| Tumorigenesis is usually thought that oncogene's activation and tumor suppressor gene's losing activation disturb the normal regulation on the proliferation and differentiation which lead to hyperplasia and less differentiation. But more and more people find tumorigenesis is not only related to the growing speed but also to the mortality speed of tumor cell. The defect or block of apoptosis is also an important factor that results in the tumorigenesis and developing .So cancer is not only the disease of abnormal growth and differentiation, but also the disease of abnormal apoptosis. Many oncogenes and antioncogenes regulate apoptosis at the molecular level, and the apoptosis-regulating genes have been regarded as a new kind of oncogene which regulates apoptosis and plays an important role in the tumorigenesis with other oncogenes. Survivin (SVV) is recently found a new apoptosis-regulating gene. As amember of lAP-family (inhibitor of apoptosis, LAP) gene, it can inhibit apoptosis induced by a variety of factors, and plays important roles during mitosis and cytokinesis of cells. Studies indicate that it's a tumor -specific antiapoptosis factor. Survivin is expressed during embryonal develompment but lacks expression in terminally differentiated adult tissues. Interestingly, it becomes re-expressed in transformed cell line and in a variety of human tumors. The over-expression of Survivin is a prognostic factor of tumors and is implicated in the resistance to chemotherapy of cells. The change of Survivin is closely correlated with carcinogenesis and progression of cancers ,such as breast tumor , squamous cell cervical carcinoma, non-small-cell lung cancer, neuroblastoma etc .But there is no any report about the expression of Survivin , bcl-2, p53 gene and the AI simultaneously in Laryngeal squamous cell carcinoma (LSCC) development. The purpose of this study is to elucidate the correlation of the expression of Survivin, bcl-2, p53 gene and the apoptosis in LSCC. The expressions of Survivin, bcl-2 and p53 gene were detected in immunohistochemistry S-P method in 40 cases of LSCC, 20 cases of laryngeal atypical hyperplasia (LAH) and 20 cases of polyp of vocal cord. The apoptosis cells are detected by the technology of terminal deoxyuncleotidyl transferase mediated d-UTP nike end labeling (TUNEL) in the above-mentioned three tissues and AI are calculated.Results:l.The positive expression rate of Survivin gene in LSCC, LAH, polyp tissues were 87.50%(35/40), 80.00%(16/40) and 45.00%(9/20) respectively. The expressions of Survivin in LSCC, LAH were significantly higher than that in polyp (P<0.05); The positive expression rate of Survivin gene in grade I and II of LSCC were 69.23% and 96.30% respectively. The higher the tumor grade was, the higher Survivin expression rate was. There was significant difference between grade I and II (P<0.05).The positive rate of Survivin staining was 82.60% (19/23) in the cases of I+II stage, while 94.11%(16/17) in the cases of III+IV stage, and there was no significant difference between them (P>0.05). The expression of Survivin had no obvious correlation with lymph node metastasis(P>0.05).2.The positive expression rate of bcl-2 gene in groups of LSCC, LAH and vocal cord polyp tissues were 60.00% (24/40), 30.00% (6/20) and 10.00% (2/20) and there was significant difference among the three groups (/><0.05). The positive expression rates of bcl-2 decrease with the increase of the histological grades and the clinical stages but difference was not found(P>0.05). In addition, there was no difference between the positive expressions of bcl-2 in lymph-node-metastasis group and in non-lymph-node-metastasis group. (P>0.05).3.The positive expression rates of p53 in LSCC, LAH and polyp group were 67.50% (27/40), 35.00% (7/20) and 15.00% (3/20) respectively, and they went higher from vocal cord polyp, LAH to LSCC. Comparing LSCC with vocal cord polyp and LAH,the differences were evident (P< 0.05).The positive expression of p53 had obvious correlation with the clinical stages and l...
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