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Hypermethylation status of APC inversely correlates with the presence of submucosal invasion in laterally spreading colorectal tumors
Author(s) -
Hashimoto Kazuo,
Shimizu Yoshihisa,
Suehiro Yutaka,
Okayama Naoko,
Hashimoto Shinichi,
Okada Toshiyuki,
Hiura Mikako,
Ueno Koji,
Hazama Shoichi,
Higaki Shingo,
Hamanaka Yuichiro,
Oka Masaaki,
Sakaida Isao,
Hinoda Yuji
Publication year - 2008
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.20363
Subject(s) - methylation , biology , adenomatous polyposis coli , dna methylation , epigenetics , methyltransferase , cancer research , microsatellite instability , cpg site , polymerase chain reaction , colorectal cancer , cancer , dna , gene expression , gene , genetics , microsatellite , allele
Abstract Little is known about epigenetic alterations in laterally spreading colorectal tumors (LSTs). The goal of the present study was to elucidate the epigenetic background of LSTs and compare the methylation status of DNA CpG islands (CGIs) with clinicopathologic features. Methylation of MINT1 , MINT2 , MINT31 , p16 , O 6 ‐methylguanine‐DNA methyltransferase (MGMT) , adenomatous polyposis coli (APC) , and human MutL homologue 1 (hMLH1) in 42 LSTs was assessed by methylation‐specific polymerase chain reaction (MSP) and compared with clinicopathologic parameters. The frequency of hypermethylation was 12.5% (4/32) for MINT1 , 40.0% (16/40) for MINT2 , 25.0% (10/40) for MINT31 , 25.7% (9/35) for p16 , 7.7% (3/39) for hMLH1 , 26.5% (9/34) for MGMT , and 35.9% (14/39) for APC . APC methylation was inversely associated with submucosal invasion ( P = 0.034), which was not found in any of 14 LST cases with APC methylation, whereas submucosal invasion was present in 8 of 25 (32.0%) cases without APC methylation. These data suggest that hypermethylation of APC could be a predictive marker for the absence of submucosal invasion of LSTs. © 2007 Wiley‐Liss, Inc.