Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dimethylbenzanthracene (DMBA)-induced mouse mammary tumors characteristically contain an activated c-H-ras-1 gene with an A----T transversion in the 61st codon which is expressed as a rapidly migrating p21 c-H-ras. The role of the activated c-H-ras-1 locus in the initiation of mammary neoplasia was analysed by studying seven transplantable, DMBA-induced Balb/c premalignant mammary hyperplasias. The DNAs from these hyperplasias had no evidence of activation of the c-H-ras-1 gene. One of the fifteen tumors arising from untreated hyperplastic outgrowths had a 61st codon mutation. In contrast, 67% of the tumors developing in DMBA-treated hyperplasias had the characteristic 61 codon mutation. All of the tumors with the characteristic mutation expressed the corresponding rapid p21 c-H-ras. These data suggest that although c-H-ras-1 activation may play an important role in neoplastic progression, it had no definable role in the initiation or the maintenance of the mammary hyperplasias studied here.
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PMID:c-H-ras-1 expression in 7,12-dimethyl benzanthracene-induced Balb/c mouse mammary hyperplasias and their tumors. 284 17

Cytogenetic studies were performed on endometrial specimens of four patients with hyperplasia. Six with adenocarcinoma and one with mixed mesodermal tumor. All 65 cells obtained from hyperplasia specimens excluding one cell, had a normal female karyotype. However, cells from five adenocarcinoma specimens had chromosomal abnormalities, though a specimen of a well differentiated adenocarcinoma showed a normal karyotype. A few numerical abnormalities which were clonal in origin, were noted in one case each. Three kinds of structural abnormalities involving chromosomes 1 were identified as clonal in origin; del (1) (p21), t. dic(1; 16) (p21; q24), and i (lq). Since carcinoma cells had two chromosomes 1 of normal morphology, the presence of the marker chromosome led to the partial trisomy or tetrasomy of the long arm of a chromosome 1, being characteristic of cells from adenocarcinoma of the endometrium. A successively transplantable tumor has been produced from a poorly differentiated carcinoma cells with the t. dic (1; 16) (p21; q24) marker chromosome. Histological and chromosomal examinations were performed in cells from the passage 1, 4 and 5 tumors in order to explore the role of this marker played in the formation of the endometrial carcinoma. Though the degree of differentiation status of tumor cells had been changed during transplantations, the t. dic (1; 16) (p21; q24) marker were observed consistently among these cells. This suggested that the rearrangement of chromosome 1 was not produced as a result of genetic instability due to tumor progression, but rather specifically associated with the endometrial carcinogenesis. None of karyotypic changes excluding the marker and the tetraploid was responsible for these phenotypic changes.
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PMID:[Cytogenetic study of endometrial carcinoma]. 301 54

The expressions of epidermal growth factor (EGF), EGF receptor, transforming growth factor (TGF) alpha and c-Ha-ras p21 in human gastric carcinomas were studied immunohistochemically. Any of these four marker proteins from gastric tumor cells was closely correlated with the depth of tumor invasion. The incidences of cases with EGF or synchronous expression of TGF alpha and c-Ha-ras in metastatic tumors were significantly higher than those in primary tumors (p less than 0.05 or p less than 0.01). Patients with synchronous expression of EGF and its receptor or TGF alpha and ras p21 had a far poorer prognosis than those without such synchronous expression. These findings strongly suggest that the EGF-related growth factors, EGF-receptor and ras p21 mutually play an important role in tumor progression and could be useful as potential metastatic and/or prognostic markers for gastric carcinoma.
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PMID:[Growth factors as biological markers of malignancy]. 326 Apr 65

Samples of 37 fresh human ovarian tumor biopsies were screened to detect proto-oncogene amplification and ras mutations. Three samples showed c-K-ras2 amplification; none of the other oncogenes tested revealed any gene amplification. 5-, 25-, and 120-fold amplifications were assessed by dilution experiments and soft laser densitometry. Corresponding elevated levels of c-K-ras2 mRNA and p21 ras protein were found in the three tumors. Analysis by the polymerase chain reaction method to detect point mutations of codon 12 or codon 61 of Harvey-, Kirsten-, or N-ras showed only the wildtype sequence in all specimens. No correlation was found between ras activation and degree of tumor progression or histological subtype. DNA from one of the tumors with c-K-ras2 amplification proved to have high transforming activity in the NIH 3T3 tumorigenicity assay, but the transforming gene was not c-K-ras2.
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PMID:ras oncogene activation in human ovarian carcinoma. 328 94

Expression of ras p21 oncogene and DNA content of paraffin-embedded tissues from 55 smooth muscle tumors of the gastrointestinal tract were analysed simultaneously by using immunofluorescence and flow cytometry. All of 14 leiomyomas were found to be DNA diploid and lower-expression of ras p21. Four cases of DNA aneuploidy (33%) and 9 cases of ras p21 overexpression (75%) were found in 12 potential malignant smooth muscle tumors, while all 29 cases of leiomyosarcomas were aneuploidy (100%) (P < 0.005), but the rate of ras p21 overexpression was not increased continuously (72%) (P < 0.005). 24 of 33 aneuploid tumors (73%) were found to be ras p21 overexpression, while in 22 diploid tumors, there were only 6 cases (27%) (P < 0.005). The outcome of the patients with ras p21 lower-expressed diploid tumor was excellent, compared to the patients with ras p21 overexpressed aneuploid tumor it was worst (P < 0.005). It was suggested that DNA aneuploidy and ras p21 overexpression could be regarded as the mark of malignancy. The overexpression of ras p21 oncogene was always presented in the early stage of malignant smooth muscle tumors, when the cell proliferation was active but the DNA content was still normal, and stable in the whole procss of the tumor progression. ras p21 expression and DNA content could supply a deficiency each other in the diagnosis and could be used as objective parameters in distinguishing malignancy from benign and predicting the prognosis of the patients with smooth muscle tumors of the gastrointestinal tract.
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PMID:[Quantitation of Ras p21 oncogene and DNA content of gastrointestinal smooth muscle tumors and prognostic significance]. 758 76

The human beta-catenin gene (CTNNB1) has been localized to 3p22-->p21.3 by fluorescence in situ hybridization. Recent studies have suggested the presence of one or more tumor suppressor genes on the short arm of chromosome 3. This raises the possibility that CTNNB1, for which important features are already known, is involved in tumor progression.
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PMID:Assignment of the human beta-catenin gene (CTNNB1) to 3p22-->p21.3 by fluorescence in situ hybridization. 773 93

The purpose of this study was to determine the correlation between expression of ras oncoproteins and the tumor stage or outcome of patients with gastric carcinoma. After the specificity of each anti-ras monoclonal antibody was confirmed by protein immunoblot analysis, immunohistochemical assays for a common-ras antigen present in N-, Harvey- and Kirsten (K)-ras oncoproteins, as well as for K-ras specific antigen, were performed on paraffin-embedded carcinoma tissue from 110 patients who underwent curative resection. By Western blot analysis, there was more p21 in fresh cancer specimens than in normal specimens. K-ras expression distinguished advanced from early gastric carcinoma and correlated with depth of cancer invasion. Among the 110 patients, survival rates of those with carcinomas positive for the common-ras or K-ras antigens were significantly lower than of those with antigen-negative carcinomas (p < 0.05). In a multivariate analysis, nodal involvement (p = 0.002), serosal invasion (p = 0.012) and K-ras p21 expression (p = 0.044) were independently predictive of the recurrence. These results suggest that K-ras p21 is a useful marker of tumor progression and poor prognosis after curative resection.
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PMID:Expression of Kirsten-ras p21 in gastric cancer correlates with tumor progression and is prognostic. 798 94

A recent trend in cancer control programmes is the development of early detection strategies and chemoprevention of premalignant lesions. The present study evaluates the potential of selected markers in the biological staging of tumor progression in oral mucosa for better management of the disease. The expression patterns of various cytokeratin protein types such as 10/11, 13 & 16, 19, 18, 14 and pancytokeratin, involucrin, ras p21, epidermal growth factor (EGF) and its receptor (EGFR) were assessed immunohistochemically in various stages of tumor progression in oral mucosa. Statistical analyses such as the Kruskal-Wallis one-way ANOVA, Spearman's rank correlation and multiple regression analysis were carried out to see which proteins have a significant association with tumor progression in oral mucosa. Statistical analysis showed that the expression patterns of cytokeratin types 10/11, 14 and 19, involucrin and epidermal growth factor were significantly correlated with tumor progression in oral mucosa in both univariate and multivariate analysis. Thus the biological stage of a lesion can be calculated from the multiple regression equation derived for these proteins, which could be more useful in assessing the stage of tumor progression in oral mucosa than histopathological grading.
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PMID:Potential biological markers for the staging of tumor progression in oral mucosa: a multivariate analysis. 877 6

p21/WAF1/CIP1/SDI1 is an important cell-cycle mediator with tumor suppressor gene capabilities, and its inactivation could potentially lead to tumor progression. Because tumor suppressor genes are commonly inactivated by somatic and germline mutations, we analyzed a variety of human tumor cell lines for p21 mutations. We used single-strand conformational analysis and direct sequencing to identify possible mutations in the p21 coding region. Two base-alterations were observed in 41 immortalized human tumor cell lines. A previously reported polymorphism that results in a serine-to-arginine amino-acid substitution at codon 31 was found in 24% (10 of 41) of the tumor cell lines but was also found in 10% (six of 62) of normal parental DNAs tested and 7% (three of 43) of normal DNAs from patients with primary endometrial tumors. Another nucleotide substitution found at codon 80 resulted in the replacement of threonine with methionine. Codon 80 changes were found in 7% (three of 41) of the tumor cell lines (all endometrial) and in 2% (one of 62) of the normal parental DNAs. This change was not found in any of the primary endometrial tumors examined. The biological activity of these base changes was analyzed by using in vitro cyclin-dependent kinase 2-cyclin A kinase assays and calcium phosphate transfections. We observed that wild-type p21 and the p21 variants had similar growth-inhibitory abilities. Thus, our results suggest that mutation of the p21 gene is not prevalent in human tumor cell lines and is not a probable mechanism of inactivation of this gene.
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PMID:Mutational analysis of the p21/WAF1/CIP1/SDI1 coding region in human tumor cell lines. 878 65

Alterations of the N-linked carbohydrate core structure of cell surface glycoproteins (beta 1-6 branching) can be detected by phytohemagglutinin (PHA-L) lectin binding and has been linked to tumor progression and K-ras activation in colon cancer. The purpose of this study was to determine the prevalence of this carbohydrate alteration and its relationship to K-ras activation in pancreatic cancer. Nine human pancreatic cancer cell lines and 4 colon lines as controls were grown under standard tissue culture conditions. K-ras genome analysis was performed by polymerase chain reaction amplification and sequencing. The proportion of cellular p21-ras bound to GTP (ras-GTP level) was determined using immunoprecipitation of 32P-labeled cell lysates followed by thin layer chromatography and phosphoimaging analysis. Lectin blot analysis was performed on crude membrane preparations. Sensitivity to lectins was assessed with cell culture thymidine incorporation. Of 9 pancreatic cancer lines tested, 3 had wild type K-ras, 2 had heterozygous and 4 had homozygous mutations in codon 12 of K-ras. These genotypes correlated strongly with the level of ras-GTP measured. K-ras mutants had increased levels of ras-GTP compared to wild-type cell lines. PHA-L binding to cell membranes correlated positively with ras-GTP levels in 7 out of 9 cell lines. PHA-L toxicity was greatest in cells with positive PHA-L reactivity on Western blotting. A positive correlation between the presence of K-ras mutation, increased ras-GTP level, and increased cell surface beta 1-6 N-linked carbohydrate exists in pancreatic cancer cell lines.
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PMID:Phytohemagglutinin-L (PHA-L) lectin surface binding of N-linked beta 1-6 carbohydrate and its relationship to activated mutant ras in human pancreatic cancer cell lines. 894 26


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