Abstract
Whole genome sequencing has identified actionable mutations in MYD88 and CXCR4 in lymphoplasmacytic cells from Waldenstrom’s Macroglobulinemia (WM) patients that promote multiple survival cascades that include Bruton’s Tyrosine Kinase (BTK), PI3Kδ/AKT, and ERK1/2. Transcriptome studies have also identified aberrations in MYD88, CXCR4, and BCL2 survival signaling. Novel treatment options for WM include inhibitors that target BTK, PI3Kδ/AKT, CXCR4, and BCL2. Ibrutinib, an inhibitor of BTK, has shown high rates of activity and durable responses in relapsed/refractory WM patients. Both MYD88 and CXCR4 tumor mutation status impact ibrutinib response.
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