Etiology of gastric cancer: what is new?
Recent advances in understanding of risk factors for gastric cancer have focused attention on genetic polymorphisms in both the human host and in Helicobacter pylori. Variation in genes for cytokines such as interleukin-1beta and its receptor antagonist may allow identification of those individuals predisposed to mount an immune response that puts them at elevated risk for gastric cancer. Likewise, analysis of how genetic variation in the genome of H. pylori may modulate the action of virulence factors like CagA may prove useful in identification of persons for whom H. pylori eradication efforts would be most important. This review examines recent studies on interleukin-1beta polymorphisms and H. pylori CagA variation with respect to their modulation of risk for gastric cancer.
Correa
Pelayo
P
Department of Pathology, Louisiana State University Health Sciences Center, 1901 Perdido Street, Box P5-1, New Orleans, LA 70112, USA. correa@lsuhsc.edu
Schneider
Barbara G
BG
D000942:Antigens, Bacterial / Q000235:genetics* / Q000276:immunology; D001426:Bacterial Proteins / Q000235:genetics* / Q000276:immunology; D014644:Genetic Variation / Q000235:genetics / Q000276:immunology; D016480:Helicobacter pylori / Q000235:genetics* / Q000276:immunology / Q000472:pathogenicity; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000382:microbiology*; D018793:Interleukin-13 / Q000235:genetics*; D011110:Polymorphism, Genetic; D012307:Risk Factors; D013274:Stomach Neoplasms / Q000209:etiology* / Q000235:genetics / Q000382:microbiology
D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D018793:Interleukin-13; C080866:cagA protein, Helicobacter pylori