东印度人群肿瘤坏死因子- α基因(- 308 G/A, - 238 G/A和- 857 C/T)多态性与胃癌风险的评估

IF 1.5 Q3 GASTROENTEROLOGY & HEPATOLOGY
Kanishka Uthansingh, G. Pati, P. Parida, Jimmy Narayan, S. Pradhan, M. Sahu, R. Padhy
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引用次数: 2

摘要

胃癌(GC)是世界范围内癌症相关死亡的主要原因之一。幽门螺杆菌在胃和十二指肠的感染引起肿瘤坏死因子α (TNF-α)的炎症。该研究的目的是将- 308 G/A、- 238 G/A和- 857 C/T位置的三种TNF-α基因多态性与GC风险联系起来并进行评估。方法:共有156名年龄在18岁以上的个体(连续诊断为95例GC患者和61例对照组)入组研究。上消化道内窥镜检查(UGIE)正常的健康个体,不论其胃癌或消化性溃疡家族史,均被纳入对照组。采用聚合酶链反应-限制性片段长度多态性(RFLP)对引用的3个TNF-α基因多态性进行评价。结果:作为遗传因素的基因多态性分布TNF-α - 308 GA/AA(22.1%比14.8%,p = 0.2)、TNF-α - 238 GA/AA(21%比19.6%,p = 0.8)和TNF-α - 857 CT/TT(8.4%比11.5%,p = 0.5)在胃癌患者与健康对照组之间无显著差异。对幽门螺杆菌阳性患者的亚组分析显示,GA/AA多态性在TNF-α - 308中的分布无显著差异(15(45.5%)vs. 3(23%);P = 0.17)和- 238 (12(36.3%)vs. 2(15.4%);p = 0.17), TT/CT - 857 CT/TT分布(13例(39.4%)vs 2例(15.4%);p = 0.13)。结论:GA/AA与GG基因型在- 308 (OR = 1.6, 95% CI: 0.6-3.8)、- 238 (OR = 1.09, 95% CI: 0.4-2.4)、TT/CT与CC基因型在- 857 (OR = 0.7, 95% CI: 0.2-2.1)的统计学比较均未提示TNF-α与胃癌的相关性。因此,TNF-α (- 308 G/A, - 238 G/A和- 857 C/T)可能不是PCR-RFLP方法确定的GC发病率的相关因素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Evaluation of Tumor Necrosis Factor-Alpha Gene (−308 G/A, −238 G/A and −857 C/T) Polymorphisms and the Risk of Gastric Cancer in Eastern Indian Population
Introduction: Gastric cancer (GC) is one of the leading causes of cancer-related decimations worldwide. The gastric infection at both the stomach and duodenum with Helicobacter pylori causes inflammation by the tumor necrosis factor-alpha (TNF-α). The aim of the study was to associate and evaluate the three TNF-α gene polymorphisms at positions −308 G/A, −238 G/A, and −857 C/T with the risk of GC. Methods: A total of 156 individuals (consecutively diagnosed 95 GC patients and 61 controls) above the age of 18 years were enrolled in the study. Healthy individuals with normal upper gastrointestinal endoscopy (UGIE) irrespective of their family history of GC or peptic ulcer were included as controls. The cited three TNF-α gene polymorphisms were evaluated using polymerase chain reaction-restriction fragment length polymorphism (RFLP). Results: There was no significant difference in the distribution of gene polymorphisms as genetic factors, TNF-α−308 GA/AA (22.1% vs. 14.8%, p = 0.2), TNF-α−238 GA/AA (21% vs. 19.6%, p = 0.8), and TNF-α−857 CT/TT (8.4% vs. 11.5%, p = 0.5), between GC cases and healthy controls. A subgroup analysis of H. pylori-positive patients showed that there was no significant difference in the distribution of GA/AA polymorphisms in TNF-α−308 (15(45.5%) vs. 3(23%); p = 0.17) and −238 (12(36.3%) vs. 2(15.4%); p = 0.17), and the distribution of TT/CT −857 CT/TT (13(39.4%) vs. 2(15.4%); p = 0.13), among the GC cases and controls. Conclusion: The statistical comparisons of GA/AA vs. GG genotypes at −308 (with OR = 1.6, 95% CI: 0.6–3.8), −238 (OR = 1.09, 95% CI: 0.4–2.4) and TT/CT vs. CC genotypes at −857 (OR = 0.7, 95% CI: 0.2–2.1) did not suggest any association of TNF-α with GC in the population herein. Hence, the TNF-α (−308 G/A, −238 G/A and −857 C/T) may not be the associating factor for GC incidence determined by the PCR–RFLP method.
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来源期刊
Gastroenterology Insights
Gastroenterology Insights GASTROENTEROLOGY & HEPATOLOGY-
CiteScore
2.80
自引率
3.40%
发文量
35
审稿时长
10 weeks
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