The inactivation of the wild-type p53 function resulting from a missense mutation, or the lack of detectable wild-type p53 protein due to the translational/post-translational deregulation of p53 protein levels may be the contributing factor in the tumorigenicity of these five cases of cervical cancer.
Although a high incidence of HPV DNA integration and a low incidence of p53 mutation were confirmed in cancer of the uterine cervix, there was no inverse association between integration of HPV types 16 and/or 18 DNA and p53 mutation.
Our data indicate that loss of wild-type p53 function is important in the pathology of cervical cancer and that in the absence of an HPV-encoded gene product that mediates loss of p53 function, somatic mutation of the gene is required.
Inactivation of the protein product of the wild-type tumour suppressor gene p53 through complexing of the protein with the E6 oncoprotein of human papillomaviruses (HPV) in HPV-infected cells is thought to be important in the aetiology of cervical carcinoma.
Our data suggest that loss of wild-type p53 function is important in development of cervical carcinoma, and that this might be achieved either by mutation within the p53 gene or the presence of a virally encoded p53 binding protein.
To examine the correlations between ras oncogene expression and the development of cervical cancer, the authors studied the reactivity of cervical intraepithelial neoplasia (CIN) and microinvasive lesions of the human uterine cervix by using anti-ras p21 mouse monoclonal antibody rp35.
It was concluded that the presence of carcinoma of the uterine cervix in human females has no bearing either on spontaneous and MMC-induced SCE rates or on cell cycle progression in PHA-stimulated cultures of peripheral blood lymphocytes.
Two of the major protein species (gp88 and gp130) were common to all four cell lines used (HeLa-cervical carcinoma, T47D-breast carcinoma, and HMB2 and SK1477-two melanoma cell lines).
Two of the major protein species (gp88 and gp130) were common to all four cell lines used (HeLa-cervical carcinoma, T47D-breast carcinoma, and HMB2 and SK1477-two melanoma cell lines).
Two of the major protein species (gp88 and gp130) were common to all four cell lines used (HeLa-cervical carcinoma, T47D-breast carcinoma, and HMB2 and SK1477-two melanoma cell lines).
Two of the major protein species (gp88 and gp130) were common to all four cell lines used (HeLa-cervical carcinoma, T47D-breast carcinoma, and HMB2 and SK1477-two melanoma cell lines).