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September 15, 2020Journal of Clinical OncologyOpen Access

Long-Term Follow-Up of Ibrutinib Monotherapy in Symptomatic, Previously Treated Patients With Waldenström Macroglobulinemia

Steven P. Treon Kirsten Meid Joshua Gustine Guang Yang Lian Xu Xia Liu Christopher J. Patterson Zachary R. Hunter Andrew R. Branagan Jacob P. Laubach Irene M. Ghobrial M. Lia Palomba Ranjana H. Advani Jorge J. Castillo

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Abstract

Ibrutinib is highly active and produces long-term disease control in previously treated patients with WM. Treatment is tolerable. Response depth, time to major response, and PFS are impacted by MYD88 and CXCR4 mutation status.

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Cite This Study

Treon et al. (2020) studied this question.

synapsesocial.com/papers/69d6ba7f8dca315383ed8af4 https://doi.org/10.1200/jco.20.00555

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Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

1MYD88 L265P Somatic Mutation in Waldenström's MacroglobulinemiaOriginal Research · 2012 · 1,294 citations
2The genomic landscape of Waldenström macroglobulinemia is characterized by highly recurring MYD88 and WHIM-like CXCR4 mutations, and small somatic deletions associated with B-cell lymphomagenesisOriginal Research · 2013 · 488 citations
3A mutation in MYD88 (L265P) supports the survival of lymphoplasmacytic cells by activation of Bruton tyrosine kinase in Waldenström macroglobulinemiaCase-Control Study · 2013 · 353 citations
4HCK is a survival determinant transactivated by mutated MYD88, and a direct target of ibrutinibOriginal Research · 2016 · 136 citations
5Somatic mutations in MYD88 and CXCR4 are determinants of clinical presentation and overall survival in Waldenström macroglobulinemiaOriginal Research · 2014 · 390 citations

More related papers

Genomic Landscape of <i>CXCR4</i> Mutations in Waldenström Macroglobulinemia2015
C1013G/CXCR4 acts as a driver mutation of tumor progression and modulator of drug resistance in lymphoplasmacytic lymphoma2014
<i><scp>CXCR</scp>4 </i><scp>WHIM</scp>‐like frameshift and nonsense mutations promote ibrutinib resistance but do not supplant <i><scp>MYD</scp>88</i><sup>L265P</sup>‐directed survival signalling in <scp>W</scp>aldenström macroglobulinaemia cells2014

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