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Evaluating ibrutinib in the treatment of symptomatic Waldenstrom’s macroglobulinemia

Authors Papanota AM, Ntanasis-Stathopoulos I, Kastritis E, Dimopoulos MA, Gavriatopoulou M

Received 9 February 2019

Accepted for publication 6 August 2019

Published 27 August 2019 Volume 2019:10 Pages 291—300

DOI https://doi.org/10.2147/JBM.S183997

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Martin Bluth


Aristea-Maria Papanota,* Ioannis Ntanasis-Stathopoulos,* Efstathios Kastritis, Meletios A Dimopoulos, Maria Gavriatopoulou

Department of Clinical Therapeutics, National and Kapodistrian University of Athens, School of Medicine, Alexandra General Hospital, Athens, Greece

Correspondence: Maria Gavriatopoulou
Department of Clinical Therapeutics, National and Kapodistrian University of Athens, School of Medicine, Alexandra General Hospital, 80 Vas. Sofias Avenue, Athens 11528, Greece
Tel +30 213 216 2547
Fax +30 213 216 2511
Email mgavria@med.uoa.gr

*These authors contributed equally to this work

Abstract: Waldenstrom’s macroglobulinemia (WM) is a rare lymphoplasmacytic lymphoma with indolent course and prolonged disease course. The first-in-class Bruton’s tyrosine kinase inhibitor, ibrutinib, has shown significant activity and a distinct adverse event profile among both newly diagnosed and relapsed/refractory WM patients. Interestingly, clinical responses to ibrutinib have been shown to be dependent on patients’ MYD88 and CXCR4 mutational status. The recent outcomes of the Phase III iNNOVATE trial showed that the combination of ibrutinib with rituximab resulted in a significantly prolonged progression-free survival compared with rituximab monotherapy, which provides a novel therapeutic option in the clinical practice especially for the rituximab-refractory WM patients. However, the need for continuous drug administration along with the unique toxicity manifestations may render the patient management challenging. Furthermore, our understanding of the underlying resistant mechanisms to ibrutinib is currently being evolved.

Keywords: Waldenstrom’s macroglobulinemia, IgM, ibrutinib, Bruton’s tyrosine kinase

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