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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The c-erbB-2 gene is a v-erbB-related proto-oncogene which is distinct from the gene encoding the epidermal growth factor receptor. By using two independent methods, hybridization of both sorted chromosomes and metaphase spreads with cloned c-erbB-2 DNA, we mapped the c-erbB-2 locus on human chromosome 17 at q21, a specific breakpoint observed in a translocation associated with acute promyelocytic leukemia. Furthermore, we observed amplification and elevated expression of the c-erbB-2 gene in the MKN-7 gastric cancer cell line. These data suggest possible involvement of the c-erbB-2 gene in human cancer.
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PMID:Localization of a novel v-erbB-related gene, c-erbB-2, on human chromosome 17 and its amplification in a gastric cancer cell line. 243 Jan 75

Alteration of oncogene and loss of chromosomal heterozygosity are infrequent in human gastric carcinoma compared with those in other gastrointestinal carcinomas. Amplification of c-erbB-2 gene is observed in well differentiated adenocarcinoma, while sam gene is found in poorly differentiated adenocarcinoma or scirrhous carcinoma. sam gene, which was isolated from a gastric cancer cell line KATO-III by a DNA renaturation method, encodes tyrosine-specific protein kinase domain. A good correlation evidently exists between the synchronous expression of TGF alpha and ras p21 and biological malignancy of gastric carcinoma. c-myc and c-fos proteins are found not only in tumor cells but also in stromal cells including macrophages and fibroblast around the tumors. The prognosis of patients with c-myc p 62-positive stromal cells is significantly better than that of patient with p 62-negative stromal cells. Coamplification of the hst-1 gene and int-2 is observed in 50% of primary tumors and all metastatic tumors of esophageal carcinoma. PCR (polymerase chain reaction) technique seems to be useful for the detection of oncogene point mutation in human gastric carcinoma.
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PMID:[Oncogenes in human gastric carcinoma]. 254 46

A murine IgM monoclonal antibody, designated SV2-61, was generated against human c-erbB-2 gene-transfected NIH-3T3 (SV11) cells. SV2-61 defined a 185-kDa molecule present on the surface of SV11 cells, another line of c-erbB-2 gene-transfected NIH-3T3 (A4-15) cells, and MKN-7 human gastric cancer cell line carrying an amplified human c-erbB-2 gene. The SV2-61-defined antigen was found to show protein kinase activity in vitro. The SV2-61 was reactive with human c-erbB-2 gene-transfected NIH-3T3 cell lines but not with transfectants carrying c-erbB-2 gene mutants which lack a coding region for the extracellular domain. It was reactive with a portion of human epithelial cell lines but not with native NIH-3T3, TGF-alpha-coding gene-, activated c-raf gene- or Ha-ras gene-transfected NIH-3T3 cells, or non-epithelial human cells. These results indicate that the SV2-61 is an antibody which recognizes an extracellular domain of the c-erbB-2 gene product, 185-kDa protein.
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PMID:A murine monoclonal antibody that recognizes an extracellular domain of the human c-erbB-2 protooncogene product. 256 25

c-erbB-2 oncogene has been reported to be frequently amplified in differentiated, tubular type of gastric cancer. Here we report a human gastric cancer which bore co-amplified c-myc and c-erbB-2 oncogenes: a portion of the amplified c-erbB-2 oncogene was found to be rearranged. Furthermore, c-myc and c-erbB-2 oncogenes were over-expressed in the tumor cells. In contrast to the previous reports, this gastric adenocarcinoma was classified as a poorly differentiated type, and was highly tumorigenic in nude mice. These results might suggest that activated c-myc and c-erbB-2 oncogenes co-operate and influence the malignant state of some gastric carcinomas.
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PMID:Co-amplification of c-myc and c-erbB-2 oncogenes in a poorly differentiated human gastric cancer. 257 9

A novel v-erb-B-related gene, c-erb-B-2, which has been identified in the human genome, maps to human chromosome 17 at q21 (ref. 40), and seems to encode a polypeptide with a kinase domain that is highly homologous with, but distinct from, that of the epidermal growth factor (EGF) receptor. The c-erb-B-2 gene is conserved in vertebrates and it has been suggested that the neu gene, detected in a series of rat neuro/glioblastomas, is, in fact, the rat c-erb-B-2 gene. Amplification of the c-erb-B-2 gene in a salivary adenocarcinoma and a gastric cancer cell line MKN-7 suggests that its over-expression is sometimes involved in the neoplastic process. To determine the nature of the c-erb-B-2 protein, we have now molecularly cloned complementary DNA for c-erb-B-2 messenger RNA prepared from MKN-7 cells. Its sequence shows that the c-erb-B-2 gene encodes a possible receptor protein and allows an analysis of the similarity of the protein to the EGF receptor and the neu product. As a consequence of chromosomal aberration in MKN-7 cells, a 4.6-kilobase (kb) normal transcript and a truncated 2.3-kb transcript of c-erb-B-2 are synthesized at elevated levels. The latter transcript presumably encodes only the extracellular domain of the putative receptor.
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PMID:Similarity of protein encoded by the human c-erb-B-2 gene to epidermal growth factor receptor. 300 77

We analyzed for alterations of the c-erbB-2 oncogene in 35 human stomach cancers and 8 cell lines derived from human stomach cancer. Amplification of c-erbB-2 was found in approximately 40% (5/13) of the tubular adenocarcinomas of the stomach examined, including 4 of 10 fresh tumors and one of 3 cell lines, but not in other histological types of stomach cancer examined (0/30), including 25 fresh tumors and 5 cell lines. This result strongly suggests that amplification of c-erbB-2 occurs frequently in tubular carcinomas in stomach cancer. Rearrangement of c-erbB-2 was also detected in one tubular adenocarcinoma. The rearranged fragment carried the 3' half, but not the 5' sequence, of the c-erbB-2 gene. Furthermore, one of the cellular homologues of v-erbA was amplified in 3 of 4 fresh tumors carrying the amplified c-erbB-2 gene. Both c-erbB-2 and the v-erbA homologue were expressed in all the stomach cancer cell lines tested.
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PMID:Genetic alterations of the c-erbB-2 oncogene occur frequently in tubular adenocarcinoma of the stomach and are often accompanied by amplification of the v-erbA homologue. 328 Oct 95

The effects of treatment in a hydrated autoclave (121 degrees C, 2 atm for 20 min), microwave oven (in water), and simple heating (60 degrees C overnight in distilled water or 90 degrees C for 10 min in ZnSO4) on the stainability of 56 antigens by commercially available antibodies in formalin-fixed paraffin-embedded tissue sections were evaluated. The detectability of nuclear antigens, glycoprotein, lymphocytic surface markers, and chromogranin A was significantly and reproducibly improved by these treatments, whereas the detectability of viral antigens and peptide hormones was attenuated or unchanged. This enhancement includes not only the distinctiveness of the positive staining, but also the number of positive cells, as revealed by comparing serial sections. Among these four heating procedures, microwave heating and autoclaving were more effective than the others on p53, c-erbB-2, and CA125, whereas simple heating was best for smooth-muscle actin (HHF35 and CGA7). Generally the effects of the heating procedures for these antigens were consistent among the cases, but the effects on GFAP varied with the case. The alterations we observed could significantly influence the interpretation of immunohistochemical staining of currently popular tumor markers such as p53 in terms of their prevalence (28% vs 64% in gastric cancer; 36% vs 82% in metastatic liver cancer) and other diagnostically important markers.
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PMID:Alteration of immunoreactivity by hydrated autoclaving, microwave treatment, and simple heating of paraffin-embedded tissue sections. 751 73

The clinical significance of the measurement of c-erbB-2 oncogene product was evaluated. The subjects consisted of 404 patients, including 248 with cancer of the digestive organs and 128 with benign digestive diseases. Serum c-erbB-2 protein levels were measured by sandwich immunoenzyme assay. The positive rates of c-erbB-2 protein, at a cut-off value of 17.0 U/ml, were, for cancers: hepatocellular carcinoma 61.6%, biliary tract cancer 54.8%, pancreatic cancer 25.0%, esophageal cancer 33.3%, gastric cancer 16.9%, and colorectal cancer 5.0%. For benign digestive diseases, the rates were: liver cirrhosis 63.3%, chronic hepatitis 43.2%, acute hepatitis 42.9%, other liver diseases 42.8%, cholelithiasis 30.0%, and chronic pancreatitis 0%. Serum c-erbB-2 protein levels were significantly correlated with the markers of hepatic functional reserve, the indocyanine green retention rate and the hepaplastin test. These findings suggest that serum c-erbB-2 protein levels are greatly influenced by liver dysfunction and that their clinical usefulness as a serum tumor marker is questionable.
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PMID:Serum levels of c-erbB-2 protein in digestive diseases. 752 80

We have examined the selective cytotoxicity of immunoliposomes containing doxorubicin (chemoimmunoliposomes, CILs) targeting the c-erbB-2 gene product (gp185) or gp125. Anti-gp185 and anti-gp125 CILs were prepared by conjugation of doxorubicin-containing liposomes with monoclonal antibodies SER4 (IgG) and HBJ127 (IgG) respectively. Both CILs bound to human SKBr-3 breast cancer cells and MKN-7 human gastric cancer cells, which express both antigens in high density. The IC50 of anti-gp185 CILs on protein synthesis by SKBr-3 cells was respectively 2- and 25-fold lower than that of anti-gp125 CILs and unmodified liposomes. Furthermore, anti-gp185 CILs significantly inhibited neither the phytohaemagglutin response of normal lymphocytes nor protein synthesis of gp185-negative T24 bladder cancer. Quantitative analysis of cell-associated doxorubicin revealed that, compared with anti-gp125 CILs, anti-gp185 CILs required, respectively 4.5 and 4.3 times less doxorubicin association in SKBR-3 and MKN-7 cells, for 50% cytotoxicity. In addition, flow cytometric analysis showed that both SKBr-3 and MKN-7 internalised more anti-gp185 CILs and processed them more efficiently than anti-gp125 CILs. These results suggest that anti-gp185 CILs act selectively against gp185-expressing cancer cells and that gp185 is a more sensitive antigen for CIL cytotoxicity associated with endocytosis activity.
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PMID:Cytotoxicity of anti-c-erbB-2 immunoliposomes containing doxorubicin on human cancer cells. 766 78

Gastric cancer involves changes in multiple oncogenes and multiple suppressor genes, and it causes genetic instability. Aberrant expression and amplification of the c-met gene, inactivation of the p53 gene, and CD44 abnormal transcripts are common events of both well differentiated and poorly differentiated gastric cancers. Amplification of the cyclin E gene is also observed in gastric cancer regardless of histologic type. Decreased expression of the pic1 (p21) gene occurs independent of the p53 mutations. In addition, K-ras mutations, c-erbB-2 gene amplification, loss of heterozygosity (LOH) and mutations of the APC gene, LOH of the bcl-2 gene, and LOH at the DCC locus are preferentially associated with well differentiated gastric cancer. Moreover, LOH on chromosome 1q is involved in the progression of well differentiated cancer. Precancerous lesions, including hyperplastic polyp, intestinal metaplasia, and adenoma, share genetic changes found in well differentiated cancers. Conversely, genetic instability may be involved in the first step of stomach carcinogenesis of the poorly differentiated type. Reduction or loss of cadherin and catenins, K-sam gene amplification, and c-met gene amplification are necessary for the development and progression of poorly differentiated or scirrhous carcinoma. Interaction between cell-adhesion molecules in the c-met expressed tumor cells and hepatocyte growth factor from stromal cells is implicated in the morphogenesis of two types of gastric cancer.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Molecular biology of gastric cancer. 767 88


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