
<ArticleTitle>Differential sensitivity of human papillomavirus type 16(+) and type 18(+) cervical carcinoma cells to <prot>CD95</prot>-mediated apoptosis.</ArticleTitle>
<AbstractText>When cervical carcinoma cells were monitored for apoptotic signals, HPV18(+) lines were found to be highly sensitive to agonistic <prot>CD95</prot> antibodies or recombinant <prot>CD95</prot> ligands after co-exposure with CHX (<prot>CD95</prot>(S)). In contrast, HPV16(+) cervical carcinoma cells and HPV16-immortalized non-malignant human keratinocytes were <prot>CD95</prot>-resistant (<prot>CD95</prot>(R)) under equivalent conditions. Somatic cell hybridization between <prot>CD95</prot>(S) and <prot>CD95</prot>(R) cervical carcinoma cell lines revealed that <prot>CD95</prot> sensitivity was a dominant trait, which could be correlated with abundant <prot>c-Myc</prot> and low <prot>Bcl-X</prot>(L) expression. Although <prot>CD95</prot>(R) cervical carcinoma cells expressed even higher levels of <prot>p53</prot> and <prot><prot>CD95</prot> receptor</prot> at the surface, resistance could be attributed to the inability to form a functional DISC, necessary for successful transmission of the apoptogenic response. These data indicate that resistance to apoptotic stimuli represents an important immunological escape mechanism during virus-induced carcinogenesis.</AbstractText>
