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口腔鳞状细胞癌(OSCC)患者中新型p53密码子240丝氨酸>苏氨酸编码区突变

Novel p53 codon 240 Ser > Thr coding region mutation in the patients of oral squamous cell carcinoma (OSCC).

作者信息

Saleem S, Abbasi Z A, Hameed A, Qureshi N R, Khan M A, Azhar A

机构信息

The Karachi Institute of Biotechnology and Genetic Engineering (KIBGE), University of Karachi, Karachi, Pakistan,

出版信息

Tumour Biol. 2014 Aug;35(8):7945-50. doi: 10.1007/s13277-014-2062-2. Epub 2014 May 16.

Abstract

Chewing habits of tobacco, betel quid (paan), and betel nut (chhaliya) are common traditions in Pakistan. Different other preparations and combination of flavors with tobacco, paan, and chhaliya ingredients are commonly available in the market and have received considerable attention as sources of carcinogens that promote OSCC. Mutagens can damage DNA and generate promutagenic lesions. The germ line mutation/polymorphism of p53 gene has been reported to be involved in multiple steps of carcinogenesis. This study aims to find out the loss of TP53 functions due to mutation/polymorphism caused by genomic alteration and interaction with tobacco-related ingredients.Tissue and blood specimens from 260 OSCC patients were collected and compared with blood samples of 260 age- and sex-matched controls. Mutations in exons 2-11 of p53 gene were examined by PCR-SSCP and directly sequenced.A novel mutation was found in exon 7 of p53 gene. This mutation was observed in the tumors of the OSCC patients. The blood samples of the patients and the controls did not show the nucleotide change in this region. The "AGT" to "ACT" missense mutation was identified at position 719 at TP53. This results in the substitution of amino acid serine with threonine at codon 240 of p53 protein.This novel missence mutation in the DNA-binding domain indicated that the DNA structure may be damaged by the use of exogenous DNA-damaging agents, including tobacco-related carcinogens present in gutka, niswar, and manpuri, which may result in the loss of p53 protein function.

摘要

咀嚼烟草、槟榔和槟榔果是巴基斯坦的常见传统习俗。市场上通常有不同的其他制剂以及烟草、槟榔和槟榔果成分与其他口味的组合,它们作为促进口腔鳞状细胞癌(OSCC)的致癌物来源受到了相当多的关注。诱变剂会破坏DNA并产生前诱变损伤。据报道,p53基因的种系突变/多态性参与了致癌作用的多个步骤。本研究旨在找出由于基因组改变以及与烟草相关成分相互作用导致的突变/多态性所引起的TP53功能丧失。收集了260例口腔鳞状细胞癌患者的组织和血液样本,并与260例年龄和性别匹配的对照者的血液样本进行比较。通过聚合酶链反应-单链构象多态性(PCR-SSCP)检测p53基因外显子2至11的突变,并进行直接测序。在p53基因的外显子7中发现了一个新的突变。在口腔鳞状细胞癌患者的肿瘤中观察到了这种突变。患者和对照者的血液样本在该区域未显示核苷酸变化。在TP53的719位鉴定出“AGT”到“ACT”的错义突变。这导致p53蛋白第240位密码子处的丝氨酸被苏氨酸取代。DNA结合域中的这种新的错义突变表明,使用包括古特卡、尼什瓦尔和曼普里中存在的烟草相关致癌物在内的外源性DNA损伤剂可能会破坏DNA结构,这可能导致p53蛋白功能丧失。

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