Abstract
Bruton’s tyrosine kinase (BTK), a member of the Tec family of nonreceptor protein tyrosine kinases, is critical for early B cell development and mature B cell activation and survival, and is downregulated in plasma cells. Mutation of BTK leads to human X-linked agammaglobulinemia (XLA) and murine X-linked immunodeficiency (Xid). Here we investigate BTK function in multiple myeloma (MM) cells. Although rare mutations were found in the promoter and coding sequence of the BTK gene, elevated BTK at mRNA level was detected in MM cell lines and CD138 positive primary cells from 3 out of 8 cases of patients with MM. At protein level, BTK was upregulated in some of MM as well as myeloid leukemia cell lines. Specific inhibitor of BTK also suppressed proliferation of MM cells. These data suggest a role for BTK to play in MM pathogenesis.