Abstract
TP53-disrupted chronic lymphocytic leukaemia (CLL) patients show a suboptimal long-term response to ibrutinib. We hereby report that ibrutinib-induced invitro apoptosis and proliferation inhibition were significantly lower in TP53-mutated (TP53-M) CLL cells compared to TP53 wild-type cells. Contrariwise, venetoclax effectively killed TP53-M cells. Gene expression profile analysis ofTP53-M cells revealed a downmodulation of B-cell receptor (BCR)-related genes and an upmodulation of genes withanti-apoptotic/pro-survival activity, suggesting that the survival and proliferation ofTP53-M cells are less dependent on the BCR pathway. These observations further support the use of drug combinations for the optimal management ofTP53-M CLL patients.
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