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S.F. De Meyer PhD

Articles

Gene therapy for von Willebrand Disease

BJH - volume 14, issue 8, december 2023

S. Vandelanotte MSc, B. Calcoen MD, C. Tersteeg PhD, K. VanHoorelbeke PhD, S.F. De Meyer PhD

SUMMARY

von Willebrand disease (VWD) is the most common inherited bleeding disorder, caused by mutations in the von Willebrand factor (VWF) gene. These mutations can affect the biosynthesis, secretion, function or clearance of VWF. As a result, quantitative or qualitative abnormalities of VWF lead to the bleeding phenotype found in VWD patients. Current management of VWD aims at correcting the bleeding phenotype via the use of supportive therapy, stimulating the release of endogenous VWF reserves and implementation of replacement strategies. Despite current treatment options, VWD patients experience a substantial negative impact on their overall health-related quality-of-life (HRQoL). Development of long-term approaches to manage VWD would not only avoid the current limitations of short-term therapies but could also significantly ameliorate the HRQoL of VWD patients. Gene therapy for VWD offers the potential of a long-term, if not lifelong, correction of VWF deficiency. During the last two decades, gene therapy for VWD has been studied via different strategies. The aim of this review is to give an overview of the different strategies and improvements that were investigated to develop a gene therapy for VWD.

(BELG J HEMATOL 2023;14(8):326–30)

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P30 VWF DEFICIENCY IS ASSOCIATED WITH RETICULOCYTOSIS AND INCREASED PARASITE ACCUMULATION IN EXPERIMENTAL MALARIA-ASSOCIATED ACUTE RESPIRATORY DISTRESS SYNDROME

BJH - 2019, issue ?, february 2019

S. Kraisin , S. Verhenne , T.-T. Pham , K. Martinod , I. Portier , N. VanDePutte , H. Deckmyn PhD, K. VanHoorelbeke PhD, P.E. Van Den Steen , S.F. De Meyer PhD

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P28 THE MECHANISM OF THE LOSS OF HMW VWF MULTIMERS AFTER LEFT VENTRICULAR ASSIST DEVICE IMPLANTATION IS DIFFERENT BETWEEN HUMANS AND SHEEP

BJH - 2019, issue ?, february 2019

S. Deconinck , A.-S. Schelpe , S. Jacobs , C. Nix , S. Barth , H.B. Feys PhD, N. VanDePutte , C. Tersteeg PhD, H. Deckmyn PhD, S.F. De Meyer PhD, B. Meyns , K. VanHoorelbeke PhD

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P27 VON WILLEBRAND FACTOR DEFICIENCY DOES NOT INFLUENCE ANGIOTENSIN I I-INDUCED ABDOMINAL AORTIC ANEURYSM FORMATION IN MICE

BJH - 2019, issue ?, february 2019

I. Portier , K. Martinod , L. Desender , N. VanDePutte , H. Deckmyn PhD, K. VanHoorelbeke PhD, S.F. De Meyer PhD

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P22 ANTI-CUB1 OR ANTI-SPACER ANTIBODIES THAT INCREASE ADAMTS13 ACTIVITY ACT BY ALLOSTERICALLY ENHANCING METALLOPROTEASE DOMAIN FUNCTION

BJH - 2019, issue ?, february 2019

A.-S. Schelpe , A. Petri , N. VanDePutte , H. Deckmyn PhD, S.F. De Meyer PhD, J.t.b. Crawley , K. VanHoorelbeke PhD

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P21 A NOVEL ADAMTS13 CONFORMATION ELISA SHOWS CONFORMATIONAL ACTIVATION OF RAT ADAMTS13 WITH EXPOSURE OF CRYPTIC EPITOPES IN VITRO

BJH - 2019, issue ?, february 2019

C. Dekimpe , L.c. VelÁsquez Pereira , J. Voorberg , H. Deckmyn PhD, S.F. De Meyer PhD, K. VanHoorelbeke PhD

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O07 THE VWF-GPIB INTERACTION MEDIATES THROMBO-INFLAMMATION IN EXPERIMENTAL STROKE VIA RECRUITMENT OF MONOCYTES, NEUTROPHILS AND T-CELLS TO THE BRAIN

BJH - 2019, issue ?, february 2019

F. Denorme , K. Martinod , A. Vandenbulcke , C.v. Denis , P.j. Lenting , H. Deckmyn PhD, K. VanHoorelbeke PhD, S.F. De Meyer PhD

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