Clinical Significance of Expression of p53 Oncoprotein and Human Papillomavirus in Cervical Cancer. |
K W Lee, M J Oh, B W Yeom |
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Abstract |
Human papillomavirus (HPV) infection is clearly associated with cervical carcinoma. High risk HPVs including HPV type 16 and 18 are closely associated with carcinoma of the uterine cervix. Cellular protein p53 is associated with growth control of normal cells and transformation. The wild type p53 gene could specially suppress the growth of human cancer cell line with a p53 allelic deletion and mutation. Wild type p53 gene may function as a suppressor of neoplastic growth and that deletion or mutation of this gene may lead to a loss of the suppressive activity. The transforming potential of HPV type 16 and 18 is located on the E6 and E7 genes in vitro. It is revealed that the E6 protein encoded by the high risk HPVs promotes the degradation of p53. In this study, we examined the presence of HPV genomes and the expression of p53 protein in invasive cervical cancer samples and analyzed a possible relationship between the clinicopathological factors of disease and the presence of HPV or expression of p53 protein. The results were as follows: 1. The detection rate of HPV type 16 was 61.2 % (30/49). 2. The proportion of carcinoma with HPV type 16 positivity increased with age, stage and invasion depth, whereas no correlation was found between HPV type 16 positivity and the other clinical parameters. 3. The rate of p53 protein overexpression was 36.7 % (18/49). 4. The overexpression of p53 protein was correlated with age, tumor size, invasion depth and nodal status. 5. There is no inverse correlation between HPV infection and p53 protein overexpression. In tumorigenesis of the cervical carcinoma other mechanism independent of p53 inactivation may also be involved. |
Key Words:
p53, Human papillomavirus, Cervical cancer |
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