| Literature DB >> 32083995 |
Steven P Treon1,2, Lian Xu1, Maria Luisa Guerrera1,2, Cristina Jimenez1,2, Zachary R Hunter1,2, Xia Liu1,2, Maria Demos1, Joshua Gustine1, Gloria Chan1, Manit Munshi1, Nicholas Tsakmaklis1, Jiaji G Chen1, Amanda Kofides1, Romanos Sklavenitis-Pistofidis2,3,4, Mark Bustoros2,3, Andrew Keezer1, Kirsten Meid1, Christopher J Patterson1, Antonio Sacco3,4, Aldo Roccaro4, Andrew R Branagan5, Guang Yang1,2, Irene M Ghobrial2,3, Jorge J Castillo1,2.
Abstract
Next-generation sequencing has revealed recurring somatic mutations in Waldenström macroglobulinemia (WM), including MYD88 (95%-97%), CXCR4 (30%-40%), ARID1A (17%), and CD79B (8%-15%). Deletions involving chromosome 6q are common in patients with mutated MYD88 and include genes that modulate NFKB, BCL2, Bruton tyrosine kinase (BTK), and apoptosis. Patients with wild-type MYD88 WM show an increased risk of transformation and death and exhibit many mutations found in diffuse large B-cell lymphoma. The discovery of MYD88 and CXCR4 mutations in WM has facilitated rational drug development, including the development of BTK and CXCR4 inhibitors. Responses to many agents commonly used to treat WM, including the BTK inhibitor ibrutinib, are affected by MYD88 and/or CXCR4 mutation status. The mutation status of both MYD88 and CXCR4 can be used for a precision-guided treatment approach to WM.Entities:
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Year: 2020 PMID： 32083995 PMCID： PMC7351339 DOI： 10.1200/JCO.19.02314
Source DB: PubMed Journal: J Clin Oncol ISSN： 0732-183X Impact factor: 44.544