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Query: UMLS:C0001418 (adenocarcinoma)
 68,496 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relationship of tumor size, status of disease in the TNM classification, and stage of disease to ras oncogene expression was studied in human non-small cell lung cancer materials immunohistochemically using monoclonal antibody rp-35 against ras 21. Materials of adenocarcinoma and squamous cell carcinoma obtained from primary sites larger than 30 mm in diameter exhibited intensely positive reactions with rp-35 significantly more frequently than those with primary sites, 30 mm in diameter or smaller (p less than 0.01). Furthermore in the TNM classification, cases with T2 (with primary sites larger than 30 mm in diameter) or T3 (with direct extension to adjacent structures) showed significantly higher reaction with rp-35 than those with T1 (with primary sites 30 mm in diameter or smaller) (p less than 0.01), although N and M status did not correlate with ras p21 expression. These results suggest that ras oncogene may play a significant role in growth or tumorigenesis at the primary site in human non-small cell lung cancer.
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PMID:The relationship of clinical classification to ras p21 expression in human non-small cell lung cancer. 284 11

It is not yet clear whether some polymorphic variants of the Ha-ras-1 gene confer genetic predisposition to cancer. However, recent data on myelodysplasia and lung cancer are controversial. To clarify this point, 62 colorectal adenocarcinoma patients were examined for the Ha-ras-1 gene restriction fragment length polymorphism and results were compared with those of 108 healthy blood donors. No Ha-ras-1 polymorphic variants specifically associated with the cancer patients were detected. However, a specific genotype was significantly more frequent in the healthy donors than in the cancer patients (16% versus 5%), suggesting an interaction between the two alleles of the gene.
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PMID:Ha-ras-1 restriction fragment length polymorphism and susceptibility to colon adenocarcinoma. 288 94

Proto-oncogenes, which have been widely implicated in the pathogenesis of malignant human tumors, frequently demonstrate restriction fragment length polymorphism (RFLP). Population studies of such restriction alleles is of potential interest for genetic analysis of cancer susceptibility. Some of the initial date of Krontiris et al (1985) showing a significant increase of rare c-ha-ras-l alleles in individuals with tumors, have been confirmed in certain types of cancer (breast cancer, lung adenocarcinoma), whereas others have been refuted (myelodysplasia, melanoma, colon adenocarcinoma). Other significant associations have been found between other proto-oncogene RLFPs and tumors (c-mos and breast cancer, c-raf and non Hodgkins lymphoma, L-myc and lung carcinoma metastasis). Although they are controversial, these studies should be extended, in order to determine whether the presence of certain alleles is a contributing factor in the development of certain tumors.
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PMID:[Genetic polymorphism and susceptibility to cancer]. 289 51

Activated c-Ki-ras with a point mutation (GGT to CGT) at codon 12, resulting in the substitution of arginine for glycine, was found in DNA from metastatic pancreatic adenocarcinoma in a lymph node. By means of restriction endonuclease length polymorphism with SacI digestion, we were able to demonstrate that the same point mutation of c-Ki-ras was present in the primary tumor and in metastases in lymph nodes. DNA from the normal spleen of the patient did not have this type of point mutation. Moreover, amplifications of 3- to 6-fold of the activated c-Ki-ras and 50-fold of c-myc were found in the primary tumor and the metastases in the two lymph nodes, indicating that point mutation had occurred at a relatively early stage of the tumor development, before amplification of the gene. This is the first clear demonstration of amplification of activated c-Ki-ras accompanied by amplification of c-myc in both primary and metastatic human tumors in vivo.
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PMID:Amplifications of both c-Ki-ras with a point mutation and c-myc in a primary pancreatic cancer and its metastatic tumors in lymph nodes. 300 77

The role of extracellular amines such as noradrenaline and serotonin and their interaction with cyclic nucleotides and intracellular polyamines in the regulation of intestinal epithelial cell proliferation is reviewed with particular reference to the differences between normal and neoplastic cells. In respect to the normal epithelium of the small intestine there is a strong case to support the notion that cell proliferation is controlled by, amongst other things, sympathetic nerves. In colonic carcinomas, antagonists for certain serotonin receptors, for histamine H2 receptors and for dopamine D2 receptors inhibit both cell division and tumour growth. Because of the reproducible variations between tumour lines in the response to these antagonists, this inhibition appears to be due to a direct effect on the tumour cells rather than an indirect effect via the tumour host or stroma. This conclusion is supported by the cytocidal effects of toxic congeners of serotonin on the tumour cells. The most salient difference between the amine responses of normal and neoplastic cells relates to the issue of amine uptake. Proliferation of crypt cells is promoted by amine uptake inhibitors, presumably because they block amine re-uptake by the amine secreting cells--sympathetic neurones and enteroendocrine cells. However, tumour cell proliferation is strongly inhibited by amine uptake inhibitors, suggesting that neoplastic cells can, and need to take up the amine before being stimulated by it. Recent revelations in the field of oncogenes also support an important association between amines, cyclic nucleotides and cell division. The ras oncogenes code for a protein that is a member of a family of molecules which relay information from extracellular regulators, such as biogenic amines, to the intracellular regulators, including cyclic nucleotides. Evidence is presented suggesting that enteroendocrine cells, enterocytes, carcinoid tumour cells and adenocarcinoma cells all have the same embryonic origin and that cells exhibiting an admixture of endocrine and proliferative properties exist in colonic tumours, but not in the normal intestinal epithelium. Thus, it appears that in the normal intestine a clear structural and functional distinction exists between the regulating cells (i.e. the sympathetic neurones and enteroendocrine cells) and the regulated cells (i.e. the undifferentiated crypt cells): cells that have acquired a regulating role are no longer able to divide and cells which are able to divide do not take up or store amines.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Biogenic amines as regulators of the proliferative activity of normal and neoplastic intestinal epithelial cells (review). 303 70

An expression of ras p21 proteins on cholangiocarcinoma (CC) (intrahepatic bile duct carcinoma) cells was examined by an immunoperoxidase method using an appropriate dilution of mouse monoclonal antibody RAP-5, with which no positive staining was obtained in livers with normal histology. Of 44 CCs examined 39 were positive for the antigens; well-differentiated adenocarcinoma usually showed a diffuse weak, cytoplasmic staining in nearly all tumor cells with the same staining intensity, while in moderately and poorly differentiated adenocarcinoma the expression of p21 varied markedly in intensity from cell to cell in the same cell nest. The number of positive cells decreased with the grade of tumor, and no or little staining was observed in undifferentiated areas. These findings indicate that the expression of ras p21 antigens was lost with increasing dedifferentiation of tumor cells. Carcinoembryonic antigens (CEA) were positive in 42 of 44 CCS. Well-differentiated adenocarcinoma expressed CEA along the apical surfaces of the tumor glands. With the dedifferentiation of tumor cells, the expression of CEA became prominent not only at the apical surfaces but also on the basolateral surfaces and in the cytoplasms, and further in the surrounding stromal tissue. There was no clear-cut correlation between the expression of p21 antigens and the production of CEA in CCs.
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PMID:Immunohistochemical localization of ras p21 and carcinoembryonic antigens (CEA) in cholangiocarcinoma. 303 84

47 tumor samples, 45 of which were obtained at thoracotomy for non-small cell lung cancer were examined for mutational activation of the oncogenes H-ras, K-ras, and N-ras. A novel, highly sensitive assay based on oligonucleotide hybridization following an in vitro amplification step was employed. ras gene mutations were present in nine of 35 adenocarcinomas of the lung (all K-ras), in two of two lung metastases of colorectal adenocarcinomas (1 x K-ras, 1 x N-ras) and in one adenocarcinoma sample obtained at autopsy (H-ras). All K-ras and H-ras mutations were in either position 1 or 2 of codon 12, while the N-ras mutation was in position 2 of codon 61. The potential clinical significance of K-ras activation was analyzed using the combined results of this and of our earlier study (S. Rodenhuis et al., New Engl. J. Med., 317: 929-935, 1987). Lung adenocarcinomas with K-ras mutations tended to be smaller and were less likely to have spread to regional lymph nodes at presentation. With a median follow up of 10 months, survival data are still immature. None of six adenocarcinomas of nonsmokers had a K-ras mutation and only one of four who had stopped smoking more than 5 years before. We conclude that mutational K-ras activation is present in about a third of adenocarcinomas of the lung and that the mutational event may be a direct result of one or more carcinogenic ingredients of tobacco smoke. Studies involving larger numbers of patients are required to confirm the association of K-ras activation with smoking and the inverse relation with tumor progression.
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PMID:Incidence and possible clinical significance of K-ras oncogene activation in adenocarcinoma of the human lung. 304 48

To investigate the role of oncogenes in the development of metastatic ability by prostatic cancer, the viral-Harvey-ras (v-H-ras) oncogene was introduced into the Dunning rat prostate adenocarcinoma cell line, AT2.1 by means of DNA transfection. The AT2.1 cell line is a cloned cell line that is anaplastic, rapidly growing, and has low metastatic potential; after subcutaneous (s.c.) inoculation in syngeneic rats, fewer than 10% of inoculated rats develop distant metastases. Calcium phosphate mediated DNA transfections of AT2.1 cells were performed with the v-H-ras oncogene or with control DNA. The in vitro growth rate of cloned transfectants, which contain and express the v-H-ras oncogene is similar to that of untransfected AT2.1 cells and of control transfectants. After s.c. inoculation in syngeneic rats, all transfectants produced rapidly growing tumors with similar growth rates. While control transfectants had low metastatic ability comparable to untransfected AT2.1 cells, the H-ras expressing transfectants metastasized in over 80% of inoculated rats. While the mechanism by which nonmetastatic Dunning tumor sublines spontaneously develop high metastatic ability in vivo during serial s.c. passage has not been addressed in the present studies, these studies do demonstrate that expression of an activated H-ras oncogene can reproducibly convert a tumorigenic nonmetastatic prostatic cell line to a highly metastatic state.
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PMID:Expression of a transfected v-Harvey-ras oncogene in a Dunning rat prostate adenocarcinoma and the development of high metastatic ability. 305 38

The Y13 259 monoclonal antibody to the ras p21 protein was used in an immunohistochemical assay to study the levels of ras p21 in human uterine lesions as compared to normal tissue. Out of 73 hysterectomies obtained we have examined ras p21 expression in separately made sections from the endometrium, the cervix and leiomyomas found in the same specimens. A total of 155 tissue sections were finally evaluated and included: 55 endometrial mucosae (normal, hyperplastic and atrophic), 13 leiomyomas, 60 cervicitis (mild, moderate and severe with or without dysplasia), 3 in situ and 7 invasive carcinoma of the cervix, 12 invasive adenocarcinoma of the endometrium and 5 endometrial adenocarcinomas, which involved the cervical canal. Out of the 73 hysterectomy specimens 27 lesions were malignant and showed elevated expression of ras p21. The remaining 128 were normal or atrophic mucosae and benign or premalignant lesions, which were mostly negative. However, all cases of severe cervicitis and dysplasias and 6 out of the 12 hyperplastic endometrial lesions were found to be moderately or highly positive. Our results suggest that elevated expression of ras oncogenes may play an important role in the development of human uterine lesions.
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PMID:Immunohistochemical study of ras oncogene expression in endometrial and cervical human lesions. 306 21

Using NIH3T3 cell transfection assay, activated c-K-ras was detected in two cell lines, TRb and TSb, obtained from a single colon adenocarcinoma induced in a rat by 1,2-dimethylhydrazine. TRb cells give rise to progressive and metastatic tumors in the syngeneic rats, whereas TSb cells only induce regressive tumors. Levels of K-ras transcripts in TRb and TSb cells were higher than that of NIH3T3 cells, but no difference was found between TRb and TSb cells. No significant difference was observed in expression levels of c-myc in these two cell lines. c-fos expression was, however, significantly lower in TRb than TSb cells.
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PMID:Activated K-ras in tumorigenic and non-tumorigenic cell variants from a rat colon adenocarcinoma, induced by dimethylhydrazine. 313 Mar 59


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