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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using the NIH 3T3 transformation assay system, an activated c-Ha-ras transforming gene has been identified in three distinct early passage colon carcinoma cell lines isolated from an invasive, differentiated, adenocarcinoma. The p21 c-Ha-ras gene product from these cell lines displayed an altered electrophorectic mobility and a point mutation in the DNA coding sequence leading to an amino acid substitution at position 12.
Carcinogenesis 1985 Oct
PMID:c-Ha-ras not c-Ki-ras activation in three colon tumour cell lines. 299 2

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

Expression of the ras oncogene product p21 (ras p21) in benign and malignant human colonic tissues was studied using the monoclonal antibody RAP-5 and the avidin-biotin-peroxidase technique. Histologically normal colonic mucosa and hyperplastic mucosa adjacent to carcinomas (transitional mucosa) were found, in most cases, to be negative for reactivity with the antibody or showed weak staining of a few epithelial cells. Similar findings were observed in hyperplastic and juvenile polyps. Of the 145 adenomas studied, 47 (32.4%) showed detectable levels of ras p21 expression. RAP-5 immunohistochemical staining was significantly associated with the degree of epithelial dysplasia (P less than 0.01) and the size of adenoma (P less than 0.05), but not with the histological type. Fifty-four of 70 primary adenocarcinomas (77.1%) were reactive with RAP-5 and usually demonstrated a higher percentage of stained cells and more intense cytoplasmic staining than that observed in adenomas. Although metastases often displayed a similar or even higher levels of ras p21 expression compared with the primary carcinomas, in 10 cases one or more metastatic lesions showed lower levels of ras p21. These results suggest that enhanced ras p21 expression may, at times, occur in the early stages of human colon carcinogenesis but are probably not associated with metastatic tumour progression.
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PMID:ras p21 oncoprotein expression in human colonic neoplasia--an immunohistochemical study with monoclonal antibody RAP-5. 304 43

Oncogenic forms of the p21ras genes have been found in a large variety of human malignancies and tumours induced in animals by chemical carcinogens or irradiation. The active form of the p21 ras proteins is the GTP bound state and oncogenic mutations result in the protein being constitutively in the GTP bound active state. There is evidence to suggest that activating mutations can occur either as initiating steps in carcinogenesis or as later events in the evolution to frank neoplasia. To transduce a signal for proliferation and transformation the active GTP form of p21ras must interact with one or more cellular targets. Genetic experiments suggest that one potential effector molecule is the GTPase activating protein GAP. However, the mechanism by which interaction with GAP results in proliferation and transformation remains to be elucidated.
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PMID:The ras oncogenes. 307 34

Remarkable progresses have been made in the field of oncogenes in the last several years. More than 40 oncogenes or proto-oncogenes were identified by transfection assay and by weak homology of base sequences with known oncogenes. Many of them were shown to play a specific role in regulation of cell growth and signal transduction, but their exact roles in development and progression of human cancers are still not clear. Study of oncogenes and their expression at cellular level using immunohistochemistry and in situ hybridization will contribute to understand how oncogenes are involved in the multiple steps of carcinogenesis. In this article, application of newly established monoclonal antibodies to ras p21 for immunohistochemistry and immunoblotting analysis and possibilities of DNA analysis using formalin-fixed paraffin-embedded blocks are discussed.
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PMID:[Analysis of oncogene and its expression at cellular level]. 315 11

A transforming N-ras gene was isolated from the SHAC human stomach fibrosarcoma cell line. A single-point mutation resulting in the substitution of histidine for glutamine at codon 61 was found in the SHAC transforming allele. The N-ras gene is overexpressed in the tumor cells and transformant cells. The N-ras p21 product was studied by immunoprecipitation and showed no alteration in mobility as compared to the normal p21 protein. The c-myc gene is amplified and overexpressed in these cells. This report gives evidence that an amplified c-myc and a mutated N-ras gene are both present in this tumor cell line and provides support for the idea that co-operation of at least 2 activated cellular oncogenes is required for carcinogenesis.
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PMID:Both N-ras and c-myc are activated in the SHAC human stomach fibrosarcoma cell line. 328 24

DNA prepared from the 3-methylcholanthrene (3MC)-transformed human 312H cell line induced foci on NIH/3T3 cells, whereas DNAs prepared from 7,12-dimethylbenz[a]-anthracene-transformed and the dimethylsulfoxide control 312H cell lines failed to induce foci. The transformed gene from the 3MC-transformed 312H cells was identified as an activated form of the human cellular transforming H-ras oncogene. Analysis of the ras oncogene p21 product in this transformant by immunoprecipitation and gel electrophoresis suggested that this gene was activated by mutation in the 61st codon. These findings demonstrate that activation of a member of the ras gene family can occur in a chemically transformed human cell line.
Carcinogenesis 1987 Aug
PMID:Activation of H-ras oncogene in 3-methylcholanthrene-transformed human cell line. 330 Oct 48

After long-term feeding of a choline-devoid diet to rats, the authors analyzed rasK, rasH, and rasN transcripts and gene structure in livers and liver tumors. They controlled their analysis by studying cell lines derived from chemically induced hepatomas. Transcripts from all three genes were elevated in all tumors, but not in the livers from which they arose. The transcript elevations may represent an effect of active cell proliferation in the tumors. Clone HiHi-3, derived from the Kirsten murine sarcoma virus, detected a large number of hybridization bands, most of which were not part of the rasK-p21 gene. Most tumors had an altered band at 2.6 kb; some had other altered bands. No alterations were seen in liver DNA, and none of the cell lines showed the 2.6 kb band. At low stringency, a rasH probe, which contains a short segment of a similar viral sequence, also detected altered bands in tumors and a single treated liver. These changes in endogenous viral sequences of the rat genome appear to be characteristic of carcinogenesis by a choline-devoid diet.
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PMID:Analysis of ras genes and linked viral sequences in rat hepatocarcinogenesis. 331 28

A new human carcinoma cell line (HEC-1), which was derived from low differentiated adenocarcinoma of the endometrium, has been established. Cells from tumor tissues grown in athymic mice were cultured in minimal essential medium supplemented with 20% fetal calf serum. Contaminated mouse fibroblasts were removed from the culture by the absorption of anti-mouse serum. Continuous cell growth (doubling time: 51.6 hrs) could be observed during 64 passages. The cultured cells appeared monolayer and the cellular arrangement was a pavement-like pattern. The morphology of cells was analogous to the one of adenocarcinoma cells. The modal number of chromosomes of the original tumor cells were 46. The t. dic (1; 16)(p21; q24) marker which had been identified as the clonal abnormality in the original tumor cells, was also observed consistently in cultured cells, though the loss of chromosome 19 was disappeared during the passage. This suggested that the rearrangements of the long arm of chromosome 1 played an important role for the endometrial carcinogenesis.
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PMID:[Establishment and characterization of the cell line derived from low differentiated adenocarcinoma of the endometrium]. 346 29

An affinity purified sheep IgG antibody to a 20 amino acid peptide from the carboxyterminal end of RasHa p21 was used to localize RasHa p21 on fixed tissue sections of Harvey sarcoma (HaSV) virus-infected mice by the avidin-biotin-peroxidase immunocytochemical technique. Control sera included immune sheep sera absorbed with the peptide, preimmune sheep sera and a goat polyclonal antibody to Rauscher leukemia virus p30. Neonatal BALB/c mice were injected with HaSV/Moloney leukemia virus (MoLV), MoLV alone or buffer. Short-term fixation in Bouin's fixative was found to be the most effective method for demonstrating p21 in fixed tissue sections. RasHa p21 was found in 5-80% of the induced sarcoma cells, depending on the tissue fixative and antibody dilution. The antigen was localized to the cell membrane and in the cytoplasm. Tumors induced by NIH 3T3 cells transformed with cellular Ha-ras oncogenes had less than 1% immunoreactive tumor cells. Splenic erythroblasts in HaSV-induced erythroblastosis contained membrane antigen as did some reticular cells in lymph nodes draining the sarcomas. Normal tissues of virus-inoculated mice, uninoculated controls or fetuses and selected naturally occurring or induced liver tumors of mice, chemically induced skin tumors of mice, N-nitrosomethylurea-induced mammary tumors of rats, and naturally occurring tumors of F344/NCr rats did not contain immunoreactive p21. Thus, with the use of affinity purified IgG sheep polyclonal antibody to a peptide in RasHa p21, we were able to demonstrate RasHa p21 in tumors and other cells. The degree of immunoreactivity was related to the expected level of p21 expression.
Carcinogenesis 1986 Apr
PMID:Immunocytochemical localization of RasHa p21 in normal and neoplastic cells in fixed tissue sections from Harvey sarcoma virus-infected mice. 351 33


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