MYD88 L265P mutations identify a prognostic gene expression signature and a pathway for targeted inhibition in CLL

Br J Haematol. 2019 Mar;184(6):925-936. doi: 10.1111/bjh.15714. Epub 2018 Dec 9.

Abstract

The L265P somatic mutation in the Myeloid Differentiation Primary Response 88 (MYD88) gene is a recurrent mutation in chronic lymphocytic leukaemia (CLL). This mutation has functional effects in various haematological malignancies but its role in CLL remains to be fully elucidated. Here, we report that MYD88 L265P mutations are associated with mutated immunoglobulin heavy-chain gene (IGHV-M) status and that among IGHV-M patients, the presence of MYD88 L265P is associated with younger age at diagnosis. Using microarray and RNA-Seq gene expression analysis, we further observe that the MYD88 L265P mutation is associated with a distinctive gene expression signature that predicts both failure-free survival and overall survival. This association was validated in an independent cohort of patients. To determine whether MYD88 L265P mutations can be therapeutically exploited in CLL, we treated primary cells with an inhibitor of interleukin 1 receptor-associated kinase 4 (IRAK4), a critical effector of the MYD88 pathway. IRAK4 inhibition decreased downstream nuclear factor-κB signalling and cell viability in CLL cells, indicating the potential of the MYD88 pathway as a therapeutic target in CLL.

Keywords: CLL; gene expression; prognostic factors; somatic mutation; therapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Cohort Studies
  • Cytokines / biosynthesis
  • Female
  • Genes, Immunoglobulin Heavy Chain
  • Humans
  • Interleukin-1 Receptor-Associated Kinases / antagonists & inhibitors
  • Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy
  • Leukemia, Lymphocytic, Chronic, B-Cell / genetics*
  • Leukemia, Lymphocytic, Chronic, B-Cell / metabolism
  • Male
  • Middle Aged
  • Molecular Targeted Therapy
  • Mutation
  • Myeloid Differentiation Factor 88 / genetics*
  • Myeloid Differentiation Factor 88 / metabolism
  • Prognosis
  • Signal Transduction
  • Transcriptome

Substances

  • Cytokines
  • MYD88 protein, human
  • Myeloid Differentiation Factor 88
  • IRAK4 protein, human
  • Interleukin-1 Receptor-Associated Kinases