Analysis on expression of tumor related antigen and its clinical application in oral cancers.

采用荧光原位杂交技术（FISH）对27例口腔鳞癌（SCC）患者17号染色体的数值畸变进行了研究，并探讨了其与p53和Bcl-2蛋白表达的关系。由于SCC中17号多体细胞显著增加（p=0.0005），因此17号染色体异常似乎与口腔SCC的癌变有关。17号染色体异常情况因人而异，异常程度与疾病分期、SCC的组织学分化、疾病复发及淋巴结转移无关。然而，17型多体与p53免疫反应性存在相关性（p=0.0228）。P53免疫反应性与疾病复发相关（p=0.044 1）。p53与Bcl-2免疫反应性呈负相关（p=0.042）。综上所述，我们认为17号多体与口腔SCC的癌变密切相关，且17号多体与p53过表达显著相关。这一现象的可能机制假设为：17号多体与p53突变有关，导致p53异常蛋白的积累，其激活导致p53蛋白的增加。

Numerical aberrations of chromosome 17 was studied by fluorescence in situ hybridization (FISH) using pericentromere specific DNA probe in 27 oral squamous cell carcinoma (SCC), and its relationship with p53 and Bcl-2 protein expression was investigated. Since cells with polysomy 17 significantly increased in SCC (p=0.0005), chromosome 17 abnormality seems to be correlated with carcinogenesis of oral SCC.Chromosome 17 abnormality varied from case to case, and the degree of the abnormality did not correlate with the stage of the disease, the histological differentiation of SCC, relapse of the disease and lymph node matastasis . However, there was the correlation between polysomy 17 and p53 immunoreactivity (p=0.0228). p53 immunoreactivity showed correlation with relapse of the disease (p=0.044 1). An inverse relationship was found between p53 and Bcl-2 immunoreactivity (p=0.042 1). In conclusion, we suggest that polysomy 17 is in close relation to carcinogenesis of oral SCC, and that polysomy 17 significantly correlated with p53 overexpression. The possible mechanism of this phenomenon is assumed that polysomy 17 correlates with mutation of p53 which results in an accumulation of aberrant p53 protein, and that its activation causes an increase of p53 protein.