In conclusion, this study provides evidence for elevated LAP2α expression in cervical cancer and suggests that E2F and p53 activities associate with the positive and negative regulation of LAP2α expression, respectively.
Thus, polymorphism of the p53 itself as well as in combination with HPV infection may not be a genetic risk for cervical cancer and therefore much attention should be paid to other risk factors such as sexual behavior and smoking.
To better understand the role of this polymorphism in cervical cancer etiology, we investigated the association between p53R72P and cervical cancer risk in Chinese women from southern Han.
In additional, interaction between these p53 and p21 polymorphisms increased the risk of cervical cancer in a multiplicative manner, with the OR being 3.96 (95% CI, 1.51-10.41) for subjects carrying both p53 Arg/Arg and p21 Ser/Ser genotypes.
The intratumoral delivery of exogenous E1A carried by SDION increases p53 expression but inhibits HER-2/neu expression, and enhances the radiosensitivity of human cervical cancer in xenograft mice.
Although genetic variation in TP53 might affect the natural history of HPV and cervical cancer, further work is needed to elucidate the possible mechanism.
MVP, p53 and angiogenesis, together with tumor oxygenation, were determined in forty-three consecutive patients suffering from localized cervix carcinoma.
Our results showed low incidence of p53 mutations and prevalence of Arg/Arg genotype polymorphic variant of codon 72 of p53 gene in early stages of cervical carcinoma.
To analyze aberrant expression of the apoptotic protein p53 and the anti-apoptotic protein Bcl-2 in premalignant lesions of the uterine cervix induced by human papillomavirus (HPV) infection and its significance for early diagnosis of cervical cancer.
Hypoxia may inhibits the NHEJ DNA repair through downregulating Ku70/80 expression and combined with an increased angiogenesis and altered p53 expression would be responsible for tumor progression in cervical carcinoma.
In this study, we compared the expression of the HPV16 E6 oncogene to the conditional genetic disruption of p53 in the context of a mouse model for cervical cancer in which estrogen is a critical cofactor.
Cervical carcinoma is associated with certain types of human papillomaviruses expressing the E6 and E7 oncogenes, which are involved in carcinogenesis through their interactions with the p53 and pRB pathways, respectively.
hMSH2 immunoreactivity was correlated with p53 and weakly correlated with apoptosis. hMSH2 immunoreactivity could not be correlated to any tumour markers, while apoptosis correlated significantly with T stage, FIGO classification and the relative risk of death from cervical cancer.
The purpose of this study was to determine whether activation of the p53 and retinoblastoma (Rb) pathway by HPV-16 E6 and E7 repression was responsible for apoptosis and senescence of cervical cancer cells and to explore the potential of an antisense RNA (AS) transcript for gene therapy of cervical cancer.
Thus, we investigated whether E6 oncoprotein could regulate VEGF expression in HPV18-positive cervical cancer-derived HeLa cells harboring a wild-type p53.
However, few reports have corroborated this data, and the role of the p53 codon 72 polymorphism in the development of cervical cancer requires further elucidation.
Most importantly, the antitumor effect of hydralazine and valproate in cervical cancer may at least partially depend on an up-regulating effect on p53 gene and on the valproate-induced hyperacetylation of p53 protein, protecting it from degradation by E6.
No relationship observed between human p53 codon-72 genotype and HPV-associated cervical cancer in a population group with a low arginine-72 allele frequency.