducted in Spain and Colombia to assess the relationship between cervical cancer and exposure to human papillomavirus (HPV), selected aspects of sexual and reproductive behaviour, use of oral contraceptives, screening practices and smoking. The study included 436 cases of histologically confirmed squamous‐cell carcinoma and 387 age‐stratified controls randomly selected front) the general population that generated the cases. The presence of HPV DMA in cervical scrapes was assessed by PCR‐based methods and was the strongest risk factor (OR = 23.8; 13.4–42.0). Risk estimates for any other factor were only slightly modified after adjusting for HPV status. Among women found positive for HPV DNA, only the use of oral contraceptives was a risk factor for cervical cancer (OR = 6.5; 1.3–31.4 for ever vs. never use). Patients with cervical cancer who were HPV DMA‐negative retained most of the established epidemiological features of this disease. This suggests that some instances of HPV infection went undetected or that other sexually transmitted factor(s) contribute to the causation of cervical cancer. Early age at first intercourse (OR = 4.3; 2.1–9.0 for age < 16 vs. 24+) and early age at first birth (OR = 5.0; 1.8–14.2 for 9ge < 16 vs. 24+) were associated with increased risk of cervical cancer; these effects were independent of one another. Low educational level was a risk factor (OR = 2.5; l.6–3.9). Number of sexual partners was in our study a surrogate for HPV infection. Smoking and parity after age 24 were weakly and inconsistently associated with the risk of cervical cancer. Previous screening (OR = 0.7; 0.5–1.0) and ever having undergone a Caesarean section (OR = 0.4; 0.2–0.8) were protective factors. © 1992 Wiley‐Liss, Inc.
Transforming growth factor β1 (TGF‐β1) inhibits growth of a human ovarian carcinoma cell line (OVCCR1) and is expressed in human ovarian tumors
Authors: Jozan S. , Guerrin M. , Mazars P. , Dutaur M. , Monsarrat B. , Cheutin F. , Bugat R. , Martel P. , Valette A. 
Published: February 2007

AbstractThe effects of EGF and TGF‐β1 on the proliferation of 2 ovarian carcinoma cell lines (IGROV1 and OVCCR1) were evaluated. The cell lines were adapted to grow in a restricted serum (0.5%) medium. EGF was required for proliferation of both ovarian cell lines. Low doses of TGF‐β1 inhibited clonogenic capacity and attenuated the EGF‐mediated stimulation of DNA synthesis in OVCCR1 cells. TGF‐β1 inhibited OVCCR1 cell proliferation by blocking the cell cycle at the G1/S transition. TGF‐β1 did not affect either clonal or monolayer growth of IGROV1 cells. Both cell lines express type‐I and type‐III TGF‐β1 receptors, suggesting that the unresponsiveness of IGROV1 cells to TGF‐β1 occurs at a post‐receptor level. TGF‐β1 mRNA was detected in OVCCR1 cells and in 8 out of 11 of the ovarian tumor specimens examined. © 1992 Wiley‐Liss, Inc.
H‐2Db gene transfer into highly metastatic D122 cells results in tumor rejection in allogeneic recipients, but does not affect metastasis in syngeneic recipients. Implications for mechanisms of allorejection
Authors: Plaksin Daniel , Gelber Cochava , Eisenbach Lea 
Published: February 2007

AbstractHighly metastatic, weakly immunogenic Lewis lung carcinoma clones express very low levels of H‐2Kb and moderate levels of H‐2Db class‐1 major histocompatibility complex antigens. These cells metastasize spontaneously in mice with C57BL/6 genetic background possessing the H‐2Db locus, and grow as local tumors across allogeneic barriers. Transfection of the H‐2Db genes into the highly metastatic clone D122 did not alter the growth or metastatic capacity of these cells in syngeneic mice. However, these cells were rejected in allogeneic mice. Transfection of the H‐2Kd or H‐2Kk genes into D122 elicited a CTL population that cross‐reacted with cells bearing native H‐2Db antigens. These data suggest that overlapping allo‐CTL populations are induced by a native alloantigen and by alloantigen peptides presented through self class‐l molecules. © 1992 Wiley‐Liss, Inc.
Treatment of liver metastases of human colon cancers in nude mice with somatostatin analogue RC‐160
Authors: Qin Yunfeng , Schally Andrew V. , Willems Gerard 
Published: February 2007

AbstractHepatic metastases of colon 320 DM and WidR human colon cancers in nude mice were treated by s.c. injections of somatostatin analogue RC‐160 for 4 weeks. Chronic administration of RC‐160 significantly inhibited the incidence and growth of liver metastases of these 2 colon‐cancer cell lines. After RC‐160 treatment, the incidence of liver metastases decreased by 25% for colon 320 DM cells and by 37.5% for WidR cells. The mean number of metastatic tumors in each liver decreased by 47.9% for colon 320 DM and 42.6% for WidR. Survival times of mice with liver tumors of colon 320 DM and WidR cells were prolonged by 20 days and 7 days, respectively. The inhibitory effect of RC‐160 on the growth of these 2 colon cancers implanted s.c. was also observed. After administration of RC‐ 160 for 4 weeks, the mean tumor volume in the treated groups was only 39.8% of that of controls for the colon 320 DM line and 58% for the WidR line. Tumor‐growth rate and final tumor weight were also significantly decreased, while tumor‐volume doubling time and tumor‐growth delay time were prolonged. The effect of RC‐160 on cellular proliferation in the tumors was studied by in vivo labelling with bromodeoxyuridine and immunoperoxidase staining. The mean labelling index in the treatment group was reduced by 14.9% and 19.5%, respectively, for colon 320 DM and WidR tumors. The cytostatic effect of RC‐160 was also evident from the apparent reduction in DNA and protein content in the tumor tissues of these cancer lines. Our findings suggest that somatostatin analogue RC‐160 may be useful for the treatment of patients with hepatic metastases of colon cancer. © 1992 Wiley‐Liss, Inc.
Early superoxide dismutase alterations during SV40‐transformation of human fibroblasts
Authors: Bravard A. , Hoffschir F. , Sabatier L. , Ricoul M. , Pinton A. , Cassingena R. , Estrade S. , Luccioni C. , Dutrillaux B. 
Published: February 2007

AbstractThe expression of superoxide dismutases (SOD) 1 and 2 was studied in 4 clones of human fibroblasts after their infection by simian virus 40 (SV40), in parallel with the alterations of chromosomes 21 and chromosome 6q arms, carrying the genes that encode for SOD1 and SOD2 respectively. For all clones, a similar scheme with 2 main phases was observed for both chromosome and SOD variations. The first phase, defined as the pre‐crisis phase, was characterized by chromosomal instability, but maintenance of normal numbers of chromosome 6q arms and chromosomes 21. The level of SOD2 mRNA was high, while SOD2 activity and immunoreactive protein were low. SOD1 protein and activity were decreased. In the second phase, defined as the post‐crisis phase, the accumulation of clonal chromosomal rearrangements led to the loss of 6q arms, while the number of chromosomes 21 remained normal. SOD2 mRNA level was decreased and SOD2 immunoreactive protein and activity remained low. SOD1 protein and activity increased with passages, reaching values similar to those of control cells at late passages. As in established SV40‐transformed human fibroblast cell lines, good correlation was found between SOD2 activity and the relative number of 6q arms. These results allow us to reconstruct the sequence of events leading to the decrease of SOD2, a possible tumor‐suppressor gene, during the process of SV40‐transformation of human fibroblasts. © 1992 Wiley‐Liss, Inc.
Effect of IL‐1 on experimental bone/bone‐marrow metastases
Authors: Arguello Francisco , Baggs Raymond B. , Graves Brian T. , Harwell Shari E. , Cohen Harvey J. , Frantz Christopher N. 
Published: February 2007

AbstractBone metastasis is a common event and a major cause of morbidity in cancer patients. The hematopoietic marrow of the bones, rather than the bone tissue per se, is the target organ in bone metastasis. In the bone marrow, IL‐1 induces the release of hematopoietic growth factors that may affect tumor‐cell growth. We treated groups of mice with rhulL‐1α to examine its role in the establishment of experimental bone/bone‐marrow metastasis. We found that injection of 2 μg of rhulL‐1α 24 hr prior to, simultaneously with or 24 hr after the injection of 104B16 melanoma cells into the left cardiac ventricle of mice resulted in a 2‐fold increase in the average number of colonized bones per mouse. GM‐CSF is produced by bone‐marrow stromal cells in response to IL‐1, and its receptor has been found on tumor cells, including melanoma cells. However, the administration of rmuGM‐CSF to mice by either multiple injections or continuous infusion did not affect the number of colonized bones. Many of the biologic effects of IL‐1 are mediated by prostaglandins. Treatment of mice with 100 μg of indomethacin, a potent inhibitor of prostaglandin synthesis, prior to the injection of rhulL‐ 1α, prevented the increase in number of bone metastases. To determine whether constitutive productions of IL‐1 and/or prostaglandins are involved in the pathogenesis of bone/bone marrow metastasis, we treated mice with antimouse IL‐1α neutralizing antibodies, rhulRAP (an inhibitor of IL‐1 activity) or indomethacin. We found no difference in the average number of colonized bones per mouse between treated and control mice. We conclude that exogenous administration of IL‐1 enhances experimental bone/bone‐marrow metastases, and that this phenomenon is mediated through prostaglandins. However, neither the constitutive production of IL‐1 nor that of prostaglandins appear to play a role in the pathogenesis of bone/bone‐marrow metastasis in our murine model system. © 1992 Wiley‐Liss, Inc.