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目的探讨p16/MTS1基因结合缺失与结直肠癌的发生及临床病理关系。方法采用聚合酶链反应方法,对68例结直肠癌组织中p16/MTS1基因纯合缺失进行检测。并用Fisher精确检验的方法,对p16/MTS1基因纯合缺失与临床病理关系进行统计分析。结果68例结直肠癌组织,p16/MTS1基因纯合缺失率为35.29%。DuckesC、D期的缺失率明显高于DuckesA、B期(P<0.05)。低分化腺癌p16/MTS1基因纯合缺失率(11/16)高于高分化腺癌肿瘤(4/25)(P<0.05)。侵犯到浆膜及浆膜外者p16/MTS1基因纯合缺失率高于侵犯在浆膜内者(P<0.05)。结论p16/MTS1基因纯合缺失与结直肠癌的临床分期、病理分化、肌层浸润等生物学特征有关。
Objective To investigate the relationship between the deletion of p16 / MTS1 gene and the occurrence and clinicopathological changes of colorectal cancer. Methods The homozygous deletion of p16 / MTS1 gene in 68 colorectal cancer tissues was detected by polymerase chain reaction. The relationship between p16 / MTS1 homozygous deletion and clinical pathology was statistically analyzed with Fisher exact test. Results The rate of homozygous deletion of p16 / MTS1 gene was 35.29% in 68 cases of colorectal cancer. DuckesC, D loss rate was significantly higher than DuckesA, B (P <0.05). The homozygous deletion rate of p16 / MTS1 gene in poorly differentiated adenocarcinoma (11/16) was higher than that in well-differentiated adenocarcinoma (4/25) (P <0.05). The rate of homozygous deletion of p16 / MTS1 gene invaded serosa and serosa was higher than those invaded serosa (P <0.05). Conclusion The homozygous deletion of p16 / MTS1 gene is related to the biological characteristics of colorectal cancer such as clinical stage, pathological differentiation and myometrial invasion.