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目的 :探讨抑癌基因p16在胃癌组织中是否存在甲基化异常及其与胃癌发生发展的关系。方法 :对 2 0例胃癌组织及相应正常胃粘膜组织应用甲基敏感酶 (HpaII)和甲基非敏感酶 (MspI)酶切 ,结合PCR扩增技术 ,对p16基因外显子 1、外显子 2的二核苷酸胞嘧啶特定序列 5’ CCGG 3’位点甲基化进行检测。结果 :2 0例胃癌组织中 ,p16基因外显子 1、2异常甲基化分别为 5例 (2 5 % )和 9例 (45 % ) ,正常组织未发现甲基化异常 ;14例高甲基化标本中 ,中分化胃癌 4例 ,低分化 7例 ,高分化 1例 ;有 2例存在外显子 1、2同时甲基化异常 ,二者均为低分化胃癌 ,进展期胃癌 (Ⅲa、Ⅳ期各 1例 )中 1例呈现泳动易位 ;外显子 2甲基化异常多发生于晚期肿瘤患者 (P <0 .0 5 )。结论 :p16基因甲基化异常可能会造成基因功能丧失 ,从而失去对细胞增殖的负性调控作用 ,导致胃癌发生与进展 ;外显子 2高甲基化与临床进展有关 ,可能为晚期事件
Objective : To investigate whether the tumor suppressor gene p16 has abnormal methylation and its relationship with the occurrence and development of gastric cancer. Methods: 20 cases of gastric cancer tissues and corresponding normal gastric mucosa tissues were digested with methyl-sensitive enzyme (HpaII) and methyl-non-sensitive enzyme (MspI), combined with PCR amplification technology, to exon 1 and exon 1 of p16 gene. The dinucleotide cytosine-specific 5’ CCGG 3’ site of subunit 2 was methylated for detection. Results: In 20 cases of gastric cancer, abnormal methylation of exon 1 and 2 of p16 gene was found in 5 cases (25%) and 9 cases (45%). No abnormal methylation was found in normal tissues; 14 cases were hypermethylated. Among the specimens, moderately differentiated gastric cancer was found in 4 cases, poorly differentiated in 7 cases, and well differentiated in 1 case; in 2 cases, exon 1 and 2 simultaneous methylation abnormalities were present, both poorly differentiated gastric cancer and advanced gastric cancer (IIIa, In one case of stage IV, one case showed a swimming movement translocation; the exon 2 methylation abnormalities mostly occurred in patients with advanced tumor (P < 0.05). Conclusion : Abnormal methylation of p16 gene may lead to loss of gene function and loss of negative regulation of cell proliferation, leading to the occurrence and progression of gastric cancer. Hypermethylation of exon 2 is associated with clinical progress and may be a late event.