Articles

Venetoclax-Azacitidine, the new standard of care for AML patients unfit for intensive treatment: A guide for clinical practice

BJH - volume 14, issue 2, march 2023

I. Moors MD, D. Deeren , C. Jacquy MD, PhD, A. Jaspers MD, PhD, T. Kerre MD, PhD, V. Havelange MD, PhD, D. Selleslag MD, C. Spilleboudt MD, N. Straetmans MD, PhD, F. Van Obbergh MD, A. De Voeght MD, S. Anguille MD, PhD, A. Schauwvlieghe MD, PhD, N. De Beule MD, PhD, A. De Becker MD, D. Breems MD, PhD

SUMMARY

Acute myeloid leukaemia is an aggressive form of bone marrow cancer with poor prognosis, especially in elderly, unfit patients. The VIALE-A study showed an impressive improvement in complete remission rate and overall survival with the addition of venetoclax, a BCL-2 inhibitor, to azacitidine. This combination therapy is now reimbursed in Belgium for newly diagnosed adult AML patients who are considered unfit for intensive chemotherapy based on age and/or comorbidities. In this article, we provide recommendations on the use of this new combination, as well as on prophylaxis and management of specific side effects.

(BELG J HEMATOL 2023;14(2):59–66)

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The clinical relevance of calreticulin mutations in myeloproliferative neoplasms

BJH - volume 13, issue 8, december 2022

V. Havelange MD, PhD, S.N. Constantinescu MD, PhD

SUMMARY

Calreticulin mutations are driver mutations detected in around 20–25% of essential thrombocythemia and in 25–30% of primary myelofibrosis patients. The most recurrent mutations are type-1 (a deletion of 52 bp in the exon 9) and type-2 (an insertion of 5 bp in the exon 9). This review describes the distinct clinical features, prognosis and outcome of calreticulin mutated patients from JAK2V617F or MPL (thrombopoietin receptor) mutated patients. The subtypes of calreticulin mutations were also associated with distinct clinical characteristics. Several treatment guidelines were adapted for calreticulin-mutated patients. The mechanism by why the three driver mutations, which all activate JAK/STAT signalling pathway can trigger diseases with quite different features is still not known. The recent progress in the understanding of calreticulin mutation biology will allow the development of new target therapies with the hope to cure the disease in the next years.

(BELG J HEMATOL 2022;13(8):293–301)

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P27 Role of FOXO1 mutations in the development of diffuse large B-cell lymphoma

BJH - 2018, issue Abstract Book BHS, february 2018

E. Bollaert , A. Velghe , G. Dachy , V. Havelange MD, PhD, J.B. Demoulin

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P16 Preleukemic phase of chronic myeloid leukemia presenting with an isolated peripheral basocytosis

BJH - 2018, issue Abstract Book BHS, february 2018

F. Dall’Armellina , Y. Berners , L. Maindiaux , A. Capes , J-P. Defour PhD, P. Saussoy MD, PhD, V. Havelange MD, PhD, M-C. Vekemans MD

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P79 Atypical bone pain after allogeneic bone marrow transplantation for myelofibrosis

BJH - volume 8, issue Abstract Book BHS, february 2017

G. Verstraete , S. Lefevre , S. Bailly MD, G. Di Prinzio , J. Devreux , J-P. Defour PhD, P. D’Abadie , P. Van Eeckhout , F. Kino , C. Goemare , N. Lepage , L. Michaux MD, PhD, V. Havelange MD, PhD, E. Van den Neste MD, PhD, C. Lambert MD, L. Knoops MD, PhD, M-C. Vekemans MD, X. Poiré MD, PhD

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PP31 Roles of microRNAs in myeloid malignancies driven by activated tyrosine kinases

BJH - volume 8, issue Abstract Book BHS, february 2017

M. Claus , A. Essaghir , P. Saussoy MD, PhD, L. Michaux MD, PhD, J.B. Demoulin , V. Havelange MD, PhD

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P38 Coexistence of inversion (16) et Bcr-Abl rearrangement in acute myeloid leulemia: a clinical description

BJH - volume 8, issue Abstract Book BHS, february 2017

J. Devreux , G. Di Prinzio , S. Bailly MD, S. Lefebvre , G. Verstraete , K. van Renterghem , A. Charlot , P. Saussoy MD, PhD, J-P. Defour PhD, N. Straetmans MD, PhD, X. Poiré MD, PhD, L. Michaux MD, PhD, M-C. Vekemans MD, V. Havelange MD, PhD

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