CXCR4WHIM-like frameshift and nonsense mutations promote ibrutinib resistance but do not supplantMYD88L265P-directed survival signalling in Waldenström macroglobulinaemia cells

Author:

Cao Yang12,Hunter Zachary R.13,Liu Xia12,Xu Lian1,Yang Guang12,Chen Jie1,Tsakmaklis Nickolas1,Kanan Sandra1,Castillo Jorge J.12ORCID,Treon Steven P.12

Affiliation:

1. Bing Center for Waldenstrom's Macroglobulinemia; Dana Farber Cancer Institute; Boston MA USA

2. Department of Medicine; Harvard Medical School; Boston MA USA

3. Department of Pathology; Boston University Medical School; Boston MA USA

Funder

Leukemia and Lymphoma Society

Publisher

Wiley

Subject

Hematology

Reference20 articles.

1. Activation of TAK1 by MYD88 L265P drives malignant B-cell growth in non-Hodgkin lymphoma;Ansell;Blood Cancer Journal,2014

2. Regulation of CXCR4 signaling;Busillo;Biochimica Biophysica Acta,2007

3. Site-specific phosphorylation of CXCR4 is dynamically regulated by multiple kinases and results in differential modulation of CXCR4 signaling;Busillo;Journal of Biological Chemistry,2010

4. The WHIM-like CXCR4S338X somatic mutation activates AKT and ERK, and promotes resistance to ibrutinib and other agents used in the treatment of Waldenstrom's Macroglobulinemia;Cao;Leukemia,2014

5. Clinical and genetic features of Warts, Hypogammaglobulinemia, Infections and Myelokathexis (WHIM) syndrome;Dotta;Current Molecular Medicine,2011

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