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Marcel Nijland
dr.

I work as a hematologist and my main focus is on patients with aggressive B-cell lymphomas and CNS lymphomas. My research is centered on the application of novel diagnostic and therapeutic strategies into clinical trials. These include imaging-studies like 18F-FDG-PET, Zr-Brentuximab-PET and Zr-atezolizumab-PET. In addition, I aim to implement novel strategies to measure minimal residual disease, and prognostic gene expression profiles in DLBCL. Linked to this I also focus on mutational analysis to study clonal evolution and prognostic / predictive values of mutations. These studies are carried out in a close collaboration with HOVON and other departments in the UMCG.

Late relapses in diffuse large B-cell lymphoma: where to move next?
Published in: Leukemia & Lymphoma
Diagnostic performance of FDG-PET/CT of post-transplant lymphoproliferative disorder and factors affecting diagnostic yield
Published in: European Journal of Nuclear Medicine and Molecular Imaging
PURPOSE: Post-transplant lymphoproliferative disorder (PTLD) is a serious complication after solid organ and hematopoietic stem cell transplantation, requiring a timely and accurate diagnosis. In this study, we evaluated the diagnostic performance of FDG-PET/CT in patients with suspected PTLD and examined if lactate dehydrogenase (LDH) levels, Epstein-Barr virus (EBV) load, or timing of FDG-PET/CT relate to detection performance of FDG-PET/CT. METHODS: This retrospective study included 91 consecutive patients with clinical suspicion of PTLD and a total of 97 FDG-PET/CT scans within an 8-year period. Pathology reports and a 2-year...
MYD88 mutations identify a molecular subgroup of diffuse large B-cell lymphoma with an unfavorable prognosis
Published in: Haematologica
The 2016 World Health Organization classification defines diffuse large B-cell lymphoma (DLBCL) subtypes based on Epstein-Barr virus (EBV) infection and oncogenic rearrangements of MYC/BCL2/BCL6 as drivers of lymphomagenesis. A subset of DLBCL, however, is characterized by activating mutations in MYD88/CD79B. We investigated whether MYD88/CD79B mutations could improve the classification and prognostication of DLBCL. In 250 primary DLBCL, MYD88/CD79B mutations were identified by allele-specific polymerase chain reaction or next-generationsequencing, MYC/BCL2/BCL6 rearrangements were analyzed by fluorescence in situ hybridization, and EBV was studied by EBV-encoded RNA in situ hybridization. Associations...
Joost S. Vermaat, Sebastiaan F. Somers, Liesbeth C. de Wreede, Willem Kraan, Ruben A. L. de Groen, Anne M. R. Schrader, Emile D. Kerver, Cornelis G. Scheepstra, Henriette Berenschot, Wendy Deenik, Jurgen Wegman, Rianne Broers, Jan-Paul D. De Boer, Marcel Nijland, Tom van Wezel, Hendrik Veelken, Marcel Spaargaren, Arjen H. Cleven, Marie Jose Kersten, Steven T. Pals
WEE1 inhibition synergizes with CHOP chemotherapy and radiation therapy through induction of premature mitotic entry and DNA damage in diffuse large B-cell lymphoma
Published in: Therapeutic advances in hematology
Background: Diffuse large B-cell lymphoma (DLBCL) is a heterogeneous disease, characterized by high levels of genomic instability and the activation of DNA damage repair pathways. We previously found high expression of the cell cycle regulator WEE1 in DLBCL cell lines. Here, we investigated the combination of the WEE1 inhibitor, AZD1775, with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) and radiation therapy (RT), with the aim of improving first-line treatment. Methods: Cell viability experiments were performed to determine synergistic combinations. Levels of DNA damage were established using flow cytometry for...
Mathilde R. W. de Jong, Myra Langendonk, Bart Reitsma, Pien Herbers, Monique Lodewijk, Marcel Nijland, Anke van den Berg, Emanuele Ammatuna, Lydia Visser, Tom van Meerten
Heterogeneous Pattern of Dependence on Anti-Apoptotic BCL-2 Family Proteins upon CHOP Treatment in Diffuse Large B-Cell Lymphoma
Published in: International Journal of Molecular Sciences
Expression of the anti-apoptotic B-cell lymphoma 2 (BCL-2) protein in patients with diffuse large B-cell lymphoma (DLBCL) strongly correlates with resistance to standard therapy with cyclophosphamide, vincristine, doxorubicin, prednisolone, and rituximab (R-CHOP). Although studies focus mainly on the contribution of BCL-2, here we also investigate the contribution of other anti-apoptotic proteins to CHOP-therapy resistance in DLBCL. Functional dynamic BCL-2 homology (BH)3 profiling was applied to DLBCL cell lines upon CHOP treatment or single CHOP compounds. Cell-specific anti-apoptotic dependencies were validated with corresponding BH3-mimetics. We found high expression of...
Mathilde Rikje Willemijn de Jong, Myra Langendonk, Bart Reitsma, Marcel Nijland, Anke van den Berg, Emanuele Ammatuna, Lydia Visser, Tom van Meerten