A mutation in MYD88 (L265P) supports the survival of lymphoplasmacytic cells by activation of Bruton tyrosine kinase in Waldenström macroglobulinemia-Reference-Cited by-同舟云学术

A mutation in MYD88 (L265P) supports the survival of lymphoplasmacytic cells by activation of Bruton tyrosine kinase in Waldenström macroglobulinemia

Published:2013-08-15 Issue:7 Volume:122 Page:1222-1232
ISSN:0006-4971
Container-title:Blood
language:en
Short-container-title:

Author:

Yang Guang¹²,Zhou Yangsheng¹²,Liu Xia¹²,Xu Lian¹,Cao Yang¹²,Manning Robert J.¹,Patterson Christopher J.¹,Buhrlage Sara J.²³,Gray Nathanael²³,Tai Yu-Tzu²⁴,Anderson Kenneth C.²⁴,Hunter Zachary R.¹²,Treon Steven P.¹²

Affiliation:

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

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

3. Department of Cancer Biology, and

4. Jerome Lipper Center for Multiple Myeloma, Dana-Farber Cancer Institute, Boston, MA

Abstract

Key Points MYD88 L265P is a widely expressed somatic mutation in WM patients that supports NF-κB signaling through stimulation of BTK and IRAK 1/4. Combined suppression of BTK and IRAK in MYD88 L265P expressing WM cells promotes synergistic inhibition of NF-κB signaling and WM cell killing.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Link

http://ashpublications.org/blood/article-pdf/122/7/1222/1373442/1222.pdf

Reference32 articles.

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3. IGHV gene features and MYD88 L265P mutation separate the three marginal zone lymphoma entities and Waldenström macroglobulinemia/lymphoplasmacytic lymphomas.;Gachard;Leukemia,2013

4. MYD88 L265P in Waldenström macroglobulinemia, immunoglobulin M monoclonal gammopathy, and other B-cell lymphoproliferative disorders using conventional and quantitative allele-specific polymerase chain reaction.;Xu;Blood,2013

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