Publication: Genetic and epigenetic alterations of tumor
suppressor and tumor-related genes in gastric cancer
Authors
Tamura, G.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Both genetic and epigenetic alterations of
tumor suppressor and tumor-related genes involved in
the pathogenesis of gastric cancer are reviewed here, and
molecular pathways of gastric carcinogenesis are
proposed. Gastric carcinomas are believed to evolve
from native gastric mucosa or intestinal metaplastic
mucosa that undergoes genetic and epigenetic alterations
involving either the suppressor pathway (defects in
tumor suppressor genes) or mutator pathway (defects in
DNA mismatch repair genes). Methylation of E -
c a d h e r i n in native gastric mucosa results in
undifferentiated carcinomas (suppressor pathway), while
methylation of hMLH1 results in differentiated foveolartype
carcinomas (mutator pathway). The majority of
d i fferentiated gastric carcinomas however, arise from
intestinal metaplastic mucosa and exhibit structural
alterations of tumor suppressor genes, especially p 5 3.
They appear to be related to chronic injury, perhaps due
to Helicobacter pylori infection. Approximately 20% of
differentiated carcinomas (ordinary-type) have evidence
of mutator pathway tumorigenesis. Mutations of E -
c a d h e r i n are mainly involved in the progression of
d i fferentiated carcinomas to undifferentiated tumors.
The molecular pathways of gastric carcinogenesis
depend on the histological background, and gastric
carcinomas show distinct biological behaviors as a result
of discernible cellular genetic and epigenetic alterations.
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