BJH - volume 7, issue 4, september 2016
I. Moors MD
The state of the art in acute myeloid leukaemia (AML) in 2016 is changing dramatically. This is the result of the availability of new techniques for genome sequencing leading to understanding of the AML ontogeny at the molecular level, redefining minimal residual disease status in daily practice, the optimised use of induction and post-remission strategies and the introduction of many novel agents. Hopefully this will ultimately lead to the long expected improvement in survival for our individual patients.
(BELG J HEMATOL 2016;7(4):137–42)
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A. Janssens MD, PhD
(BELG J HEMATOL 2016;7(4):145–8)
Read moreBJH - volume 7, issue 4, september 2016
L. Zuurbier PhD
The standard of care is curative in the large majority of primary Hodgkin lymphoma (HL) patients and in approximately two-third of non-Hodgkin lymphoma (NHL) patients.1,2 Treatment strategies mainly consist of a combination of chemotherapy and radiotherapy.2 However, a substantial number of patients will develop relapsed or refractory (R/R) disease with poor prognosis. These patients often receive additional chemotherapy and stem cell transplantation (SCT).2 During the annual European Hematology association (EHA) conference, outcomes of various treatment regimes in lymphoma patients were discussed. In recent years, new agents for treatment of lymphoma were developed, including promising antibody-drug conjugates and inhibitors against programmed death 1 (PD-1) signalling. Results of clinical trials with these agents were presented at the EHA. Thus far, current treatment schemes are mainly dependent on clinical risk factors. Unfortunately, these treatment regimens coincide with many side-effects that affect the quality of life and morbidity of patients. To this end, personalised treatment needs further implementation and predictive and prognostic factors that can define patient-specific optimal therapies are therefore needed. These are currently under investigation and were also discussed at EHA 2016.
(BELG J HEMATOL 2016;7(4):151–7)
Read moreBJH - volume 7, issue 4, september 2016
K. Beel MD, PhD
(BELG J HEMATOL 2016;7(4):166–9)
Read moreBJH - volume 7, issue 4, september 2016
T. Feys MBA, MSc
Defects in the platelet haemostasis can lead to the development of thrombocytopaenia and thrombosis. During the 2016 annual meeting of the European Hematology Association (EHA) several presentations focussed on prognostic, clinical and biochemical aspects of these conditions. In addition to this, several new therapeutic options were discussed together with a study looking into cancer-associated thrombosis.
(BELG J HEMATOL 2016;7(4):170–3)
Read moreBJH - volume 7, issue 4, september 2016
T. Feys MBA, MSc
Haemophilia B is a genetic condition that is caused by a shortage in clotting factor IX (FIX). The severity of the haemophilia is determined by the clotting activity of FIX in the blood. The standard of care for patients with haemophilia B consists of substitution therapy with FIX. In this procedure, FIX, either prepared from human plasma or a recombinant form, is administered through an intravenous (IV) infusion with a frequency that depends on the severity of the haemophilia. These infusions are given once or twice a week and lay a heavy burden on patients. In addition to this, the presence of inhibitory antibodies in haemophilia patients can hamper the treatment. In these cases, FIX is no longer active, or is sometimes even eradicated. More recently, important advances have been made in the development of gene therapy for haemophilia B patients. With this technique, a non-mutated FIX gene is introduced into the DNA of patients using a viral vector that targets the hepatocytes of patients. As such, the missing clotting factor is reintroduced in patients allowing them to produce sufficient amounts of the clotting factor. During the 2016 annual EHA meeting, several haemophilia studies addressed this technique.
(BELG J HEMATOL 2016;7(4):174–5)
Read moreBJH - volume 7, issue 2, april 2016
A. Bosly MD, PhD
Overview of the ASH 2015 plenary scientific session held on Sunday, December 6th, 2015.
(BELG J HEMATOL 2016;7(2):90–2)
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