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目的:分析与探讨燃煤型砷中毒患者中抑癌基因p16突变与甲基化的情况及意义。方法:选取120例2013年4月-2015年5月在我院收治的燃煤型砷中毒患者,依照皮肤病变病理学诊断结果,将所有患者分为癌前组(24例)、癌病组(20例)及普通病变组(76例),通过PCR与PCR-SSCP产物克隆测序检测突变热点显子,并通过甲基化内切酶分析第1外显子。结果:通过PCR与PCR-SSCR产物克隆测序对燃煤型砷中毒病人外周血DNA进行分析,没有检测出抗癌基因p16第2外显子发生突变。通过Sma I酶切燃煤型砷中毒病人外周血DNA后,癌变组患者中,扩增出抗癌基因p16第1外显子片段4例,普通病变组与癌前组患者没有检测出Sma I位点甲基化情况。结论:研究表明,p16基因由于高度甲基化是造成p16基因在砷性肿瘤中失活的关键方式,而且在砷致癌中发挥着重要作用。
Objective: To analyze and discuss the mutation and methylation of tumor suppressor gene p16 in patients with coal-burning arsenism. Methods: A total of 120 patients with coal-burning arsenic poisoning who were treated in our hospital from April 2013 to May 2015 were selected and all patients were divided into precancerous group (24 cases), cancer group (20 cases) and common lesion group (76 cases). Mutant hot spots were detected by PCR and PCR-SSCP product sequencing. Exon 1 was analyzed by methylation endonuclease. Results: The peripheral blood DNA of coal-fired arsenism patients was analyzed by PCR and PCR-SSCR product cloning and sequencing. No mutation of exon 2 of anti-oncogene p16 was detected. After Sma I digested the peripheral blood DNA of coal-fired arsenism patients, 4 cases of the first exon of the anti-oncogene p16 were amplified in patients with canceration and no Sma I was detected in the normal and precancerous groups Site methylation. CONCLUSIONS: Studies show that p16 gene is a key way to inactivate p16 gene in arsenic tumors due to its high degree of methylation, and plays an important role in arsenic carcinogenesis.