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Mutation of ras oncogene in gastric adenocarcinoma: Association with histological phenotype

DC Field Value Language
dc.contributor.authorKim, TY-
dc.contributor.authorBang, YJ-
dc.contributor.authorKim, WS-
dc.contributor.authorKang, SH-
dc.contributor.authorLee, KU-
dc.contributor.authorChoe, KJ-
dc.contributor.authorKim, NK-
dc.date.accessioned2021-01-31T11:00:56Z-
dc.date.available2021-01-31T11:00:56Z-
dc.date.created2020-12-22-
dc.date.issued1997-03-
dc.identifier.citationAnticancer Research, Vol.17 No.2B, pp.1335-1339-
dc.identifier.issn0250-7005-
dc.identifier.other119569-
dc.identifier.urihttps://hdl.handle.net/10371/172965-
dc.description.abstractIn order to explore the role of ras oncogene in gastric carcinomas from Korean patients, we examined the frequency of point mutations all three ras oncogenes (Ki-, Ha-, and N-ras). A total of 57 DNA samples were prepared from 3 gastric carcinoma cell lines, 10 malignant ascites, and 44 frozen gastric tremor tissues. Exons I and 2 of each ras oncogene were amplified by polymerase chain reaction (PCR), and analyzed by single strand conformation polymorphism (SSCP) and direct sequencing. Mutated ms genes were detected in 6 out of 57 samples (10%). One cell line and 2 tumors showed a mutation at exon 1 of Ki-ras. N-ras mutations were also detected at exon I of 3 tumors. Histologically, all the ras mutation cases exhibited a diffuse phenotype. In summary, we performed a comprehensive analysis to investigate the mutation of all three ms oncogenes in gastric carcinoma. The results demonstrate infrequent mutations of Ki-and N-ras which may favor the development of diffuse type gastric carcinomas, implicating a different genetic pathway in diffuse and intestinal type gastric carcinomas.-
dc.language영어-
dc.publisherInternational Institute of Anticancer Research-
dc.titleMutation of ras oncogene in gastric adenocarcinoma: Association with histological phenotype-
dc.typeArticle-
dc.contributor.AlternativeAuthor방영주-
dc.citation.journaltitleAnticancer Research-
dc.identifier.wosidA1997WU02400019-
dc.identifier.scopusid2-s2.0-0030894070-
dc.citation.endpage1339-
dc.citation.number2B-
dc.citation.startpage1335-
dc.citation.volume17-
dc.identifier.sciA1997WU02400019-
dc.description.isOpenAccessN-
dc.contributor.affiliatedAuthorKim, TY-
dc.contributor.affiliatedAuthorBang, YJ-
dc.contributor.affiliatedAuthorLee, KU-
dc.contributor.affiliatedAuthorChoe, KJ-
dc.contributor.affiliatedAuthorKim, NK-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlusPOLYMERASE CHAIN-REACTION-
dc.subject.keywordPlusPOINT MUTATIONS-
dc.subject.keywordPlusCANCERS-
dc.subject.keywordPlusGENE-
dc.subject.keywordPlusCARCINOMA-
dc.subject.keywordPlusOVEREXPRESSION-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusCODON-12-
dc.subject.keywordPlusDNA-
dc.subject.keywordAuthorgastric carcinoma-
dc.subject.keywordAuthorras oncogene-
dc.subject.keywordAuthorpoint mutation-
dc.subject.keywordAuthorpolymerase chain reaction-
dc.subject.keywordAuthorsequencing-
dc.subject.keywordAuthordifferentiation-
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  • Department of Medicine
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