Deficiency of MSH2 expression is associated with clear cell renal cell carcinoma.

Abstract:

:DNA hypermethylation plays a major role in the regulation of gene expression in differentiation, development and diseases. The DNA mismatch repair system, which includes Mut-S-Homologon-2 (MSH2) protein, is essential to maintain the stability of the genome during repeated duplication. This study aimed to investigate tumoral MSH2 immunohistochemical expression in clear cell renal cell carcinoma (RCC), and the associations between tumoral MSH2 immunohistochemical expression and clinicopathological parameters. Previously, we reported a high-throughput method for analyzing the methylation status of 807 preselected genes; Illumina's GoldenGate Methylation Cancer Panel I microarray. The MSH2 gene was identified to be hypermethylated in cancer tissue compared with normal tissue. From January 2000 to December 2012, 129 clear cell RCC cases (median age, 61 years) were included in the immunohistochemical analysis of the present study. Patients were divided according to MSH2 expression status (MSH2-negative, n=53; MSH2-positive, n=76). T stage was significantly higher in the MSH2-negative group than in the MSH2 positive-group (P=0.021). There was no significant difference in terms of N stage, M stage and Fuhrman's nuclear grade between the MSH2-negative and MSH2-positive group (N stage, P=0.072; M stage, P=0.759; Fuhrman's nuclear grade, P=0118). The MSH2-negative group showed decreased rates of recurrence-free survival, progression-free survival and overall survival, without statistically significant results (P=0.232, P=0.268 and P=0.311, respectively). MSH2 protein expression may be a useful marker for predicting TNM stage and prognosis and, thus, MSH2 may be a prognostic factor in clear cell RCC.

journal_name

Oncol Lett

journal_title

Oncology letters

authors

Yoo KH,Won KY,Lim SJ,Park YK,Chang SG

doi

10.3892/ol.2014.2482

subject

Has Abstract

pub_date

2014-11-01 00:00:00

pages

2135-2139

issue

5

eissn

1792-1074

issn

1792-1082

pii

ol-08-05-2135

journal_volume

8

pub_type

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