Articles

Practical management of chronic myeloid leukaemia in Belgium

BJH - volume 6, issue 1, march 2015

F. S. Benghiat MD, PhD, Y. Beguin MD, PhD, B. Dessars MD, PhD, T. Devos MD, PhD, P. Lewalle MD, PhD, P. Mineur MD, N. Straetmans MD, PhD, K. Van Eygen MD, G. Verhoef MD, PhD, L. Knoops MD, PhD

Summary

Imatinib has drastically changed the outcome of patients with chronic myeloid leukaemia, with the majority of them showing a normal life span. Recently, the development of second and third generation tyrosine kinase inhibitors and the possibility of treatment discontinuation made the management of these patients more challenging. In this review, practical management guidelines of chronic myeloid leukaemia are presented adapted to the Belgian situation in 2014. In first line chronic phase patients, imatinib, nilotinib and dasatinib can be prescribed. While second generation tyrosine kinase inhibitors give faster and deeper responses, their impact on long-term survival remain to be determined. The choice of the tyrosine kinase inhibitor depends on chronic myeloid leukaemia risk score, priority for a deep response to allow a treatment-free remission protocol, age, presence of comorbid conditions, side effect profile, drug interactions, compliance concerns and price. Monitoring the response has to be done according the 2013 European LeukemiaNet criteria, and is based on the bone-marrow cytogenetic response during the first months and on the blood molecular response. Molecular follow-up is sufficient in patients with a complete cytogenetic response. For patients who fail frontline therapy, nilotinib, dasatinib, bosutinib and ponatinib are an option depending on the type of intolerance or resistance. T315I patients are only sensitive to ponatinib, which has to be carefully handled due to cardiovascular toxicity. Advanced phase diseases are more difficult to handle, with treatments including allogeneic stem cell transplantation, which is also an option for patients failing at least two tyrosine kinase inhibitors. The possibility of treatment-free remission and pregnancy are also discussed.

(BELG J HEMATOL 2015;6(1): 16–32)

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P1.06 Bilateral Bell’s palsy leading to the diagnosis of chronic lymphocytic leukemia

BJH - volume 6, issue Abstract Book BHS, january 2015

C. Cornil , E. Collinge MD, G. Di Prinzio , A. Devresse , J-P. Defour PhD, P. Saussoy MD, PhD, L. Michaux MD, PhD, L. Knoops MD, PhD, M.C. Vekemans MD, A. Ferrant

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P3.11 Remitting seronegative symmetrical synovitis with pitting edema after allogeneic stem cell transplantation

BJH - volume 6, issue Abstract Book BHS, january 2015

A. Devresse , S. Daens , R. Lhommel , L. Knoops MD, PhD, D. Bauwens , E. Van den Neste MD, PhD, X. Poiré MD, PhD

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P2.03 Belgian Stop IMatinib trial

BJH - volume 6, issue Abstract Book BHS, january 2015

P. Mineur MD, C. Doyen MD, N. Straetmans MD, PhD, K. Van Eygen MD, D. Pranger MD, A. Bosly MD, PhD, M. André MD, PhD, T. Devos MD, PhD, L. Knoops MD, PhD

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P1.07 Unusual progression of a B-cell non-Hodgkin’s lymphoma

BJH - volume 6, issue Abstract Book BHS, january 2015

E. Collinge MD, A. vanden Daelen , L. Marot , A. Camboni MD, PhD, J-P. Defour PhD, P. Saussoy MD, PhD, L. Michaux MD, PhD, M.C. Vekemans MD, L. Knoops MD, PhD

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O.4 Functional characterization of activating mutants of the JAK3 tyrosine kinase implicated in tumoral transformation of T lymphocytes

BJH - volume 5, issue Abstract Book BHS, january 2014

E. Losdyck , L. Springuel , T. Hornakova , J.C. Renauld , L. Knoops MD, PhD

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P2.11 Activating JAK1 and JAK3 mutations cooperate to confer growth signal self-sufficiency and increased resistance to JAK inhibitors in a mouse in vitro leukemia model

BJH - volume 5, issue Abstract Book BHS, january 2014

L. Springuel , E. Losdyck , T. Hornakova , L. Knoops MD, PhD, J.C. Renauld

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