Since E6 and E7 viral protein interaction with cell proteins pRb and p53 is mandatory for cell transformation, HPV RNA CISH is functionally relevant and acutely reflects active oncogenic HPV infection.
Considering that HPV could affect tumor protein 53 (TP53) degradation via E6 oncoprotein, we evaluated the expression of TP53 according to HPV infection and E6 expression.
Similarly, we have demonstrated that persistent hr-HPV infection 16/18 and p53 overexpression are associated with treatment failure after endoscopic ablation of BD/EAC.
Furthermore, TP53 codon 72 polymorphism was not significant associated with oral carcinoma susceptibility in tobacco or alcohol use, and HPV infection status.
The study was performed to investigate the value of HPV infection and the expression of p16<sup>INK4A</sup> and TP53 in rare primitive cancers of the cervix.
Aim of our study was to evaluate the relationship between the polymorphisms of TP53 pathway genes <i>TP53</i>, <i>MDM2</i>, <i>MDM4</i>, the polymorphisms of HPV-associated genes <i>MTHFR</i>, <i>CASP8</i>, <i>CCR5</i>, and HPV infection with survival of LC patients.SNPs were genotyped using PCR-RFLP. qRT-PCR was used to detect, identify, and quantify HPV.
Lentiviral shRNA attenuation of PTTG or PBF expression in HNSCC cells with either wild-type or mutant p53, and with and without HPV infection, led to dysregulated expression of p53 target genes involved in DNA repair and apoptosis.
Finally, the absence of differences in p53 and p16 expressions is at variance with other epithelia where the classical pathway is associated with human papillomavirus infection and can be explained by the fact that both AK pathways share identical mechanisms of actinic oncogenesis.
This study aimed to identify biomarkers of active HPV infection in Barrett's metaplasia, (BM)/BD/OAC by immunohistochemical staining (IHC) of formalin-fixed paraffin embedded (FFPE) tissue for aberrations of p53 and the retinoblastoma (pRb) pathway, which are targets for the viral oncoproteins, E6/E7, respectively.
In contrast, the pure G-ECAs were characterized by the absence of HPV infection and frequent HIK1083 expression and aberrant p53 expression, similar to that of HPV-unrelated G+U ECAs.
The combination of relative low HPV infection and variant TP53 72C allele overtransmission provide a plausible explanation for the low incidence of cervical cancer in our population.
<b>CONCLUSIONS:</b> These results suggest that hr-HPV types are not associated with the development of ESCC and that p53 and p16 protein expression have no relationship with HPV infection in normal or cancerous esophagus.
This study found that 26-30% of oropharyngeal carcinoma was associated with HPV infection, mostly HPV16, and that smoking which predisposes to TP53 mutations was another important risk factor.
Further evaluation of the associations between PrP expression and the data concerning p53 abnormalities and human papillomavirus (HPV) infection in these samples as previously described, revealed that PrP-positive staining was more frequently detected in the tissues with p53-positive accumulation and the wild-type TP53 gene.
The data obtained suggest that HIV-infected women are more susceptible to be infected by low-risk HPV (LR-HPV) genotypes than by high-risk (HR-HPV), and Pro72Pro of TP53 gene and TG of MDM2 SNP309 genotypes apparently seem to be protective factors among HIV-infected women for HPV acquisition and HR-HPV infection, respectively, in a sample of Southern Brazilian woman.