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慢性幽门螺杆菌感染患者胃黏膜中p53的评估

p53 evaluation in gastric mucosa of patients with chronic Helicobacter pylori infection.

作者信息

Marinone C, Martinetti A, Mestriner M, Seregni E, Geuna M, Ferrari L, Strola G, Bonardi L, Fea E, Bombardieri E

机构信息

Division of Internal Medicine Ospedale San Vito, Torino, Italy.

出版信息

Anticancer Res. 2001 Mar-Apr;21(2A):1115-8.

Abstract

Gastric cancer is often associated with p53 over-expression and Helicobacter pylori (HP) infection. In this study we have investigated the production of the p53 protein and mutation of its gene in precancerous gastric lesions with HP infection. For this purpose 130 patients who underwent endoscopy for dyspepsia were enrolled in the study. To assess p53 production and mutation of the p53 gene we employed an immunoluminometric assay and polymerase chain reaction single strand conformation polymorphism (PCR-SSCP) analysis, respectively. Histologically, 52 of the 130 enrolled patients showed intestinal metaplasia type I (IM) (90.4% of these were also HP positive), 47 had HP-related gastritis and 31 were normal. p53 cytosol levels were significantly higher in patients with IM or HP-related gastritis than in normal patients (p = 0.0137 and p = 0.0411, respectively). All DNAs extracted from gastric mucosa samples with higher p53 values and examined for p53 mutations by PCR-SSCP analysis were characterized by a normal run. Our data indicate, that irreversible genetic changes in the p53 protein has not yet occurred in morphologically non-neoplastic gastric mucosa with IM and HP-related chronic gastritis. In conclusion, the increase in p53 cytosolic levels found in our study is due to an increased production of the wild-type protein probably related to an inflammatory response induced by HP infection.

摘要

胃癌常与p53过表达和幽门螺杆菌(HP)感染相关。在本研究中,我们调查了HP感染的胃癌前病变中p53蛋白的产生及其基因的突变情况。为此,选取了130例因消化不良接受内镜检查的患者纳入研究。为评估p53的产生及p53基因的突变,我们分别采用了免疫荧光测定法和聚合酶链反应单链构象多态性(PCR - SSCP)分析。组织学检查显示,130例入选患者中52例表现为I型肠化生(IM)(其中90.4%也为HP阳性),47例有HP相关性胃炎,31例正常。IM或HP相关性胃炎患者的p53胞浆水平显著高于正常患者(分别为p = 0.0137和p = 0.0411)。通过PCR - SSCP分析对所有从p53值较高的胃黏膜样本中提取的DNA进行p53突变检测,结果均显示电泳条带正常。我们的数据表明,在形态学上非肿瘤性的伴有IM和HP相关性慢性胃炎的胃黏膜中,p53蛋白尚未发生不可逆的基因改变。总之,我们研究中发现的p53胞浆水平升高是由于野生型蛋白产量增加,这可能与HP感染诱导的炎症反应有关。

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