T. Feys Archives - Page 15 of 17

From June 3^rd till June 6^th, Chicago again formed the background for the biggest cancer congress in the world. Notwithstanding the fact that solid tumours remain the main focus of the annual meeting of the American Society of Clinical Oncology (ASCO), the meeting program also included some interesting lectures on haematological malignancies. The aim of this report is not to discuss all these studies, but will address some of the key presentations on haematological cancer from ASCO 2016. For a more complete overview we would like to refer to the congress website, where all abstracts and a plethora of webcasts can be found.

(BELG J HEMATOL 2016;7(5):203–6)

Innovations in the management of thrombocytopaenia and thrombosis

BJH - volume 7, issue 4, september 2016

T. Feys MBA, MSc

Summary

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)

New advances in the treatment of haemophilia B

BJH - volume 7, issue 4, september 2016

T. Feys MBA, MSc

Summary

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 In these cases, FIX is no longer active, or is sometimes even eradicated.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)