Somatic mutations in MYD88 and CXCR4 are determinants of clinical presentation and overall survival in Waldenström macroglobulinemia

Author:

Treon Steven P.12,Cao Yang12,Xu Lian12,Yang Guang12,Liu Xia12,Hunter Zachary R.13

Affiliation:

1. Bing Center for Waldenström's Macroglobulinemia, Dana-Farber Cancer Institute, Boston, MA;

2. Department of Medicine, Harvard Medical School, Boston, MA; and

3. Department of Pathology, Boston University School of Graduate Medical Sciences, Boston, MA

Abstract

Key Points Activating MYD88 as well as nonsense and frameshift WHIM-like CXCR4 somatic mutations are common in WM. CXCR4 NS mutations are present in aggressive cases including hyperviscosity syndrome, and MYD88 status is a determinant of survival.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Reference22 articles.

1. How I treat Waldenström macroglobulinemia.;Treon;Blood,2009

2. MYD88 L265P somatic mutation in Waldenström’s macroglobulinemia.;Treon;N Engl J Med,2012

3. The genomic landscape of Waldenstöm’s Macroglobulinemia is characterized by highly recurring MYD88 and WHIM-like CXCR4 mutations, and small somatic deletions associated with B-cell lymphomagenesis [published online ahead of print December 23, 2013].;Hunter;Blood

4. Regulation of CXCR4 signaling.;Busillo;Biochim Biophys Acta,2007

5. Site-specific phosphorylation of CXCR4 is dynamically regulated by multiple kinases and results in differential modulation of CXCR4 signaling.;Busillo;J Biol Chem,2010

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