Genomic and genetic alterations influence the progression of gastric cancer.

Abstract

Gastric cancer is one of the leading causes of cancer-related deaths worldwide, although the incidence has gradually decreased in many Western countries. Two main gastric cancer histotypes, intestinal and diffuse, are recognised. Although most of the described genetic alterations have been observed in both types, different genetic pathways have been hypothesized. Genetic and epigenetic events, including 1q loss of heterozygosity (LOH), microsatellite instability and hypermethylation, have mostly been reported in intestinal-type gastric carcinoma and its precursor lesions, whereas 17p LOH, mutation or loss of E-cadherin are more often implicated in the development of diffuse-type gastric cancer. In this review, we summarize the sometimes contradictory findings regarding those markers which influence the progression of gastric adenocarcinoma.

• Authors: Stefania Nobili, Lorenzo Bruno, Ida Landini, Cristina Napoli, Paolo Bechi, Francesco Tonelli, Carlos A Rubio, Enrico Mini, Gabriella Nesi
• Journal: World journal of gastroenterology (World J Gastroenterol) Vol. 17 Issue 3 Pg. 290-9 (Jan 21 2011) ISSN: 2219-2840 [Electronic] United States
• PMID: 21253387 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Topics

• DNA Methylation
• Disease Progression
• Epigenomics
• Genome, Human
• Genomic Instability
• Humans
• Loss of Heterozygosity
• Microsatellite Repeats
• Mutation
• Signal Transduction (genetics)
• Stomach Neoplasms (genetics, physiopathology)