Abstract
MYD88(L265P) is the most common mutation in lymphoplasmacytic lymphoma/Waldenström macroglobulinemia (LPL/WM) and one of the most frequent in poor-prognosis subtypes of diffuse large B-cell lymphoma (DLBCL). Although, inhibition of MYD88(L265P) activity has been shown to be toxic to LPL/WM and DLBCL cells, providing crucial insight for potential targeted therapies, these studies were conducted in the context of pre-quiescent tumor suppressor signaling and the results bear limited information on the role of MYD88(L265P) in tumor initiation, which remains uncertain.
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