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Clinicopathological Significance of Elevated PIK3CA Expression in Gastric Cancer

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dc.contributor.authorJang, Si-Hyong-
dc.contributor.authorKim, Kyung-Ju-
dc.contributor.authorOh, Mee-Hye-
dc.contributor.authorLee, Ji-Hye-
dc.contributor.authorLee, Hyun Ju-
dc.contributor.authorCho, Hyun Deuk-
dc.contributor.authorHan, Sun Wook-
dc.contributor.authorSon, Myoung Won-
dc.contributor.authorLee, Moon Soo-
dc.date.accessioned2021-08-11T17:43:48Z-
dc.date.available2021-08-11T17:43:48Z-
dc.date.issued2016-06-
dc.identifier.issn2093-582X-
dc.identifier.issn2093-5641-
dc.identifier.urihttps://scholarworks.bwise.kr/sch/handle/2021.sw.sch/9068-
dc.description.abstractPurpose: PIK3CA is often mutated in a variety of malignancies, including colon, gastric, ovary, breast, and brain tumors. We investigated PIK3CA expression in gastric cancer and explored the relationships between the PIK3CA expression level and clinicopathological features as well as survival of the patients. Materials and Methods: We examined PIK3CA expression in a tissue microarray of 178 gastric adenocarcinomas by immunohistochemistry and reviewed patients' medical records. Results: In our study, 112 of the 178 gastric cancer patients displayed positive PIK3CA expression. Overexpression of PIK3CA was correlated with low grade differentiation (P=0.001), frequent lymphatic invasion (P=0.032), and high T stage (P=0.040). Patients with positive PIK3CA staining were more likely to display worse overall survival rate than those with negative PIK3CA staining, as determined by Kaplan-Meier survival analysis with log-rank test (P=0.047) and a univariate analysis using the Cox proportional hazard model (hazard ratio=1.832, P=0.051). Conclusions: Elevated PIK3CA expression was significantly correlated with tumor invasiveness, tumor phenotypes, and poor patient survival.-
dc.format.extent8-
dc.language영어-
dc.language.isoENG-
dc.publisher대한위암학회-
dc.titleClinicopathological Significance of Elevated PIK3CA Expression in Gastric Cancer-
dc.typeArticle-
dc.publisher.location대한민국-
dc.identifier.doi10.5230/jgc.2016.16.2.85-
dc.identifier.scopusid2-s2.0-84975882627-
dc.identifier.wosid000382463300004-
dc.identifier.bibliographicCitationJournal of Gastric Cancer, v.16, no.2, pp 85 - 92-
dc.citation.titleJournal of Gastric Cancer-
dc.citation.volume16-
dc.citation.number2-
dc.citation.startPage85-
dc.citation.endPage92-
dc.type.docTypeArticle-
dc.identifier.kciidART002122639-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClassesci-
dc.description.journalRegisteredClasskci-
dc.relation.journalResearchAreaOncology-
dc.relation.journalResearchAreaGastroenterology & Hepatology-
dc.relation.journalWebOfScienceCategoryOncology-
dc.relation.journalWebOfScienceCategoryGastroenterology & Hepatology-
dc.subject.keywordPlusCOLORECTAL-CARCINOMA-
dc.subject.keywordPlusPATHWAY ALTERATIONS-
dc.subject.keywordPlusPOOR-PROGNOSIS-
dc.subject.keywordPlusHIGH-FREQUENCY-
dc.subject.keywordPlusMUTATIONS-
dc.subject.keywordPlusCELLS-
dc.subject.keywordPlusGENE-
dc.subject.keywordPlusCLASSIFICATION-
dc.subject.keywordPlusRESISTANCE-
dc.subject.keywordPlusGROWTH-
dc.subject.keywordAuthorPIK3CA-
dc.subject.keywordAuthorStomach neoplasms-
dc.subject.keywordAuthorImmunohistochemistry-
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