Detection of MYD88 and CXCR4 mutations in cell-free DNA of patients with IgM monoclonal gammopathies
Author:
Publisher
Springer Science and Business Media LLC
Subject
Oncology,Cancer Research,Hematology
Link
http://www.nature.com/articles/s41375-018-0197-7.pdf
Reference35 articles.
1. Treon SP, Xu L, Yang G, Zhou Y, Liu X, Cao Y, et al. MYD88 L265P somatic mutation in Waldenstrom′s macroglobulinemia. N Eng J Med. 2012;367:826–33.
2. Hunter ZR, Xu L, Yang G, Zhou Y, Liu X, Cao Y, et al. The genomic landscape of Waldenstrom macroglobulinemia is characterized by highly recurring MYD88 and WHIM-like CXCR4 mutations, and small somatic deletions associated with B-cell lymphomagenesis. Blood. 2014;123:1637–46.
3. Treon SP, Cao Y, Xu L, Yang G, Liu X, Hunter ZR. Somatic mutations in MYD88 and CXCR4 are determinants of clinical presentation and overall survival in Waldenstrom macroglobulinemia. Blood. 2014;123:2791–6.
4. Burnworth B, Wang Z, Singleton TP, Bennington A, Fritschle W, Bennington R, et al. Clone-specific MYD88 L265P and CXCR4 mutation status can provide clinical utility in suspected Waldenstrom macroglobulinemia/lymphoplasmacytic lymphoma. Leuk Res. 2016;51:41–8.
5. Abeykoon JP, Paludo J, King RL, Ansell SM, Gertz MA, LaPlant BR, et al. MYD88 mutation status does not impact overall survival in Waldenström macroglobulinemia. Am J Hematol. 2018 Feb;93(2):187-194.
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3. Clinical, biological, electrophysiological and therapeutic profile of patients with anti-MAG neuropathy according to MYD88L265P and CXCR4 mutations and underlying haemopathy;Journal of Neurology;2023-11-18
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