Efficacy and Safety of Bruton Tyrosine Kinase Inhibitors in B-Cell Malignancies

Published: Sunday, Sep 30, 2018
B-cell malignancies are a heterogeneous subset of non-Hodgkin lymphomas in which treatment has remained essentially unchanged for the past 3 decades.1 However, greater understanding of the key pathways that drive proliferation, survival, and resistance patterns to commonly used therapeutics has led to the identification of novel therapeutic targets, thereby offering to significantly change the prognosis for patients affected by B-cell malignancies.1


BTK in B-Cell Malignancies: CLL and MCL

Despite associations with considerable genetic heterogeneity, CLL is noted to have a complex pathogenesis that is heavily influenced by genetic factors.6 The genetic heterogeneity of CLL suggests a potential need for multiple drugs or multitargeted agents to effectively address the variety of manifestations. However, as BCR signaling has been implicated to play a central role in CLL pathogenesis and cell proliferation, inhibition of this pathway yields compartment shift of malignant B cells from the tissues into the blood, resulting in transient lymphocytosis and eventual lymph node shrinkage.7 A consequence of interfering in BCR signaling in malignant B cells in this manner permits normalization of peripheral lymphocyte counts, leading to disease remission in an appreciable number of treated patients.2,7
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