Publication: Expression of beta-catenin and its mechanism of delocalization in intestinal-type early gastric cancer based on mucin expression
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Date
2009
Authors
Lee, Soo Han ; Kang, Hyun Jeong ; Shin, Dong-Hun ; Cho, Duk-Yeon ; Song, Jin Mi ; Kim, G.H. ; Song, G.A. ; So, Mee Young ; Kim, J.Y. ; Choi, K.U. ; Lee, Chian-Her ; Huh, G.Y. ; Park, D.Y. ; Lee, H.C.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
The biological characteristics of intestinaltype early gastric cancers (ICs) differ based on mucin
phenotypes. Beta-catenin delocalization is a predictive
marker of aggressive biological behavior (submucosal
invasion and lymph node metastasis) of ICs. The
presumptive causative genetic alterations leading to
delocalization of beta-catenin in ICs are still
controversial, and there are only a few reports regarding
beta-catenin expression in gastric cancer based on mucin
phenotypes. Therefore, in the current study, the
expression and mechanisms of delocalization of betacatenin were elucidated on the basis of mucin
phenotypes in 109 cases of ICs. There was increased
cytoplasmic and nuclear beta-catenin expression
(delocalization) in ICs with a predominant intestinal
mucin phenotype (ICIP; 46.3% [25/54 cases]) compared
to ICs with a predominant gastric mucin phenotype
(ICGP; 20% [11/55 cases]). There were no beta-catenin
or APC mutations in ICs. APC promoter
hypermethylation was present in 49 of 105 (46.7%)
cases of ICs. There was a significant relationship
between APC promoter hypermethylation and betacatenin delocalization in ICs, especially in ICIPs. There
was no relationship between beta-catenin delocalization
and APC gene loss of heterozygosity in ICs. In
conclusion, we showed that beta-catenin delocalization
was more evident in ICIPs, and APC promoter
hypermethylation might play a role in delocalization of
beta-catenin, especially in ICIPs.
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