食管癌组织多种肿瘤抑制基因微卫星多态位点的杂合丢失和不稳定

The loss of heterozygosity and microsatellite DNA instability of esophageal carcinomas in multiple tumor suppressor genes polymorphous sites

目的：研究ｐ５３ ，ｐ１６， Ｒｂ ， Ｄ Ｃ Ｃ， Ａ Ｐ Ｃ 等多种已知抑癌基因在食管癌组织中的缺失及与临床病理的关系。方法：采用 Ｐ Ｃ Ｒ 银染技术，检测高发区３６ 例配对的食管癌标本１４ 个微卫星 Ｄ Ｎ Ａ 多态位点的杂合丢失和不稳定性。结果：分别与ｐ５３ ，ｐ１６ 及 Ｒｂ 连锁的 Ｄ１７ Ｓ２６１ ， Ｄ９ Ｓ１６２ 、 Ｄ９ Ｓ１７１、 Ｉ Ｆ Ｎ Ａ 和 Ｄ１３ Ｓ１７０ 均有高频率的杂合丢失（ ＞ ２５ ％ ） ；两个以上的位点异常者占８６％ ，ｐ Ｔ Ｎ Ｍ Ⅲ期患者微卫星 Ｄ Ｎ Ａ 多态位点异常的频率显著高于Ⅱ期患者（ Ｐ＜ ０．０１） 。结论：同一病例有多个微卫星 Ｄ Ｎ Ａ 多态位点异常提示食管上皮癌变涉及多个抑癌基因的失活。

Objective:To study the deletion frequency of tumor suppressor genes p53,p16,Rb, DCC,APC,FHIT, PTEN in esophageal carcinoma(EC) and their relationship to clinic pathological characteristics.Method:Using PCR silver staining technique,the loss of heterozygosity(LOH) and microsatellite instability(MSI) among 14 microsatellite DNA polymorphic markers were examined in 36 matched human esophageal cancers and adjacent normal mucosal tissues. Rsults:High frequency of LOH ( >25%) was found in D17S261,D9S162,D9S171,IFNA and D13S170, which were respectively linked to p53, p16 and Rb genes.Eighty six percent (86%) of patients had 2 or more aberrant sites, the tumors of pTNM Ⅲshowed more abnormal sites than those of pTNM Ⅱ.Conclusion:Multiple microsatellite DNA abnormality in the same tissues suggested that more than one suppressor gene was deleted during the carcinogeneses of esophageal epithelia.