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Genetic testing in early diagnostics and prevention of gastric cancer

机译:基因检测对胃癌的早期诊断和预防

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Background: To determine diagnostic importance of DNA methylation in patients with chronic atrophic gastritis and induction of ''Correa'' cascade for gastric cancer prevention. Material and methods: This present study included 80 patients with chronic atrophic gastritis associated with Helicobacter pylori. Diagnoses were confirmed by endoscopic, morphologic, serologic examinations. Age of patients varied from 17 to 78 years old. There were 52 (65%) males and 28 (35%) females. The control group consisted of 32 patients with morphological verified diagnosis of stage I-II gastric cancer. Examination with the purpose to determine hypermethylation of DNA was performed simultaneously in biopsy materials and blood plasma. Provoking factors of hypermethylation in 4 tumors' genes, APE, E-Cadherin, T1MP3, hMLHI were determined by quantitative methylation with use of Polymerase Chain Reaction. To evaluate the level of methylation we compared the analysis' results of biopsy and blood plasma tests. Blood serum samples and biopsy specimens were collected at diagnosis until the therapy is started. All patients with chronic atrophic gastritis infected with H. pylori underwent anti-H. pylori therapy according to the protocol. Chronic atrophic gastritis was found at morphologic examination in 40 (50%) patients according to ''Correa'' cascade. 36 (45%) patients had intestinal metaplasia, and 4 (5%) patients had dysplasia. Reaction was considered to be positive in cases, when the level of methylation in genes listed above was higher in blood serum than in biopsy materials. Results: High concentrations of methylated APE, T1MP3 and hMLIH in genes were found in blood serum of 8 (10%) patients. In the control group, all 32 patients with gastric cancer had high methylation level in blood serum. In the remaining 72 (90%) patients, no high concentration of DNA methylation was found. After the 2-nd course of anti-H. pylori therapy, patients underwent morphologic and endoscopic examinations according to the protocol. Eradication of H. pylori was determined in 86% patients who received therapy. Intestinal metaplasia decreased from 45% to 25% (20 patients). Mild dysplasia was found in 1.2% of cases. Repeated analysis of methylation level showed its decrease after anti-H. pylori therapy in 4 (50%) out of 8 patients. Conclusion: Genetic tests show that DNA methylation in patients with chronic atrophic gastritis has high diagnostic importance. Anti-H. pylori therapy at the different stages of ''Correa'' cascade has high level of induction in transforming into non invase gastric cancer.
机译:背景:确定DNA甲基化在慢性萎缩性胃炎患者中的诊断重要性以及诱导“ Correa”级联预防胃癌的重要性。材料和方法:本研究包括80例患有幽门螺杆菌的慢性萎缩性胃炎患者。通过内窥镜检查,形态学检查,血清学检查确诊。患者年龄从17岁到78岁不等。男52例(65%),女28例(35%)。对照组包括32例经形态学证实为I-II期胃癌的患者。在活检材料和血浆中同时进行了旨在确定DNA超甲基化的检查。使用聚合酶链反应通过定量甲基化确定4种肿瘤基因APE,E-钙黏着蛋白,T1MP3,hMLHI中高甲基化的诱发因素。为了评估甲基化水平,我们比较了活检和血浆测试的分析结果。诊断时收集血清样本和活检标本,直到开始治疗为止。所有感染幽门螺杆菌的慢性萎缩性胃炎患者均接受抗H疗法。根据方案进行幽门螺杆菌治疗。根据“ Correa”级联,在形态学检查中发现40例(50%)患者患有慢性萎缩性胃炎。肠上皮化生36例(45%),不典型增生4例(5%)。当血清中上述基因的甲基化水平高于活检材料中的甲基化水平时,该反应被认为是阳性的。结果:8名(10%)患者的血清中发现了高浓度的甲基化APE,T1MP3和hMLIH基因。在对照组中,所有32例胃癌患者的血清甲基化水平较高。在其余的72名(90%)患者中,未发现高浓度的DNA甲基化。防H后第2个疗程。幽门螺杆菌治疗后,根据方案对患者进行了形态学和内镜检查。在接受治疗的86%患者中根除了幽门螺杆菌。肠上皮化生从45%下降至25%(20例患者)。在1.2%的病例中发现了轻度的不典型增生。重复分析甲基化水平显示抗H后降低。 8例患者中有4例(50%)接受了幽门螺杆菌治疗。结论:基因测试表明,DNA甲基化在慢性萎缩性胃炎患者中具有很高的诊断意义。反H。在“ Correa”级联的不同阶段进行的幽门螺杆菌疗法在转化为非侵袭性胃癌方面具有较高的诱导水平。

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