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In contrast, the p53 / Rb1 double knockout model with Cre-activated mutant Myc T58A that leads to stabilised MYC proteins, is representative of the variant subtype of human SCLC [149]
This suggests that chronic smoke exposure leads to an increase in smoke-mediated activation of the parthanatos pathway and implicates its contribution in the pathogenesis of smoke-related lung diseases
(Shihadeh et al
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