Genetic variants in gastric cancer: Risks and clinical implications

• Published in: Experimental and molecular pathology Vol. 103; no. 1; pp. 101 - 111
• Main Authors: Gigek, Carolina Oliveira, Calcagno, Danielle Queiroz, Rasmussen, Lucas Trevizani, Santos, Leonardo Caires, Leal, Mariana Ferreira, Wisnieski, Fernanda, Burbano, Rommel Rodriguez, Lourenço, Laercio Gomes, Lopes-Filho, Gaspar Jesus, Smith, Marilia Arruda Cardoso
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Inc 01-08-2017
• Subjects: CNV; DNA Copy Number Variations; Gastric cancer; Genome-Wide Association Study; GWAS; Helicobacter Infections - complications; Helicobacter Infections - diagnosis; Helicobacter pylori; Humans; Interleukin; Interleukins - genetics; Interleukins - metabolism; Meta-Analysis as Topic; mRNA expression; Polymorphism; Polymorphism, Genetic; Signal Transduction; Stomach Neoplasms - diagnosis; Stomach Neoplasms - etiology; Stomach Neoplasms - genetics; CNV; GWAS; Gastric cancer; Interleukin; Polymorphism; mRNA expression
• ISSN: 0014-4800; 1096-0945
• DOI: 10.1016/j.yexmp.2017.07.004

Cancer is a multifactorial disease that involves many molecular alterations. Gastric cancer (GC) is the third leading cause of cancer death worldwide. GC is a highly heterogeneous disease with different molecular and genetics features. Therefore, this review focuses on an overview of the genetic aspects of gastric cancer by highlighting the important impact and role of deletions and/or duplications of chromosomal segments, genomic variants, H. pylori infection and interleukin variants, as found in gene expression and newly proposed molecular classification studies. The challenge is to better understand the mechanisms and different pathways that lead to the development and progression of GC.
•Gastric cancer is a highly heterogeneous disease with different molecular and genetics features.•CNVs exert influence on gene expression by affecting the activity of various signalling pathways.•GWAS have been useful for identifying genetic variations that are associated with risk for gastric cancer.•H. pylori virulence factors and variants of interleukin play an important role in the inflammatory/immune host response.