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p16 Hypermethylation and KRAS Mutation Are Independent Predictors of Cetuximab Plus FOLFIRI Chemotherapy in Patients with Metastatic Colorectal Cancer

DC FieldValueLanguage
dc.contributor.author김남규-
dc.contributor.author노재경-
dc.contributor.author라선영-
dc.contributor.author김태일-
dc.contributor.author박규현-
dc.contributor.author신상준-
dc.contributor.author안중배-
dc.contributor.author이강영-
dc.date.accessioned2017-02-24T08:15:19Z-
dc.date.available2017-02-24T08:15:19Z-
dc.date.issued2016-
dc.identifier.issn1598-2998-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/146601-
dc.description.abstractPURPOSE: Hypermethylation of the CpG island of p16(INK4a) occurs in a significant proportion of colorectal cancer (CRC). We aimed to investigate its predictive role in CRC patients treated with 5-fluorouracil, leucovorin, irinotecan (FOLFIRI), and cetuximab. MATERIALS AND METHODS: Pyrosequencing was used to identify KRAS mutation and hypermethylation of 6 CpG island loci (p16, p14, MINT1, MINT2, MINT31, and hMLH1) in DNA extracted from formalin-fixed paraffin-embedded specimens. Logistic regression and Cox regression were performed for analysis of the relation between methylation status of CpG island methylator phenotype (CIMP) markers including p16 and clinical outcome. RESULTS: Hypermethylation of the p16 gene was detected in 14 of 49 patients (28.6%) and showed significant association with KRAS mutation (Fisher exact, p=0.01) and CIMP positivity (Fisher exact, p=0.002). Patients with p16-unmethylated tumors had significantly longer time to progression (TTP; median, 9.0 months vs. 3.5 months; log-rank, p=0.001) and overall survival (median, 44.9 months vs. 16.4 months; log-rank, p=0.008) than those with p16-methylated tumors. Patients with both KRAS and p16 aberrancy (n=6) had markedly shortened TTP (median, 2.8 months) compared to those with either KRAS or p16 aberrancy (n=11; median, 8.6 months; p=0.021) or those with neither (n=32; median, 9.0 months; p < 0.0001). In multivariate analysis, KRAS mutation and p16 methylation showed independent association with shorter TTP (KRAS mutation: hazard ratio [HR], 3.21; p=0.017; p16 methylation: HR, 2.97; p=0.027). CONCLUSION: Hypermethylation of p16 was predictive of clinical outcome in metastatic CRC patients treated with cetuximab and FOLFIRI, irrespective of KRAS mutation.-
dc.description.statementOfResponsibilityopen-
dc.format.extent208~215-
dc.languageEnglish, Korean-
dc.publisherOfficial journal of Korean Cancer Association-
dc.relation.isPartOfCancer Research and Treatment-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titlep16 Hypermethylation and KRAS Mutation Are Independent Predictors of Cetuximab Plus FOLFIRI Chemotherapy in Patients with Metastatic Colorectal Cancer-
dc.typeArticle-
dc.publisher.locationKorea-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentDept. of Surgery-
dc.contributor.googleauthorSe Hyun Kim-
dc.contributor.googleauthorKyu Hyun Park-
dc.contributor.googleauthorSang Joon Shin-
dc.contributor.googleauthorKang Young Lee-
dc.contributor.googleauthorTae Il Kim-
dc.contributor.googleauthorNam Kyu Kim-
dc.contributor.googleauthorSun Young Rha-
dc.contributor.googleauthorJae Kyung Roh-
dc.contributor.googleauthorJoong Bae Ahn-
dc.identifier.doi10.4143/crt.2014.314-
dc.contributor.localIdA00353-
dc.contributor.localIdA01290-
dc.contributor.localIdA01316-
dc.contributor.localIdA01079-
dc.contributor.localIdA04566-
dc.contributor.localIdA02105-
dc.contributor.localIdA02262-
dc.contributor.localIdA02640-
dc.relation.journalcodeJ00453-
dc.relation.journalsince2001~-
dc.identifier.pmid25943321-
dc.relation.journalbefore~2001 Journal of the Korean Cancer Research Association (대한암학회지)-
dc.subject.keywordCIMP-
dc.subject.keywordColorectal neoplasms-
dc.subject.keywordKRAS-
dc.subject.keywordMethylation-
dc.subject.keywordp16-
dc.contributor.alternativeNameKim, Nam Kyu-
dc.contributor.alternativeNameRoh, Jae Kyung-
dc.contributor.alternativeNameRha, Sun Young-
dc.contributor.alternativeNameKim, Tae Il-
dc.contributor.alternativeNamePark, Kyu Hyun-
dc.contributor.alternativeNameShin, Sang Joon-
dc.contributor.alternativeNameAhn, Joong Bae-
dc.contributor.alternativeNameLee, Kang Young-
dc.contributor.affiliatedAuthorKim, Nam Kyu-
dc.contributor.affiliatedAuthorRoh, Jae Kyung-
dc.contributor.affiliatedAuthorRha, Sun Young-
dc.contributor.affiliatedAuthorKim, Tae Il-
dc.contributor.affiliatedAuthorPark, Kyu Hyun-
dc.contributor.affiliatedAuthorShin, Sang Joon-
dc.contributor.affiliatedAuthorAhn, Joong Bae-
dc.contributor.affiliatedAuthorLee, Kang Young-
dc.citation.volume48-
dc.citation.number1-
dc.citation.startPage208-
dc.citation.endPage215-
dc.identifier.bibliographicCitationCancer Research and Treatment, Vol.48(1) : 208-215, 2016-
dc.date.modified2017-02-24-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Surgery (외과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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