Nadine Van Roy

ORCID: 0000-0003-0247-2223
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About
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Research Areas
  • Neuroblastoma Research and Treatments
  • Cancer Genomics and Diagnostics
  • Genomic variations and chromosomal abnormalities
  • Acute Myeloid Leukemia Research
  • Cancer, Hypoxia, and Metabolism
  • Acute Lymphoblastic Leukemia research
  • RNA modifications and cancer
  • Lung Cancer Research Studies
  • Sarcoma Diagnosis and Treatment
  • Microtubule and mitosis dynamics
  • Chronic Lymphocytic Leukemia Research
  • Chronic Myeloid Leukemia Treatments
  • Chromosomal and Genetic Variations
  • Epigenetics and DNA Methylation
  • Genetic factors in colorectal cancer
  • Cancer-related molecular mechanisms research
  • Cancer therapeutics and mechanisms
  • Glioma Diagnosis and Treatment
  • Prenatal Screening and Diagnostics
  • Virus-based gene therapy research
  • Protein Degradation and Inhibitors
  • Neuroendocrine Tumor Research Advances
  • Lymphoma Diagnosis and Treatment
  • Chromatin Remodeling and Cancer
  • MicroRNA in disease regulation

Ghent University Hospital
2016-2025

Cancer Research Institute Ghent
2015-2024

Ghent University
2014-2024

VIB-UGent Center for Medical Biotechnology
2024

AZ Sint-Jan
2007-2023

Cancer Research Institute
2023

Rode Kruis-Vlaanderen
2021

European Organisation for Research and Treatment of Cancer
2015

Institute of Pathology and Genetics
2014

St Anna Children's Hospital
2003-2011

Jan Van Deun Pieter Mestdagh Patrizia Agostinis Özden Akay Sushma Anand and 90 more Jasper Anckaert Zoraida Andreu Martínez Tine Baetens Els Beghein Laurence Bertier Geert Berx Janneke Boere Stephanie Boukouris Michel Bremer Dominik Buschmann James Brian Byrd Clara Casert Lesley Cheng Anna Cmoch Delphine Daveloose Eva De Smedt Şeyma Demirsoy Victoria Depoorter Bert Dhondt Tom A. P. Driedonks Aleksandra M. Dudek Abdou ElSharawy Ilaria Floris Andrew D. Foers Kathrin Gärtner Abhishek D. Garg Edward Geeurickx Jan Gettemans Farzaneh Ghazavi Bernd Giebel Tom Groot Kormelink Grace Hancock Hetty Helsmoortel Andrew F. Hill Vincent Hyenne Hina Kalra David Kim Joanna Kowal Sandra Kraemer Petra Leidinger Carina Leonelli Yaxuan Liang Lien Lippens Shu Liu Alessandra Lo Cicero Shaun Martin Suresh Mathivanan Prabhu Mathiyalagan Tamás Matusek Gloria Milani Marta Tortajada Liselot Mus Dillon C. Muth Andrea H. Németh Esther N. M. Nolte‐‘t Hoen Lorraine O’Driscoll Roberta Palmulli Michael W. Pfaffl Bjarke Primdal-Bengtson Erminia Romano Quentin Rousseau Susmita Sahoo Natália G. Sampaio Monisha Samuel Benjamin J. Scicluna Bieke Soen Anneleen Steels Johannes V. Swinnen Maarit Takatalo Safia Thaminy Clotilde Théry Joeri Tulkens Isabel Van Audenhove Susanne van der Grein Alan Van Goethem Martijn J. C. van Herwijnen Guillaume van Niel Nadine Van Roy Alexander R. van Vliet Niels Vandamme Suzanne Vanhauwaert Glenn Vergauwen Frederik J. Verweij Annelynn Wallaert Marca H. M. Wauben Kenneth W. Witwer Marijke I. Zonneveld Olivier De Wever Jo Vandesompele An Hendrix

10.1038/nmeth.4185 article EN Nature Methods 2017-02-28

Gain of genetic material from chromosome arm 17q (gain segment 17q21–qter) is the most frequent cytogenetic abnormality neuroblastoma cells. This gain has been associated with advanced disease, patients who are ≥1 year old, deletion 1p, and amplification N-myc oncogene, all which predict an adverse outcome. We investigated these associations evaluated prognostic importance status 17.

10.1056/nejm199906243402504 article EN New England Journal of Medicine 1999-06-24

The HEK293 human cell lineage is widely used in biology and biotechnology. Here we use whole-genome resequencing of six 293 lines to study the dynamics this aneuploid genome response manipulations generate common derivatives, such as transformation stable clone generation (293T); suspension growth adaptation (293S); cytotoxic lectin selection (293SG). Remarkably, observe that copy number alteration detection could identify genomic region enabled survival under selective conditions (i.c....

10.1038/ncomms5767 article EN cc-by-nc-nd Nature Communications 2014-09-03

Neurofibromatosis type 1 (NF1) is one of the most common autosomal dominant disorders and caused by mutations in NF1 gene. Mutation detection complex due to large size gene, presence pseudogenes great variety possible lesions. Although there no evidence for locus heterogeneity NF1, mutation rates rarely exceed 50%. We studied 67 unrelated patients fulfilling NIH diagnostic criteria, 29 familial 38 sporadic cases, using a cascade complementary techniques. performed protein truncation test...

10.1002/1098-1004(200006)15:6<541::aid-humu6>3.0.co;2-n article EN Human Mutation 2000-01-01

10.1038/nmeth.2697 article EN Nature Methods 2013-10-30
Sushree Sangita Sahoo Victor B. Pastor Charnise Goodings Rebecca Voss Emilia J. Kozyra and 91 more Amina Szvetnik Peter Noellke Michael Dworzak Jan Starý Franco Locatelli Riccardo Masetti Markus Schmugge Barbara De Moerloose Albert Catalá Krisztián Kállay Dominik Turkiewicz Henrik Hasle Jochen Buechner Kirsi Jahnukainen Marek Ussowicz Sophia Polychronopoulou Owen P. Smith Oksana Fabri Shlomit Barzilai Valérie de Haas Irith Baumann Stephan Schwarz‐Furlan Jan Starý Barbara De Moerloose Krisztián Kállay Owen P. Smith Valérie de Haas Gudrun Göhring Charlotte M. Niemeyer Karin Nebral Ingrid Simonitsch-Kluppp Pascale De Paepe Nadine Van Roy Vít Campr Zuzana Zemanová Erik Clasen‐Linde Tine Plesner Brigitte Schlegelberger Martina Rudelius Kalliopi N. Manola Kalliopi Stefanaki Judit Csomor Hajnalka Andrikovics David R. Betts Maureen J. O’Sullivan Yaniv Zohar Marta Jeison Rita De Vito Francesco Pasquali Jadwiga Małdyk Olga Haus Helena Alaiz Paula Kjöllerström Luís Mascarenhas‐Lemos Ivana Boďová Martin Čermák Lukáš Plank Barbara Gazić Marko Kavčič Helena Podgornik Margarita Llavador Ros José Cervera Carole Gengler Joëlle Tchinda Berna Beverloo Roos J. Leguit Marena R. Niewisch Martin G. Sauer Birgit Burkhardt Peter Lang Peter Bader Rita Beier Ingo Müller Michael H. Albert Roland Meisel Ansgar Schulz Gunnar Cario Pritam Kumar Panda Julius Wehrle Shinsuke Hirabayashi Marta Derecka Robert Durruthy-Durruthy Gudrun Göhring Ayami Yoshimi‐Noellke Manching Ku Dirk Lebrecht Miriam Erlacher Christian Flotho Brigitte Strahm Charlotte M. Niemeyer Marcin W. Włodarski

10.1038/s41591-021-01511-6 article EN Nature Medicine 2021-10-01

Purpose Neuroblastoma is a genetically heterogeneous pediatric tumor with remarkably variable clinical behavior ranging from widely disseminated disease to spontaneous regression. In this study, we aimed for comprehensive genetic subgroup discovery and assessment of independent prognostic markers based on genome-wide aberrations detected by comparative genomic hybridization (CGH). Materials Methods Published CGH data 231 primary untreated neuroblastomas were converted digitized format...

10.1200/jco.2005.06.104 article EN Journal of Clinical Oncology 2005-03-30

Purpose: Neuroblastoma (NB) is a heterogeneous disease characterized by distinct clinical features and the presence of typical copy-number alterations (CNAs). Given strong association these CNA profiles with prognosis, analysis profile at diagnosis mandatory. Therefore, we tested whether circulating cell-free DNA (cfDNA) present in plasma samples patients NB could offer valuable alternative to primary tumor for profiling.Experimental Design: In 37 NB, cfDNA using shallow whole genome...

10.1158/1078-0432.ccr-17-0675 article EN Clinical Cancer Research 2017-07-15

The classification of the until recently poorly explored group atypical adipocytic neoplasms with spindle cell features, for which term lipomatous tumor (ASLT) has been proposed, remains challenging. Recent studies have proposed ASLT as a unique entity (in at least significant subset cases) specific genetic background, namely deletions/losses 13q14, including RB1 and its flanking genes RCBTB2, DLEU1, ITM2B. Similar aberrations reported in pleomorphic liposarcomas (PLSs). This prompted us to...

10.1097/pas.0000000000000936 article EN The American Journal of Surgical Pathology 2017-09-06

Double minutes (dmin), homogeneously staining regions, and ring chromosomes are vehicles of gene amplification in cancer. The underlying mechanism leading to their formation as well structure function acute myeloid leukemia (AML) remain mysterious. We combined a range high-resolution genomic methods investigate the architecture expression pattern amplicons involving chromosome band 8q24 23 cases AML (AML-amp). This revealed that different MYC-dmin architectures can coexist within same...

10.1038/s41375-018-0033-0 article EN cc-by-nc-nd Leukemia 2018-02-21

Abstract We report on the finding of a t(1;17) in two primary neuroblastomas. Subsequent fluorescence situ hybridization (FISH) analysis revealed presence 1; 17 transfocations four out nine neuroblastoma cell lines. The chromosome 1 short arm breakpoints were determined using region‐specific probes. FISH screening also demonstrated or confirmed 11;17 translocations three lines and other rearrangements those that did not carry t(1; 17) t(11; 17). Our data extend previous cytogenetic findings...

10.1002/gcc.2870100205 article EN Genes Chromosomes and Cancer 1994-06-01

Partial and complete genome duplications occurred during evolution resulted in the creation of new genes gene families. We identified a novel intricate human family located primarily regions segmental on chromosome 1. named it NBPF, for neuroblastoma breakpoint family, because one its members is disrupted by chromosomal translocation patient. The NBPF have repetitive structure with high intragenic intergenic sequence similarity both coding noncoding regions. These similarities might expose...

10.1093/molbev/msi222 article EN Molecular Biology and Evolution 2005-08-03

Double minutes (dmin)-circular, extra-chromosomal amplifications of specific acentric DNA fragments-are relatively frequent in malignant disorders, particularly solid tumors. In acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS), dmin are observed approximately 1% the cases. Most them consist an amplified segment from chromosome band 8q24, always including MYC gene. Besides this information, little is known about their internal structure. We have characterized detail genomic...

10.1093/hmg/ddl010 article EN Human Molecular Genetics 2006-02-01

Comparative genomic hybridization (CGH) analysis was performed on 36 neuroblastomas of both low and high stage disease. This study significantly increases the number neuroblastoma tumors studied by CGH. Analysis larger series is particularly important in view different clinical subgroups that are recognized for this tumor. The present data a comparison with all published CGH provide further insights into genetic heterogeneity neuroblastoma. Stage 1, 2, 4S showed predominantly whole...

10.1002/(sici)1098-2264(199810)23:2<141::aid-gcc7>3.0.co;2-2 article EN Genes Chromosomes and Cancer 1998-10-01
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