| Aim:Vulvar dystrophy was regarded as precancerous lesions formerly, but recently studies showed that the canceration rate of vulvar dystrophy only was 0.7% , and only atypical hyperplasia had the possibility to malignant transformation, so the early diagnosis for atypical hyperplasia will be of great value to treatment and prognosis. AnnexinI, also called LipocortinI, was the substrate for epidermal growth factor receptor tyrosine kinase. Its expression level change had been found in earlier period of multiple tumor. P16 protein which is product of pl6 gene (an multiple tumor suppressor), served as inhibitor of cyclin dependent kinase ( CDK), compete with CyclinD1 for combinition with CDK4 and CDK6, down regulate cell proliferation by inhibiting the promotive effect of CyclinD1 for cell proliferation. The disproportion of regulator of cell proliferation will lead to abnormal proliferation and oncogenesis. To discuss the contribution of AnnexinI EGFR c-erbB-2 p16 and CyclinD1 to pathogenesis development and canceration of vulvar dystrophy and the significance for early diagnosis of SCC of vulva, we examined the expression of the five proteins by SABC technique of immunohistochemistry in various vulvar dystrophy and SCC of vulva.Method: The expression of Annexing EGFR, c-erbB-2 p16 and CyclinD1 was investigated by SABC technique of immunohistochemistry in 100 cases of various vulvar dystrophy and 34 cases of SCC of vulva.Results: AX-I, EGFR and c-erbB-2 all localized in plasmalemma and cytoplasm. In normal skin, AX-I and EGFR were mainly distributed in stratum basale, c-erbB-2 was mainly distributed in stratum granulosum and superior part of stratum spinosum. In atypical hyperplasia and SCC of vulva AX-I EGFR and c-erbB-2 had strong positive expression in entire epidermal. The expression of the three proteins was increased significantly in atypical hyperplasia. There were significant difference between atypical hyperplasia and other groups except the group of SCC (P>0.05): nomal tissue (P<0.01), other various dystrophy(P<0.05). EGFR and c-erbB-2 had higher expression in hyperplasia type and mixed type than normal skin ( P<0.05 ) , and the expression intensity of AX-I rised in hyperplasia type, althoug the positive rate had not significant difference between hyperplasia type and normal skin (P>0.05). In SCC of vulva, there were an overexpression of AnnexinI c-erbB-2 and a lower expression of EGFR in stagel (P<0.01) stageII(P<0.05) than stageIII.The expression of pl6 and Cyclin D1 had not significant difference betweem various vuvar dystrophy and normal skin (P>0.05) . Atypical hyperplasia group showd a dramatic reduction in pl6 protein expression and an increase in Cyclin D1 expression compared with nomal tissue and other various dystrophy(P<0.05), but there was not significant difference between atypical hyperplasia and the group of SCC of vulva (P>0.05). In SCC of vulva, p16 protein had lower expresion in stageIII than stagel (P<0.05), the positive rate of Cyclin Djin the different stage of SCC were 57.1% in staged 66.7% in stageII and 81.8% in stagelll. In addition, the expression level of Cyclin D1 was more highly significant in P16-negative cases than that in P16-positive cases(P<0.01), and the positive rate of p16 in Cyclin D1- positive cases was significantly lower than thatin Cyclin Drnegative cases (P<0.01).Conclusion: AX-I EGFR, c-erbB-2 may play an important role in vulvar squamous epidermal proliferation and malignant transformation. In SCC of vulva, the expression of three proteins was related to histology grades, EGFR mainly expressed in undifferentiation squamous carcinoma. AX-I c-erbB-2 mainly expressed in differentiation squamous carcinoma. The strong positive expression of AX-I c-erbB-2 mainly appeared in atypical hyperplasia and differentiation squamous carcinoma, these suggest that two proteins play an role mainly in earlier period of oncogenesis and have some significance for early diagnosis of SCC of vulva. EGFR mainly expressed in undifferentiation squamous carcinoma, so could b...
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