Little is known about penile carcinogenesis. The aim of this study was to evaluate the prevalence of HPV and EBV, and the methylation status of p16 in penile cancer samples, and to contribute to the understanding of the mechanisms responsible for penile cancer development. HPV DNA was detected in 63.6% of 122 cases, with HPV16 being the most prevalent type. EBV DNA was detected in 47.7%, with EBV-1 being the most prevalent type. HPV/EBV co-infections were found in 27.3% of the cases. Hypermethylation in p16 was detected in 64.5% of 110 tested cases. An association between the absence of HPV absence and p16 hypermethylation was also found. Death and/or progressive disease was associated with grade (P = 0.001), T stage (P < 0.0001), and N stage (P < 0.0001). In the multivariable model, grade and N stage were independent risk factors for disease-free survival (P = 0.008 and P < 0.001, respectively). Patients without viral infection had a median age significantly lower than that of the HPV-infected patients. We suggest at least two pathways for penile carcinogenesis, one HPV-independent linked to epigenetic events, probably via p16 inactivation; and another, dependent on HPV infection.
Cervical cancer is a major source of illness and death among women worldwide and genital infection with oncogenic human papillomavirus (HPV) its principal cause. There is evidence of the influence of the male factor in the development of cervical neoplasia. Nevertheless, the pathogenic processes of HPV in men are still poorly understood. It has been observed that different HPV types can be found among couples. The objective of the present study was to investigate HPV infections in female patients (n = 60 females/group) as well as in their sexual partners and to identify the concordance of HPV genotypes among them. By using the polymerase chain reaction, we detected a 95% prevalence of HPV DNA in women with cervical intraepithelial neoplasia (CIN) compared to 18.3% in women with normal cervical epithelium, with a statistically significant difference (P < 0.001). The HPV DNA prevalence was 50% in male partners of women with CIN and 16.6% in partners of healthy women. In the control group (healthy women), only 9 couples were simultaneously infected with HPV, and only 22.2% of them had the same virus type, showing a weak agreement rate (kappa index = 0.2). Finally, we observed that HPV DNA was present in both partners in 30 couples if the women had CIN, and among them, 53.3% shared the same HPV type, showing moderate agreement, with a kappa index of 0.5. This finding supports the idea of circulation and recirculation of HPV among couples, perpetuating HPV in the sexually active population, rather than true recurrences of latent infections.
Our study comprises a cases series of 71 men attending a dermatology clinic in Brazil during an 18-month period with anogenital HPV infection. Clinical manifestations, laboratory findings and sociodemographic factors were evaluated. Biopsy samples were subjected to histopathological analysis, generic and type-specific viral identification, and p16 INK4a quantification. The average age at diagnosis was 33 years. We observed little variation in identified viral types (HPVs 6, 11, 16 and 53), despite the inclusion of 16 HIV+ patients. The presence of high-risk HPV was associated with receptive anal sex (p<0.05), lesion malignancy (p<0.01) and p16INK4a expression (p<0.05). HIV+ was correlated with HPV16 infection, presence of perianal lesions and high-grade lesions (p<0.05) diagnosed at a younger mean age than HIV-patients (p<0.05). Our results demonstrate the unequivocal relationship between high-risk HPV infection and the presence of high-grade lesions, HPV 16 tropism in the anal epithelium, and the role of receptive anal sex as a risk factor for development of high-grade anal lesions, that present early in HIV+ men who have sex with men. As the 5 high-grade lesions (1 AINII and 4 AIN III) showed p16INK4a negativity but were related to HPV 16 presence, we believe that p16INK4a is a promising biomarker, but its use remains controversial requiring further research.
A infecção pelo papilomavírus humano (HPV) está entre as doenças sexualmente transmissíveis (DST) mais prevalentes no mundo. No entanto, ainda existem lacunas no conhecimento sobre a história natural da infecção por HPV em homens. Este estudo teve como objetivo determinar a prevalência de infecção por HPV em amostras de esfregaços penianos derivadas de uma população masculina clinicamente assintomática. Para tanto, 261 amostras foram coletadas entre janeiro de 2011 e julho de 2013 em diferentes instituições da cidade do Rio de Janeiro. As amostras foram coletadas da glande, corona, frênulo e sulco coronal. A identificação viral foi feita por meio das técnicas de Reação em Cadeia da Polimerase genérica e tipo-específica e de Polimorfismo do Comprimento do Fragmento de Restrição. A prevalência da infecção por HPV foi de 16,5% (43 indivíduos). O tipo de HPV mais prevalente foi o HPV6 (34,9%), seguido pelo HPV16 (23,3%), HPV11 (16,3%), HPV45 (9,3%) e HPV58 (2,3%). Assim, a infecção foi associada a tipos de baixo risco oncogênico em 53,7% dos indivíduos estudados e a tipos de alto risco oncogênico em 46,3% destes indivíduos. Resultados estatisticamente significativos foram encontrados para o grupo de homens que fazem sexo com homens, o grupo que afirma manter relações sexuais anais e indivíduos não circuncidados. Após ajustes estatísticos, o comportamento sexual e a não circuncisão permaneceram como fatores de risco independentes para a infecção por HPV. Acreditamos que estes resultados possam contribuir para uma visão mais clara a respeito da circulação do HPV na população masculina em geral, bem como para a identificação dos fatores de risco associados com a epidemiologia da infecção por HPV em nosso estado.
IntroductionHPV infection causes cancer at several anatomical sites. However, the natural history of the infection in non-cervical sites have been understudied, especially at the oral epithelium.MethodsIn our study, we investigated 351 samples from three different sites of 117 patients, searching for HPV By generic and specific PCR and Microarray, and related risk factors.ResultsHPV DNA prevalence was 89.5% (105/117) in the genital lesions, 53.8% (63/117) in oral samples and 59% (69/117) in anal samples. Regarding the risk factors associated with HPV in the genital lesions, we found statistically significant rates for oral (p=0.039) and anal sex practices (p=0.0000012). For oral samples, we observed a relevant correlation concerning oral contraceptive use (p=0.039), tobacco smoking (p=0.036) and alcohol use (p=0.0075) while in anal samples, we found higher risk for HPV infection in patients relating non-exclusive sexual partners (p=0.013). The presence of viral DNA in all the three sites was observed in 36.8% of the cases (43/117). Among them, 18% (21/117) presented concordant HPV genotypes, diverging from the literature, corroborating that there is still much to learn about HPV natural history, since different biological behaviours are expected within different populations.ConclusionIn our study we also evaluated if the detection of oral HPV would suggest an infection in the anogenital tract. Nevertheless, our results showed only 36.8% of correlation pointing out that it is not suitable as a an auxiliary biomarker for HPV anogenital infections.
IntroductionStudies have shown that persistent infection by high risk human papillomavirus (HR-HPV), especially type 16, is responsible for cervical cancer development. For the development of a malignant phenotype, several mechanisms are involved, among them the process of epigenetic DNA methylation, which results in gene silencing, leading to abrogation of cell cycle control, escape from senescence, and induction of proliferation, that therefore can collaborate in carcinogenesis. Understanding how the epidemiological factors can influence the mechanism of methylation related to infection of the HR-HPV is an unclear situation to be unveiled. The objective of this study was to evaluate the infections caused by HPV16 in patients attended at Gynaecology Institute, of UFRJ, in the period between 2012 and 2013, considering aspects of methylation in host gene pINK4a.MethodsThe cervical smears were submitted to the detection of HPV DNA by Polimerase Chain Reaction (PCR) using primers MY09/11, genotyped with primers for the E6 gene of HPV16, evaluated the methylation of the host pINK4a gene by Nested-MSP technique, and collected epidemiological data, which included socio-demographic and behavioural factors of each patient; and, the data of the diagnostic test that served as reference, the cytopathology.ResultsOur results showed nearly 76% of the studied samples presented some degree of gene pINK4amethylated, while 24% were unmethylated. The results showed statistical significance for the correlation of the cytopathology with sexarca (p=0.05657), smoking (p=0.0317), pregnancies (p=5938e-05), parity (p=0.004425) and number of partners (p=0.0242). The p16 gene methylation correlations that showed statistical significance were pregnancy (p=0.02725), parity (p=0.01414),and typing (p=0.008121).ConclusionWe have found that the presence of HPV16 is associated with a greater chance of methylation of p16 in the lesions. Although, we also observed that the methylation of p16 gene is increasingly accompanying the severity of lesions, but without statistical relevance.
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