Alternative mechanisms of deregulation of the p53 pathway in chronic lymphocytic leukemia
Eventually almost all cancers escape the tumor suppression control by the key genome guardian p53, most frequently by genetic mutations but also by other mechanisms. Defects in p53 are widely accepted to be the most significant marker of poor prognosis among chronic lymphocytic leukemia (CLL) patients. We hypothesize that apart from a direct genetic impairment, other mechanisms acting upon p53 protein could be driving CLL. Therefore, we plan to portray the landscape of phosphorylation modifications of p53 in primary human CLL cells treated with a clinically relevant drug set. We anticipate to identify differences among patients with distinct genetic background and with diverse clinical outcome.