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Immunohistochemical detection of p53 protein in anogenital lesions and its relationship with HPV status
1Department of Histopathology, I.R.C.C.S. S. de Bellis, Castellana Grotte, Bari, Italy.
Abstract:
The p53 tumour suppressor protein can be rendered ineffective by mutations in the p53 gene or by interactions with proteins of DNA-transforming viruses, including Human Papillomaviruses (HPVs). Our aim was to determine whether the inactivation of p53, caused by a mutation of gene itself or by HPV is involved in anogenital carcinogenesis. We studied p53 overexpression by immunohistochemical methods, and HPV/DNA by non isotopic in situ hybridization method in 137 anogenital lesions. Immunoreactivity for p53 was seen in 5% of condylomata acuminata, in 12% of low-grade CINs, in 3.5% of high-grade CINs, and in 17% of invasive cervical carcinomas. Two (67%) of three condylomata acuminate p53+ harboured HPV/DNA. The concomitant presence of p53 and HPV was not detected in intraepithelial and invasive cervical lesions. Our findings suggest that p53 inactivation does not seem to play an important role in anogenital carcinogenesis. Further investigation of the concomitant presence of p53 and HPV in condylomata acuminate and its role in recurrences or progression of these lesions is needed.
Insights
p53 protein inactivation, whether by gene mutation or Human Papillomavirus (HPV), does not appear to be a significant factor in anogenital cancers. Further research is needed on HPV and p53 in condylomata acuminata.
Area of Science:
- Oncology
- Virology
- Molecular Biology
Background:
- The p53 tumor suppressor protein is crucial for preventing cancer.
- Mutations in the p53 gene or interactions with viral proteins, such as those from Human Papillomaviruses (HPVs), can inactivate p53.
- Anogenital carcinogenesis involves complex genetic and viral factors.
Purpose of the Study:
- To investigate the role of p53 inactivation in anogenital carcinogenesis.
- To determine if p53 gene mutations or HPV infections contribute to the development of anogenital lesions.
- To assess the prevalence of p53 overexpression and HPV DNA in various anogenital lesions.
Main Methods:
- Studied 137 anogenital lesions using immunohistochemical methods for p53 overexpression.
- Employed non-isotopic in situ hybridization to detect HPV DNA.
- Correlated p53 status with HPV presence and lesion type.
Main Results:
- p53 overexpression was detected in 5% of condylomata acuminata, 12% of low-grade CINs, 3.5% of high-grade CINs, and 17% of invasive cervical carcinomas.
- HPV DNA was found in 67% of p53-positive condylomata acuminata.
- Concomitant p53 and HPV presence was not observed in intraepithelial or invasive cervical lesions.
Conclusions:
- p53 inactivation does not appear to be a major driver in anogenital carcinogenesis.
- The role of concurrent p53 and HPV in condylomata acuminata warrants further investigation regarding lesion recurrence and progression.