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目的 探讨结、直肠癌P16基因突变与癌发生、演进的关系。方法 选结、直肠癌组织、癌旁正常组织42例和7例转移淋巴结,用蛋白酶K消化,提取DNA,用多聚酶链式反应-单链构象多态分析(PCR-SSCP)及DNA测序方法分析P16基因第二外显子的突变。结果 42例癌组织中发现7例有异常泳动条带,占16.7％。在7例癌转移的淋巴结中发现3例异常泳动条带。癌旁组织中未发现异常泳动条带。第二外显子42～61,147～168编码区的核酸出现改变,为碱基G-T、T-G、G-A的碱基转换。突变的发生率与组织分型无明显相关。Duke’C期突变率高于A、B期,有淋巴结转移者突变率也高。结论 P16基因的丧失,可引起Cdk 4活性的负调节,导致细胞无限增殖。本组资料发现点突变在癌组织中占16.7％,转移淋巴结中也有。由于采用了自身正常组织对照,避免了正常多态性的干扰,结果较为可靠。P16基因的改变与临床分期及预后有一定关系。
Objective To investigate the relationship between P16 gene mutation and carcinogenesis and progression in colorectal cancer. METHODS: Selective node, rectal cancer tissue, normal tissue adjacent to tumors and metastatic lymph nodes in 42 cases were digested with proteinase K and DNA was extracted. Polymerase chain reaction-single strand conformation polymorphism analysis (PCR-SSCP) and DNA sequencing methods were used to analyze the results. Mutations in the second exon of the P16 gene. Results Abnormal motility bands were found in 7 of 42 cases of cancer tissues, accounting for 16.7%. Three abnormal migration bands were found in 7 lymph node metastases. No abnormal swimming bands were found in the adjacent tissues. The nucleic acid in the coding region of the second exons 42 to 61, 147 to 168 changed, and the bases of the bases G-T, T-G, and G-A were converted. The incidence of mutations was not significantly related to tissue typing. The Duke’C phase mutation rate was higher than that of the A and B phases, and the mutation rate was also high in patients with lymph node metastasis. Conclusion The loss of P16 gene can lead to the negative regulation of Cdk 4 activity, leading to an indefinite proliferation of cells. In this group of data, point mutations were found in 16.7% of cancers and metastatic lymph nodes. Due to the use of its own normal tissue control, normal polymorphism interference was avoided and the results were more reliable. The change of P16 gene has a certain relationship with clinical stage and prognosis.