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检测９号染色体及ｐ１６基因在口腔鳞癌发生发展中的作用。方法：应用聚合酶链反应技术，检测经显微切割的口腔鳞癌组织中两个ＤＮＡ微卫星多态标记ＤｑＳ３１９（９ｐ２１）和ＤｑＳ２９９（９ｑ２２～３１），分析染色体９ｐ、９ｑ的杂合性丢失情况。同时应用免疫组织化学方法观察其ｐ１６蛋白表达状况。结果：２９．４％出现ＤｑＳ３１９标记的ＬＯＨ，ＤｑＳ２９９标记发现较高频率ＬＯＨ（４３．８％）。ｐ１６蛋白免疫组化染色阳性率为８６．４％。其中３例未表达ｐ１６的标本中，有２例发现ＤｑＳ３１９的ＬＯＨ。结论：口腔鳞癌在染色体９ｐ２１区域频繁丢失可能与ｐ１６失活有关，而染色体９ｑ２２～３１区域在口腔鳞癌的较高频率丢失推测此区可能存在与肿瘤发生密切相关的抑癌基因。
To detect the role of chromosome 9 and p16 gene in the development of oral squamous cell carcinoma. Methods: Two microsatellite DNA microsatellite markers, DqS319 (9p21) and DqS299 (9q22 ~ 31), were used to detect the loss of heterozygosity of chromosome 9p, 9q in the microdissected oral squamous cell carcinoma by polymerase chain reaction Happening. Immunohistochemistry was used to observe the expression of p16 protein. Results: DQS319-labeled LOH appeared in 29.4%, and higher frequency LOH (43.8%) was found in DqS299. The positive rate of p16 protein immunohistochemical staining was 86.4%. Of the 3 specimens that did not express p16, 2 found LOH in DqS319. Conclusion: The frequent loss of oral squamous cell carcinoma in chromosome 9p21 may be related to the deactivation of p16, whereas the higher frequency loss of chromosome 9q22 ~ 31 in oral squamous cell carcinoma suggests that there may be a tumor suppressor gene closely related to tumorigenesis.