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Clinical significance of loss of heterozygosity for M6P/IGF2R in patients with primary hepatocellular carcinoma

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dc.contributor.authorJang, Hong Seok-
dc.contributor.authorKang, Ki Mun-
dc.contributor.authorChoi, Byung Ock-
dc.contributor.authorChai, Gyu Young-
dc.contributor.authorHong, Soon Chan-
dc.contributor.authorHa, Woo Song-
dc.contributor.authorJirtle, Randy L.-
dc.date.accessioned2022-12-27T06:11:25Z-
dc.date.available2022-12-27T06:11:25Z-
dc.date.created2022-12-13-
dc.date.issued2008-03-07-
dc.identifier.issn1007-9327-
dc.identifier.urihttps://scholarworks.bwise.kr/gnu/handle/sw.gnu/27471-
dc.description.abstractAIM: To investigate the relationship between loss of heterozygosity (LOH) for mannose 6-phosphate/insulin-like growth factor 2 receptor (M6P/IGF2R) and the outcomes for primary HCC patients treated with partial hepatectomy. METHODS: The LOH for M6P/IGF2R in primary HCC patients was assessed using six different gene-specific nucleotide polymorphisms. The patients studied were enrolled to undergo partial hepatectomy. RESULTS: M6P/IGF2R was found to be polymorphic in 73.3% (22/30) of the patients, and of these patients, 50.0% (11/22) had tumors showing LOH in M6P/IGF2R. Loss of heterozygosity in M6P/IGF2R was associated with significant reductions in the two year overall survival rate (24.9% vs 65.5%; P = 0.04) and the disease-free survival rate (17.8% vs 59.3%; P = 0.03). CONCLUSION: These results show M6P/IGF2R LOH predicts poor clinical outcomes in surgically resected primary HCC patients. (c) 2008 WJG. All rights reserved.-
dc.language영어-
dc.language.isoen-
dc.publisherBAISHIDENG PUBLISHING GROUP INC-
dc.subjectFACTOR-II RECEPTOR-
dc.subjectTUMOR-SUPPRESSOR GENE-
dc.subjectHAPLO-INSUFFICIENCY-
dc.subjectPROMOTES GROWTH-
dc.subjectEXPRESSION-
dc.subjectCANCER-
dc.subjectIGF2R-
dc.subjectLOCUS-
dc.subjectMOUSE-
dc.subjectDEATH-
dc.titleClinical significance of loss of heterozygosity for M6P/IGF2R in patients with primary hepatocellular carcinoma-
dc.typeArticle-
dc.contributor.affiliatedAuthorKang, Ki Mun-
dc.identifier.doi10.3748/wjg.14.1394-
dc.identifier.scopusid2-s2.0-41149151320-
dc.identifier.wosid000253866400015-
dc.identifier.bibliographicCitationWORLD JOURNAL OF GASTROENTEROLOGY, v.14, no.9, pp.1394 - 1398-
dc.relation.isPartOfWORLD JOURNAL OF GASTROENTEROLOGY-
dc.citation.titleWORLD JOURNAL OF GASTROENTEROLOGY-
dc.citation.volume14-
dc.citation.number9-
dc.citation.startPage1394-
dc.citation.endPage1398-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaGastroenterology & Hepatology-
dc.relation.journalWebOfScienceCategoryGastroenterology & Hepatology-
dc.subject.keywordPlusFACTOR-II RECEPTOR-
dc.subject.keywordPlusTUMOR-SUPPRESSOR GENE-
dc.subject.keywordPlusHAPLO-INSUFFICIENCY-
dc.subject.keywordPlusPROMOTES GROWTH-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusCANCER-
dc.subject.keywordPlusIGF2R-
dc.subject.keywordPlusLOCUS-
dc.subject.keywordPlusMOUSE-
dc.subject.keywordPlusDEATH-
dc.subject.keywordAuthorloss of heterozygosity-
dc.subject.keywordAuthormannose 6-phosphate/insulin-like growth factor 2 receptor-
dc.subject.keywordAuthorhepatocellular carcinoma-
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