BAG3 protein controls B-chronic lymphocytic leukaemia cell apoptosis

Dear Editor,

B-cell chronic lymphocytic leukaemia (B-CLL), the most common form of leukaemia in North America and Europe, is caused primarily by defective apoptosis.^1,2 Such defect prolongs the physiological lifespan of the cells and renders them resistant to the effects of therapy.^1,2 Advanced research on B-CLL pathogenesis and therapy therefore points to the identification of molecules that sustain cell survival and/or contrast death in this form of leukaemia.^1,2 The expression of a number of antiapoptotic proteins has been detected in B-CLL cells.^3,4,5,6 These include Bcl-2,^3,4,5,6 Mcl-1,^4,5,6 inhibitor of apoptosis proteins (IAPs)^5,6 and the cochaperone family member BAG1.^4,5 Furthermore, surface structures, such as CD40, can transduce NF-κB-mediated survival signals in B-CLL cells.⁷ Although all these molecules exert antiapoptotic activities, they do not completely account for the sustained leukaemic cell survival, to which other pathways are likely to contribute.^1,2

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