Najjar Sadeghi Rouhallah, Damavand Behzad, Vahedi Mohsen, Mohebbi Seyed Reza, Zojazi Homayon, Molaei Mahsa, Zali Mohamad Reza
Research Center for Gastroenterology and Liver Diseases, Taleghani Hospital, Shahid Beheshti University of Medical sciences, Tehran, Iran.
Asian Pac J Cancer Prev. 2013;14(1):91-6. doi: 10.7314/apjcp.2013.14.1.91.
p53 alterations have been implicated in the development of many cancers, such as gastric cancer, but there is no evidence of p53 intron alterations in gastritis lesions. The aim of this study was to investigate the p53 intron alterations in gastritis along with p53 and mismatch repair protein expression and microsatellite status.
PCR-sequencing was conducted for introns 2-7 on DNA extracted from 97 paired samples of gastritis lesions and normal adjacent tissue. Abnormal accumulation of p53 and mismatch repair proteins was investigated using immunohistochemistry. In addition, microsatellite status was evaluated with reference to five mononucleotide markers.
Gastritis cases included 41 males and 56 females in the age range of 15-83 years, 87.6% being H.pylori positive. IVS2+38, IVS3ins16 and IVS7+72 were the most polymorphic sites. Their minor allele frequency values were as follows: 0.38, 0.21 and 0.06, respectively. Samples with GG genotype at IVS2+38 and CT at IVS7+72 had no insertion. Moreover, most of the stable samples (91.9 %) had a G allele at IVS2+38. All of the samples were IHC negative for p53 protein, microsatellite stable and expressed mismatch repair proteins. p53 alterations were prominent in the HP+ group, but without statistical significance.
According to our results, some p53 polymorphisms such as IVS2+38, IVS3ins16 and IVS7+72, because of their correlations together or with microsatellite status may contribute to gastritis development. However, so far effects on p53 expression and function remain unclear. Therefore, a comprehensive survey is needed to delineate their biological significance.
p53改变与许多癌症的发生有关，如胃癌，但尚无证据表明胃炎病变中存在p53内含子改变。本研究旨在探讨胃炎中p53内含子改变以及p53和错配修复蛋白表达及微卫星状态。
对从97对胃炎病变和相邻正常组织样本中提取的DNA进行第2至7内含子的PCR测序。采用免疫组织化学研究p53和错配修复蛋白的异常积聚。此外，参照五个单核苷酸标记评估微卫星状态。
胃炎病例包括41名男性和56名女性，年龄在15至83岁之间，87.6%为幽门螺杆菌阳性。IVS2+38、IVS3ins16和IVS7+72是最具多态性的位点。它们的次要等位基因频率值分别如下：0.38、0.21和0.06。IVS2+38处为GG基因型且IVS7+72处为CT的样本无插入。此外，大多数稳定样本（91.9%）在IVS2+38处有G等位基因。所有样本p53蛋白免疫组化均为阴性，微卫星稳定且表达错配修复蛋白。p53改变在HP+组中较为突出，但无统计学意义。
根据我们的结果，一些p53多态性，如IVS2+38、IVS3ins16和IVS7+72，由于它们之间或与微卫星状态的相关性，可能有助于胃炎的发生。然而，目前对p53表达和功能的影响仍不清楚。因此，需要进行全面调查以阐明它们的生物学意义。
