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위장관 간질성 종양의 면역화학적염색법을 이용한 재진단 및 새로운 등급체계의 임상적 유용성
이채영(Chae Young Lee),김진조(Jin Cho Kim),김원우(Won Woo Kim),진현민(Hyung Min Chin),김욱(Wook Kim),박조현(Cho Hyun Park),전해명(Hae Myung Jeon),박승만(Seung Man Park),임근우(Keun Woo Lim),박우배(Woo Bae Park),김승남(Seung Nam Kim) 대한외과학회 2003 Annals of Surgical Treatment and Research(ASRT) Vol.64 No.6
Helicobacter pylori 감염과 Interleukin $1\beta$ 유전자의 다형성에 따른 위암 발생 위험도
박상협,송교영,김진조,진형민,김욱,박조현,박승만,임근우,박우배,김승남,전해명,Park, Sang-Hyub,Song-Kyo-Young,Kim, Jin-Jo,Jin-Hyung-Min,Kim, Wook,Park, Cho-Hyun,Park, Seung-Man,Lim-Keun-Woo,Park, Woo-Bae,Kim, Seung-Nam,Jeon, Hae-Myung 대한위암학회 2004 대한위암학회지 Vol.4 No.3
Purpose: According to the recent studies, it is shown that the polymorphism of Interleukin $1\beta$ gene is associated with the incidence of gastric cancer caused by the Helicobacter pylori infection. Interleukin $1\beta$ is a cytokine markedly inhibiting gastric acid secretion. Interleukin $1\beta$ production associated with Helicobacter pylori gastric infection may exacerbate mucosal damage including chronic gastritis and atrophic gastritis, may induce eventual neoplasia. Among these Interleukin $1\beta$ gene polymorphisms, polymorphisms at -31 portion and -511 portion may associated with these processes, eventually increase the risk of gastric cancer. We investigated the risk of gastric cancer according to the Helicobacter pylori infection and genetic polymorphism of Interleukin $1\beta$ in gastric cancer patients. Materials and Methods: 176 individuals with gastric cancer and 40 healthy controls were analyzed. Each group was divided into two groups whether they infected with Helicobacter pylori or not. DNA was extracted from the peripheral blood in all groups. The PCR-RFLP method was used for investigating the distribution of genotype of C/C, C/T, T/T at -31 portion and -511 portion. Results: T/T genotype at -511 portion was $19.3\%$ in gastric cancer cases and $10\%$ in controls, which was statistically significant. (P=0.0432) The risk of gastric cancer was increased 4.86 ($1.26\∼18.77$) in group which had T/T genotype. In gastric cancer cases, C/C genotype at 31 portion was $27.6\%$ in group with Helicobacter pylori infection and $12.8\%$ in group without infection, which was statistically significant. (P=0.0047) The risk of gastric cancer was increased 4.82 ($1.81\~12.81$) in group which had C/C genotype. Conclusion: T genotype at -511 portion among the Interleukin $1\beta$ genetic polymorphisms may be the risk factor of gastric cancer. And, with Helicobacter pylori infection, C genotype at -31 portion may be the risk factor of gastric cancer.