Genetic and Epigenetic Alteration in Gastric Carcinogenesis

• Type: Another Publication in an International Scientific Journal
• Date: 2010

Authors

Resende, C (Author) Other; Ristimaki, A (Author) Other; Machado JC (Author) FMUP

Journal

Title: Helicobacter

Vol. 15

Pages: 34-39

ISSN: 1083-4389

Publisher: Wiley-Blackwell

Indexing

ISI Web of Knowledge - 65 Citations

Scopus - 69 Citations

Other information

Authenticus ID: P-003-3DG

DOI: 10.1111/j.1523-5378.2010.00782.x

Abstract (EN): Gastric cancer (GC) is an important cause of morbidity and mortality worldwide. In addition to environmental factors, genetic factors also play an important role in GC etiology, as demonstrated by the fact that only a small proportion of individuals exposed to the known environmental risk factors develop GC. Molecular studies have provided evidence that GC arises not only from the combined effects of environmental factors and susceptible genetic variants but also from the accumulation of genetic and epigenetic alterations that play crucial roles in the process of cellular immortalization and tumorigenesis. This review is intended to focus on the recently described basic aspects that play key roles in the process of gastric carcinogenesis. Genetic variation in the genes DNMT3A, PSCA, VEGF, and XRCCI has been reported to modify the risk of developing gastric carcinoma. Several genes have been newly associated with gastric carcinogenesis, both through oncogenic activation (MYC, SEMA5A, BCL2L12, RBP2 and BUBR1) and tumor suppressor gene inactivation mechanisms (KLF6, RELN, PTCHIA, CLDN11, and SFRP5). At the level of gastric carcinoma treatment, the HER-2 tyrosine kinase receptor has been demonstrated to be a molecular target of therapy.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 6