Insights into the genomic landscape of MYD88 wild-type Waldenstrom macroglobulinemia.

ABSTRACT: Activating MYD88 mutations are present in 95% of Waldenström macroglobulinemia (WM) patients, and trigger NF-κB through BTK and IRAK. The BTK inhibitor ibrutinib is active in MYD88-mutated (MYD88 ^MUT ) WM patients, but shows lower activity in MYD88 wild-type (MYD88 ^WT ) disease. MYD88 ^WT patients also show shorter overall survival, and increased risk of disease transformation in some series. The genomic basis for these findings remains to be clarified. We performed whole exome and transcriptome sequencing of sorted tumor samples from 18 MYD88 ^WT patients and compared findings with WM patients with MYD88 ^MUT disease. We identified somatic mutation

SUBMITTER: Hunter ZR 

PROVIDER: S-EPMC6234368 | biostudies-literature | 2018 Nov

REPOSITORIES: biostudies-literature