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Comparison of the Clinicopathological Characteristics and Genetic Alterations Between Patients with Gastric Cancer with or Without Helicobacter pylori Helicobacter pylori Infection

机译:胃癌患者临床病理特征和胃癌术幽门螺杆菌幽门螺杆菌感染的临床病理特征和遗传改变

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Abstract Background Helicobacter pylori (HP) can induce epithelial cells and intestinal metaplasia with genetic damage that makes them highly susceptible to the development of gastric cancer (GC). Materials and Methods Between 2005 and 2010, 356 patients with gastric cancer who received curative surgery were enrolled. Analysis of HP, Epstein‐Barr virus (EBV) infection, PIK3CA amplification, and mutation analysis of 68 mutations in eight genes using a mass spectrometric single‐nucleotide polymorphism genotyping technology was conducted. The clinicopathological characteristics of patients with or without HP infection were compared. Results Among the 356 patients, 185 (52.0%) had HP infection. For intestinal‐type GC, patients with HP infection were more likely to be younger and had fewer PI3K/AKT pathway genetic mutations than those without HP infection. For diffuse‐type GC, patients with HP infection were characterized by less male predominance, less lymphoid stroma, fewer microsatellite instability‐high tumors, and fewer PI3K/AKT pathway genetic mutations than those without HP infection. Patients with HP infection had less tumor recurrence and a better 5‐year overall survival (87.7% vs. 73.9%, p ?=?.012) and disease‐free survival (64.1% vs. 51.3%, p ?=?.013) than those without HP infection, especially for intestinal‐type GC. For EBV‐negative GC, patients with HP infection had fewer PI3K/AKT pathway mutations and a better 5‐year overall survival and disease‐free survival than those without HP infection. Multivariate analysis demonstrated that HP infection was an independent prognostic factor regarding overall survival and disease‐free survival. Conclusion Patients with GC with HP infection were associated with fewer PI3K/AKT pathway genetic mutations and better survival than those without HP infection, especially for EBV‐negative and intestinal‐type GC. Implications for Practice Patients with gastric cancer with Helicobacter pylori (HP) infection had fewer PI3K/AKT pathway genetic mutations, less tumor recurrence, and better survival than those without HP infection, especially for Epstein‐Barr virus (EBV)‐negative and intestinal‐type gastric cancer. HP infection is an independent prognostic factor regarding overall survival and disease‐free survival. Future in vivo and in vitro studies of the correlation among HP infection, PI3K/AKT pathway, and EBV infection in gastric cancer are required.
机译:摘要背景幽门螺杆菌(HP)可以诱导上皮细胞和肠青细胞癌,遗传损伤使得它们对胃癌(GC)的发育非常敏感。 2005年至2010年期间的材料和方法,注册了356例接受治疗手术的胃癌患者。采用MATS谱图单核苷酸多态性基因分型技术分析HP,EPStein-BART病毒(EBV)感染,PIK3CA扩增和68个突变的突变分析。比较有或没有HP感染患者的临床病理学特征。 356例患者中的结果有185名(52.0%)有HP感染。对于肠型GC,HP感染的患者更容易发生更年轻,并且PI3K / AKT途径遗传突变较少,而不是没有HP感染的遗传突变。对于弥漫性GC,HP感染的患者的特征在于较少的男性优势,淋巴样基质较少,较少的微卫星不稳定 - 高肿瘤,以及比没有HP感染的PI3K / AKT途径遗传突变更少。患有HP感染的患者肿瘤复发性较少,5年的整体存活(87.7%vs.73.9%,p?=β.012)和无病生存率(64.1%与51.3%,p?= 013 )而不是没有HP感染的那些,特别是对于肠型GC。对于EBV阴性GC,HP感染的患者具有较少的PI3K / AKT途径突变,并且比没有HP感染的人更好的5年整体存活和无病的存活率。多变量分析表明,HP感染是关于整体存活和无病生存率的独立预后因素。结论患有HP感染的GC患者与较少的PI3K / AKT途径遗传突变和比没有HP感染的患者更好的存活率相关,特别是对于EBV阴性和肠型GC。对胃癌幽门螺杆菌(HP)感染的胃癌患者的影响具有较少的PI3K / AKT途径遗传突变,较少的肿瘤复发,比没有HP感染的那些更好的存活,特别是对于Epstein-Barr病毒(EBV) - 肠道 - 肠 - 胃癌型。 HP感染是关于整体存活和无病生存的独立预后因素。需要在体内和体外研究HP感染,PI3K / AKT路径和胃癌中的EBV感染之间的相关性。

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