Targeting precursor BCR signaling in ALL

Abstract

In this issue of Blood, Kim et al1 investigated the preclinical therapeutic potential of targeting precursor B-cell receptor (pre-BCR) signaling and its mechanism of action in acute lymphoblastic leukemia (ALL). Ibrutinib, a US Food and Drug Administration (FDA)-approved inhibitor of Bruton tyrosine kinase (BTK), was demonstrated to interfere with pre-BCR signaling and specifically suppress in vitro and in vivo cell proliferation of B-ALL cells that express a functional pre-BCR. The synergistic activity with conventional chemotherapeutic agents corroborates ibrutinib as a new therapeutic opportunity for pre-BCR+ ALL.