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Although the sensitivity to a particular stimulus varied considerably among the TGCT cell lines, the differences in response were not associated with the presence of functional p53, Mutant (mt) p53-expressing NCCIT and S2 (no p53 protein) were both readily triggered into apoptosis by cisplatin and doxorubicin, while wild-type(wt)p53-transactivation-competent 2102 EP cells failed to undergo drug-induced apoptosis, Moreover, transactivation-deficient NCCIT cells and wtp53-expressing NT2 cells were equally sensitive to cisplatin, doxorubicin, gamma radiation, and cell-permeable C-2-ceramide, Our p53 data suggest that, at least in this panel of non-isogeneic TOOT cell lines, hypersensitivity to therapeutic agents is not associated with p53 status. Next, we examined the impact of p53 inactivation on apoptosis induction in isogeneic NT2 sublines expressing human papillomavirus Et, protein. Evidently, abrogation of p53 function did not affect the hypersensitivity to apoptotic stimuli. We noted that drug-sensitive 52 cells were highly resistant to radiation-induced apoptosis, indicating distinct signalling pathways for chemotherapy and irradiation. The impaired radiation-induced apoptotic pathway in 52 and 2102 EP could not be restored by addition of cell-permeable C-2-ceramide, suggesting that the blockade is downstream of ceramide generation. Ligation of Fas/APO-I/CD95 by anti-Fas effectively induced apoptosis in pas-antigen expressing S2, 2102 EP and 833 KE. The efficient pas-mediated activation of apoptosis in drug-, radiation- and ceramide-resistant 2102 EP cells further suggests that diverse apoptosis-inducing factors may use distinct signalling pathways. In summary, we demonstrated the presence of distinct p53-independent: apoptotic pathways in TOOT cells. 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