Recurrent losses or gains of genomic material as well as mutations of key tumor suppressors (ATM and TP53) have been identified in chronic lymphocytic leukemia (CLL).
The induction of p53 by nutlin-3 in B-CLL samples was accompanied by alterations of the mitochondrial potential and activation of the caspase-dependent apoptotic pathway.
Translocations or isochromosome formations at sites of low-copy DNA repeats in 17p10 to 17p12 appear to be the mechanism for the loss of TP53 in B-CLL.