Detection of oncogenic viruses (SV40, BKV, JCV, HCMV, HPV) and p53 codon 72 polymorphism in lung carcinoma

As a part of our continuous search for oncogenic viruses in bronchial, cancer, we extended our HPV studies to anayse atso SV40, BKV, JCV and HCMV sequences in bronchiat cancer and related these data with p53 codon 72 polymorphism. Fresh tumor samples from 78 patients withjung cancer were analysed for SV40, BKV, JCV, HCMV and HPV sequences by PCR. HPV genotypes were determined using reverse Mot hybridization and sequencing, and at( HPV-positive tumors were tested for the presence of E6/E7 transcripts by RT-PCR. ALL samples were analysed for p53 codon 72 poymorphism, using PCR-based RFLP method. Of the 78 cases studied, 11 (14.1%) were positive for T-Ag gene of SV40, while BKV and JCV sequences were both amptified in 1 tumor only. Altogether, 10/78 tesions were HPV-positive; six HPV16, one HPV31, two HPV6/53 and one HPV16/18. All HPV DNA-positive samples except one also expressed E6 and E7 transcripts. HCMV was amplified in 18 (23%) cases. RFLP analysis of p53 codon 72 revealed 32 homozygotes for arglarg allete (50.8%), 26 heterozygotes for arg/pro attete (41.3%), and 5 homozygotes for prolpro altele (7.9%). P53 codon 72 poymorphism was not significantly different between cases (n =63) and controls In= 50) (p=0.455), among virus positive and negative patients, nor was it retated to HPV genotypes (p = 0.384), expression of E6 (p=0.384) and E7 oncogenes (p=0.293). Of aR possible combinations of virus co-detection, onty SV40-HCMV association was statistically significant (OR = 5.500, 95%CI 1.43-21.02; p = 0.015). Taken the known mechanisms of these individuat viruses, there is a chance that these viruses could affect cell cycle controt and inhibit apoptosis, thus potentially causing genetic instability and promote oncogenesis. (c) 2007 Etsevier Ireland Ltd. AR rights reserved.