[What is the most important factor for gastric carcinogenesis in Koreans: Helicobacter pylori, host factor or environmental factor?].
Epidemiological data including our studies demonstrated the association between Helicobacter pylori (H. pylori) infection and gastric cancer. However, this significant clinical outcome happens only in a small portion of infected person. This suggests that other contributors including host genetic and environmental factors might be involved in the disease process. Studies on the association between virulent strains of H. pylori and clinical outcomes failed to show significant results in Korea. Cytokine gene polymorphism such as interleukin-1 (IL-1) has been thought to play a role in gastric carcinogenesis. Our studies showed the controversial role of IL-1, TNF-A, IL-10 and IL-2 gene polymorphisms in the development of gastric cancer in Korea. Chronic infection and inflammation leading to tumorigenesis are mediated in part through the recognition of various stimuli by toll-like receptors (TLRs). Our studies on the polymorphisms of TLR4 and TLR2 showed no mutant form in Koreans. These discrepancies might reflect the genetic differences between Caucasians and Koreans or might be due to prevalent genetic polymorphisms with masked effect in gastric carcinogenesis in Koreans. As other candidate risk factors, there are constant or inconsistent results on the effect of dietary intake in gastric cancer. There are numerous similar risk for gastric carcinogenesis with different risk ratio including environmental factors in Caucasians and Koreans. Under the background of prevalent H. pylori infection and genetic polymorphisms, environmental factors including diet may potentiate their role in gastric carcinogenesis in Koreans.
Kim
Hak Yang
HY
Division of Gastroenterology, Department of Internal Medicine, Kangdong Sacred Heart Hospital, Hallym University College of Medicine, Gangdong-Gu, Seoul, Korea. bacter@hallym.or.kr
D014408:Biomarkers, Tumor; D016207:Cytokines / Q000235:genetics; D004032:Diet; D020022:Genetic Predisposition to Disease; D016481:Helicobacter Infections / Q000150:complications* / Q000382:microbiology; D016480:Helicobacter pylori / Q000472:pathogenicity; D006801:Humans; D007723:Korea; D011110:Polymorphism, Genetic; D012307:Risk Factors; D013274:Stomach Neoplasms / Q000209:etiology* / Q000235:genetics / Q000382:microbiology; D051197:Toll-Like Receptor 4 / Q000235:genetics; D037521:Virulence Factors
D014408:Biomarkers, Tumor; D016207:Cytokines; D051197:Toll-Like Receptor 4; D037521:Virulence Factors