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Amanda Kofides, BS
Zachary Hunter, Ph.D
Steven Treon, MD, Ph.D
Phil Brodsky, BS
Nick Tsakmaklis, BA
Kirsten Meid, BA, MPH
Jorge Castillo, MD
Christopher Patterson, MS, BASc
Shayna Sarosiek, MD
Margaret Kobs DNP, FNP-BC
Hannah Chory, FNP-BC
Nina Budano, CRC II
Julia Nguyen, CRC
Alexandra Eurell, RC II
Alberto Guijosa Ramirez, MD
Maria Luisa Guerrera, MD
Tarek Mouhieddine, MD
Camille V. Edwards, MBBS
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Pub-2019
Articles
Title
What is new in the treatment of Waldenstrom macroglobulinemia?
TP53 mutations are associated with mutated MYD88 and CXCR4, and confer an adverse outcome in Waldenstrom macroglobulinaemia
Progression Risk Stratification of Asymptomatic Waldenstrom Macroglobulinemia
Long survival in patients with Waldenstrom macroglobulinaemia diagnosed at a young age
Low risk of Pneumocystis jirovecii pneumonia and invasive aspergillosis in patients with Waldenstrom macroglobulinaemia on ibrutinib
Low levels of von Willebrand markers associate with high serum IgM levels and improve with response to therapy, in patients with Waldenstrom macroglobulinaemia
Consensus treatment recommendations from the tenth International Workshop for Waldenström Macroglobulinaemia
Ibrutinib for the treatment of Bing-Neel syndrome: A multicenter study
Human MYD88-L265P is insufficient by itself to drive neoplastic transformation in mature mouse B cells
How we manage Bing–Neel syndrome
Dual PAK4-NAMPT Inhibition Impacts Growth and Survival, and Increases Sensitivity to DNA-Damaging Agents in Waldenstrom Macroglobulinemia
CXCR4 mutations affect presentation and outcomes in patients with Waldenström macroglobulinemia: A systematic review
CXCR4 mutation subtypes impact response and survival outcomes in patients with Waldenstrom macroglobulinaemia treated with ibrutinib
CXCR4-S338X clonality is an important determinant of ibrutinib outcomes in patients with Waldenstr¨om macroglobulinemia
Cutaneous Eruptions from Ibrutinib Resembling EGFR Inhibitor-Induced Dermatologic Adverse Events
Correction: Resveratrol Exerts Antiproliferative Activity and Induces Apoptosis in Waldenstr€om Macroglobulinemia
Bruton’s Tyrosine Kinase Degradation as a Therapeutic Strategy for Cancer
TP53 mutations are associated with mutated MYD88 and CXCR4, and confer an adverse outcome in Waldenström macroglobulinaemia
Dual PAK4-NAMPT Inhibition Impacts Growth and Survival, and Increases Sensitivity to DNA-Damaging Agents in Waldenström Macroglobulinemia
Long survival in patients with Waldenström macroglobulinaemia diagnosed at a young age
Low risk of Pneumocystis jirovecii pneumonia and invasive aspergillosis in patients with Waldenström macroglobulinaemia on ibrutinib
Bruton tyrosine kinase degradation as a therapeutic strategy for cancer
Ibrutinib for the treatment of Bing-Neel syndrome: a multicenter study
Progression Risk Stratification of Asymptomatic Waldenström Macroglobulinemia