Human papillomavirus (HPV) infections are associated with benign and
malignant lesions of the female and male anogenital tract. In the current
study, we aimed to investigate the role of high-risk HPVs infection in the
pathogenesis of prostate cancer among nations or ethnic groups, in
addition to testing the role of homozygosity of arginine form at codon 72
of the p53 gene among prostate cancer patients whose prostate tissues
were infected with high-risk HPVs.
Formalin-fixed paraffin-embedded tissue samples of 123 primary prostate
adenocarcinoma cases and 267 control tissues of benign prostatic
hyperplasia were used in the study. Genomic DNA was purified and
amplified through MY09/MY11 degenerate primers, GP5+/GP6+
consensus primers, SPF1/2 cocktail of six primers using conventional,
multiplex and nested PCR techniques, and subsequently subjected to viral
load quantification, genotyping, testing of polymorphism of codon 72 of
the p53 gene and apoptosis index assessment by in situ assay. Also, the
status of the p53 tumour suppressor gene, p16INK4a transcription factor as
well as the E6 protein of the high risk HPVs have been tested by
immunohistochemistry in both the study and control groups.
High-risk HPVs were detected in 30 of 123 (24.3%) PCa and 16 of 267
(5.9%) BPH samples with positive HPV-DNA. The detection rate of the
high-risk HPV infections was 4%, 44% and 29% among the ethnic
subgroups from the Middle Eastern, Caucasian, and Afro-Caribbean of the
PCa patients. There was no association between the existence of high-risk
HPV infections and their viral load in PCa patients and the tumour
staging, grading, PSA level and patient survival rate in those patients.
Likewise, there was no significant difference in the frequency of p53 Arg
16
homozygosity between the high-risk HPV-positive and the HPV-negative
PCa samples. Moreover, it has been found that the existence of the highrisk
HPV E6 protein within the PCa samples was independent of the
status of the p53 gene, p16INK4a transcription factor, and the apoptosis
index in these samples.
Our data showed that HPV infections do exist in PCa and BPH samples
with different prevalence within ethnic groups with the least occurrence in
the Middle Eastern patients. However, the infections with high-risk HPVs
are not associated with the prostate cancer grade, stage, patient’s PSA
level, and survival rate. Therefore, our data do not support the role of
HPV infection in the pathogenesis of prostate carcinoma
