Some studies have reported an incidence of 0% to 10%[27]; other studies have reported an incidence of 10% to 50%[29]; and some studies have even reported an incidence of 50%

Some studies have reported an incidence of 0% to 10%[27]; other studies have reported an incidence of 10% to 50%[29]; and some studies have even reported an incidence of 50%.[29] Several explanations of this variability have been proposed, including sampling problems, contamination, sensitivity of the detection systems, and geographic variation.[30] None CAY10650 of the healthy controls were positive for HPV-16 and -18 DNA in BCC, which was in accordance with Aglian and colleagues.[27] In contrast, Barghi and colleagues[31] had an HPV positivity rate of one of the CAY10650 largest control groups (5%) of bladder tissue, with PCR on paraffin-embedded bladder tissue specimens. Many investigations have reported a low prevalence CAY10650 of HPV in TCC.[32] For example, Sur and colleagues,[33] from South Africa, detected HPV DNA in only 1 of 64 screened paraffin wax-embedded TCCs. and recurrence (48%, HPV-16). There was a significant association of transitional cell carcinoma (TCC) with HPV-16 in 69.2% and 61.1% of BCC and BTB, respectively. Multiple HPV types 16, 18, and 52 were significantly higher than single types (79.2% and 20.8%, respectively). The observed absolute association between seropositivity of HPV-52 (11.7%) and HPV-16 (26.7%) was significantly associated with TCC CAY10650 in patient groups only. Conclusion Our study confirmed the significant association of HPV-16, -18 and -52 with bladder cancer in Egyptian patients, with the suggestion of viral synergistic action in bladder carcinogenesis. Such HPV types were significantly associated with TCC tumors of low grade and high stage, with schistosomal affection and recurrence tendency. HPV serology would pave the way for better management and follow-up of patients and for optimal design and evaluation of HPV vaccination. Introduction Bladder cancer is a common malignancy in Egypt.[1,2] The increasing incidence of bladder carcinoma observed over the past 3 decades has stimulated research into the identification of possible etiologic agents. The significant association between human papillomavirus (HPV) infection and cancer bladder has been reported.[3,4] More than 100 HPV genomes have been characterized on the basis of nucleotide sequence homology of viral DNA, and at least 42 types have an established etiologic role in tumors of the urogenital tract and anal region. Molecular and epidemiologic studies have distinguished HPV types into oncogenic types, eg, HPV-16, -18, -31, -33, -35, -45, -52, and -58. HPV-16 is the most prevalent oncogenic HPV genotype, with regional CAY10650 variation being highest in Europe and lowest in Africa.[5] The prevalence of other HPV types varies across geographic locations: HPV-35, -45, -52, -56, and -58 are more common in HPV-positive women in sub-Saharan Africa than in Europe, whereas HPV-52 and -58 are more prevalent in Japan and China.[6] The role of HPV in the pathogenesis of carcinoma of the urinary bladder has been extensively investigated with contradictory results in non-Egyptian reports, ranging between 0%[7] and 80%.[8] Egyptian reports from the National Cancer Institute of Cairo University, Cairo, Egypt, revealed that the association between HPV and human cancer bladder ranged from 23%[9] to 49%.[10] The choice of specimen and the different techniques performed seem to influence the number of false-positive and false-negative results, eg, the use of single or multiple tumor fragments, fresh or fixed and paraffin-embedded material, the number of virus genotypes, contamination by plasmid DNA or polymerase chain reaction (PCR) products, and the use of high- or low-sensitivity techniques (Southern blot, PCR, or in situ hybridization).[11] In addition, serology with HPVL capsids, viruslike particles (VLPs), as antigens has also been used to elucidate the association of oncogenic types with cervical neoplasia.[12] Moreover, antibody response to HPV-16 L capsids was significantly associated with the development of HPV-16-positive cervical intraepithelial neoplasia in a cohort study of university women.[13] HPV-16 and/or -18 genomic sequences were identified in the urinary tract of female patients with recurrent and persistent urethritis and cystitis, and in transitional tumors of the bladder.[3,4] However, the question of whether prior infection with a given type of HPV can reduce the risk for infection with a different HPV type and subsequent intraepithelial neoplasia development is unresolved. Similarly, it is not clear whether vaccination against a given HPV strain can protect against infections with other types, especially phylogenetically related types. Recently, some prospective studies that were based on viral Mouse monoclonal to CD74(PE) DNA detection have reported that prior infection may not.