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目的 探讨人肺癌中nm2 3等位基因缺失与肺癌转移的关系。方法 应用Southern印迹杂交对 5 2例人肺癌组织中nm2 3 H1 和nm2 3 H2 等位基因缺失进行了研究 ,并以自身远离癌灶的肺组织作对照。结果 5 2例肺癌中 14例存在nm2 3 H1 等位基因的杂合缺失 ( 2 6.92 % )。 47例有nm2 3 H2 杂交信号的肺癌中 ,2例存在nm2 3 H2 等位基因缺失 ( 4 .2 6% )。伴有淋巴结和 /或远处转移的肺癌中 ,nm2 3 H1等位基因缺失率 ( 4 2 .86% )明显高于不伴有转移的肺癌 ( 8.3 3 % ) (P <0 .0 1) ;低分化和未分化癌nm2 3 H1等位基因缺失率 ( 4 5 .45 % )亦明显高于中～高分化癌 ( 13 .3 3 % ) (P <0 .0 5 )。nm2 3 H1 等位基因缺失与肺癌组织学类型、P TNM分期、原发肿瘤大小、部位 ,以及患者年龄等无明显关系 (P >0 .0 5 )。结论 本研究结果表明nm2 3基因可能参与调控肺癌的细胞分化和转移过程 ,且nm2 3 H1 基因在肺癌转移和细胞分化中的调节作用较nm2 3 H2 基因更为显著
Objective To explore the relationship between loss of nm23 allele and lung cancer metastasis in human lung cancer. Methods Southern blot hybridization was used to study the loss of nm23H1 and nm23H2 alleles in 52 human lung cancer tissues. Results The heterozygous deletion of the nm23H1 allele was found in 14 out of 52 cases of lung cancer (2 6.92%). Of the 47 lung cancers with nm23H2 hybridization signal, 2 had the loss of nm23H2 allele (4.2%). In lung cancer with lymph node and/or distant metastasis, the deletion rate of nm23 H1 allele was significantly higher (42.86%) than that of lung cancer without metastasis (8.33%) (P < 0.01). The rate of deletion of the nm23H1 allele in poorly differentiated and undifferentiated carcinomas (45.4%) was also significantly higher than that in moderately to well differentiated carcinomas (13.33%) (P < 0.05). The loss of nm23H1 allele was not significantly associated with histological type, P TNM stage, primary tumor size, location, and age of patients (P > 0.05). Conclusion The results of this study suggest that nm23 may be involved in the regulation of cell differentiation and metastasis of lung cancer, and the regulation of nm23H1 gene in lung cancer metastasis and cell differentiation is more significant than that of nm23H2 gene.