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Promoter Methylation of PTEN Is a Significant Prognostic Factor in Melanoma Survival.

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dc.contributor.author노미령-
dc.contributor.author라선영-
dc.contributor.author정기양-
dc.date.accessioned2017-02-27T07:53:13Z-
dc.date.available2017-02-27T07:53:13Z-
dc.date.issued2016-
dc.identifier.issn0022-202X-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/147023-
dc.description.abstractStructural compromise of the tumor suppressor gene, phosphatase and tensin homolog (PTEN), occurs in 10% of melanoma specimens, and loss of PTEN expression through DNA methylation of the PTEN promoter region has also been reported in a number of other malignancies. However, the role of PTEN promoter methylation in melanoma is not well understood. We thus sought to elucidate the prevalence of PTEN promoter methylation in melanoma specimens, its relationship to clinical features, and its impact on the outcome of patients with melanoma. PTEN promoter methylation data were acquired from an archived primary Korean melanoma cohort (KMC) of 158 patients and, for validation, 234 patients from The Cancer Genome Atlas melanoma (TCGA-MEL) cohort. Hierarchical clustering was performed to identify PTEN "high methylated" and "low methylated" samples. Subsequently, differences in clinical features and outcomes based on PTEN promoter methylation status were then analyzed using SPSS and R. In the KMC, all tumors were acquired from primary tumors and 65.7% (n = 105) were acral or mucosal by site, whereas in the TCGA-MEL cohort, 90.5% of the tumors were from regional lymph node and distant metastatic lesions. Overall, 17.7% and 45.7% of the specimens harbored BRAF mutations in the KMC and TCGA-MEL cohort, respectively. Neuroblastoma RAS viral oncogene homolog was mutated in 12.2% and 26.9% of the tumors in the KMC and TCGA-MEL cohort, respectively. In the KMC, 31 cases (19.6%) were included in the high methylated group versus 142 cases (60.7%) in the TCGA-MEL cohort (P < 0.001). Multivariate Cox-regression analysis revealed promoter methylation of PTEN to be an independent negative prognostic factor for survival in both the KMC (hazard ratio 3.76, 95% confidence interval = 1.24-11.12, P = 0.017) and TCGA-MEL cohort (HR 1.88, 95% confidence interval = 1.13-3.12, P = 0.015). Our results indicate that PTEN promoter methylation is an independent predictor for impaired survival in patients with melanoma.-
dc.description.statementOfResponsibilityrestriction-
dc.format.extent1002~1011-
dc.languageEnglish-
dc.publisherElsevier-
dc.relation.isPartOfJOURNAL OF INVESTIGATIVE DERMATOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAdult-
dc.subject.MESHAged-
dc.subject.MESHChi-Square Distribution-
dc.subject.MESHCluster Analysis-
dc.subject.MESHCohort Studies-
dc.subject.MESHDNA Methylation*-
dc.subject.MESHFemale-
dc.subject.MESHGene Expression Regulation, Neoplastic-
dc.subject.MESHHumans-
dc.subject.MESHMale-
dc.subject.MESHMelanoma/genetics*-
dc.subject.MESHMelanoma/mortality*-
dc.subject.MESHMelanoma/therapy-
dc.subject.MESHMiddle Aged-
dc.subject.MESHMultivariate Analysis-
dc.subject.MESHPTEN Phosphohydrolase/genetics*-
dc.subject.MESHPrognosis-
dc.subject.MESHPromoter Regions, Genetic/genetics-
dc.subject.MESHProportional Hazards Models-
dc.subject.MESHRisk Assessment-
dc.subject.MESHSkin Neoplasms/genetics*-
dc.subject.MESHSkin Neoplasms/mortality*-
dc.subject.MESHSkin Neoplasms/therapy-
dc.subject.MESHStatistics, Nonparametric-
dc.subject.MESHSurvival Analysis-
dc.titlePromoter Methylation of PTEN Is a Significant Prognostic Factor in Melanoma Survival.-
dc.typeArticle-
dc.publisher.locationUnited States-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentDept. of Dermatology-
dc.contributor.googleauthorMi Ryung Roh-
dc.contributor.googleauthorSameer Gupta-
dc.contributor.googleauthorKyu-Hyun Park-
dc.contributor.googleauthorKee Yang Chung-
dc.contributor.googleauthorMartin Lauss-
dc.contributor.googleauthorKeith T. Flaherty-
dc.contributor.googleauthorGo¨ran Jo¨nsson-
dc.contributor.googleauthorSun Young Rha-
dc.contributor.googleauthorHensin Tsao-
dc.identifier.doi10.1016/j.jid.2016.01.024-
dc.contributor.localIdA01278-
dc.contributor.localIdA01316-
dc.contributor.localIdA03582-
dc.relation.journalcodeJ01469-
dc.identifier.eissn1523-1747-
dc.identifier.pmid26854490-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0022202X16004589-
dc.contributor.alternativeNameRoh, Mi Ryung-
dc.contributor.alternativeNameRha, Sun Young-
dc.contributor.alternativeNameChung, Kee Yang-
dc.contributor.affiliatedAuthorRoh, Mi Ryung-
dc.contributor.affiliatedAuthorRha, Sun Young-
dc.contributor.affiliatedAuthorChung, Kee Yang-
dc.citation.volume136-
dc.citation.number5-
dc.citation.startPage1002-
dc.citation.endPage1011-
dc.identifier.bibliographicCitationJOURNAL OF INVESTIGATIVE DERMATOLOGY, Vol.136(5) : 1002-1011, 2016-
dc.date.modified2017-02-24-
dc.identifier.rimsid47056-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Dermatology (피부과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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