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Loss of CDC14B Expression in Clear Cell Renal Cell Carcinoma Meta-Analysis of Microarray Data Sets

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dc.contributor.authorKim, Younghye-
dc.contributor.authorChoi, Jung-Woo-
dc.contributor.authorLee, Ju-Han-
dc.contributor.authorKim, Young-Sik-
dc.date.accessioned2021-09-05T10:09:03Z-
dc.date.available2021-09-05T10:09:03Z-
dc.date.created2021-06-15-
dc.date.issued2014-04-
dc.identifier.issn0002-9173-
dc.identifier.urihttps://scholar.korea.ac.kr/handle/2021.sw.korea/98882-
dc.description.abstractObjectives: To discover significant differentially expressed genes (DEGs) in clear cell renal cell carcinoma (ccRCC) that might be unidentified by single microarray analysis. Methods: The effect sizes of five ccRCC microarray data sets were combined using a random-effects model. The most downregulated gene was validated in paired 80 ccRCC tissues by immunohistochemistry. Results: CDC14B was the most downregulated gene among 1,761 DEGs. CDC14B was strongly expressed in the apical proximal tubules in the nonneoplastic tissues, while it was completely absent in 10 (12.5%) of 80 or downregulated in 70 (87.5%) of 80 ccRCC cases. The complete loss of CDC14B correlated with high T stage (P = .038), advanced TNM stage (P = .027), tumor recurrence (P = .038), and shorter recurrence-free survival (P = .046) compared with the partial loss of CDC14B. Conclusions: Microarray meta-analysis is a useful tool for pathologists. CDC14B expression is downregulated in ccRCC, suggesting its role in renal carcinogenesis.-
dc.languageEnglish-
dc.language.isoen-
dc.publisherOXFORD UNIV PRESS INC-
dc.subjectVON-HIPPEL-LINDAU-
dc.subjectPRIMARY CILIUM-
dc.subjectPROFILES-
dc.subjectCILIOGENESIS-
dc.subjectCONTRIBUTES-
dc.subjectPROGRESSION-
dc.subjectSURVIVAL-
dc.subjectHYPOXIA-
dc.subjectBIOLOGY-
dc.titleLoss of CDC14B Expression in Clear Cell Renal Cell Carcinoma Meta-Analysis of Microarray Data Sets-
dc.typeArticle-
dc.contributor.affiliatedAuthorChoi, Jung-Woo-
dc.contributor.affiliatedAuthorLee, Ju-Han-
dc.contributor.affiliatedAuthorKim, Young-Sik-
dc.identifier.doi10.1309/AJCP4PE4JPSRGBQS-
dc.identifier.scopusid2-s2.0-84899471393-
dc.identifier.wosid000333070600017-
dc.identifier.bibliographicCitationAMERICAN JOURNAL OF CLINICAL PATHOLOGY, v.141, no.4, pp.551 - 558-
dc.relation.isPartOfAMERICAN JOURNAL OF CLINICAL PATHOLOGY-
dc.citation.titleAMERICAN JOURNAL OF CLINICAL PATHOLOGY-
dc.citation.volume141-
dc.citation.number4-
dc.citation.startPage551-
dc.citation.endPage558-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaPathology-
dc.relation.journalWebOfScienceCategoryPathology-
dc.subject.keywordPlusVON-HIPPEL-LINDAU-
dc.subject.keywordPlusPRIMARY CILIUM-
dc.subject.keywordPlusPROFILES-
dc.subject.keywordPlusCILIOGENESIS-
dc.subject.keywordPlusCONTRIBUTES-
dc.subject.keywordPlusPROGRESSION-
dc.subject.keywordPlusSURVIVAL-
dc.subject.keywordPlusHYPOXIA-
dc.subject.keywordPlusBIOLOGY-
dc.subject.keywordAuthorRenal cell carcinoma-
dc.subject.keywordAuthorMete-analysis-
dc.subject.keywordAuthorMicroarray-
dc.subject.keywordAuthorCDC14B-
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