Guy Van Camp

University of Antwerp, Antwerpen, Flemish, Belgium

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Publications (324)1550.19 Total impact

  • Annals of Oncology 05/2015; 26(suppl 3):iii11-iii11. DOI:10.1093/annonc/mdv116.04
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    ABSTRACT: Introduction and aim Recently a new phenotypic and characteristic radiologic feature of DNA9 has been discovered in a series of 9 patients, all with the same PSIS COCH gene mutation. This study adds more patients to the series. Material and methods CT en MRI imaging of 14 patients who presented between 2007 and 2014 with otovestibular deterioration all caused by the same c.1S IC>T,p.ProS ISet (PSIS) missense mutation in the COCH gene, were analyzed. The mean patients' age at the time of investigation was 62 years, and 29% were female. Results Ninety-three percent of the patients had sclerotic lesions and/or narrowing in one or more semicircular canals on CT scan with a signal loss at corresponding areas on T2-weighted MR images. The posterior canals were affected in most cases (50%), compared with the superior (25%) and lateral canals (14%) or the vestibule (4%). Only 77% of the lesions on MR images were also visible on CT scans, suggesting a fibrotic process without calcification. As the disease progresses, patients get more lesions visible on imaging and more severe hearing loss. Median PTA in unaffected ears is 60 dB HL versus 100 dB HL in affected ears. Conclusions An extended retrospective analyses of CT and MRI imaging in patients with the same P51S mutation in the COCH gene, confirmed the recently discovered characteristic radiologic feature.
    Paper presented at The Annual Meeting of the Royal Belgian Society for Ear, Nose, Throat, Head and Neck Surgery, Brussels; 03/2015
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    ABSTRACT: The human BON-1 and QGP-1 cell lines are two frequently used models in pancreatic neuroendocrine tumor (PNET) research. Data on the whole exome genetic constitution of these cell lines is largely lacking. This study presents the first whole exome profile of the BON-1 and QGP-1 cell lines. Cell line identity was confirmed by short tandem repeat profiling. Using GTG-banding and CytoSNP-12v2 Beadchip array, cell line ploidy and chromosomal alterations were determined in BON-1 and QGP-1. The exome of both cell lines was sequenced on Ilumina's HiSeq next generation sequencing (NGS) platform. Single Nucleotide Variants (SNVs) and indels were called using the Genome Analysis ToolKit. SNVs were validated with Sanger sequencing. Ploidy of BON-1 and QGP-1 was 3 and 4 respectively, with long stretches of loss of heterozygosity across multiple chromosomes, which is associated with aggressive tumor behaviour. In BON-1, 57 frameshift indels and 1725 possible protein-altering SNVs were called in the NGS data. In the QGP-1 cell line, 56 frameshift indels and 1095 SNVs were identified. ATRX, a PNET-associated gene, was mutated in both cell lines, while TSC2 contained a mutation in BON-1. NRAS showed a mutation in BON-1, while KRAS was mutated in QGP-1, implicating aberrations in the RAS pathway in both cell lines. Homozygous mutations in TP53 with possible loss of function were identified in both cell lines. Various MUC genes, implicated in cell signaling, lubrication and chemical barriers, which are frequently expressed in PNET tissue samples, showed homozygous protein-altering SNVs in the BON-1 and QGP-1 cell line.
    Journal of Molecular Endocrinology 01/2015; DOI:10.1530/JME-14-0304
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    ABSTRACT: Glucocorticoids (GCs) selectively trigger cell death in the multiple myeloma cell line MM1S which express NR3C1/Glucocorticoid Receptor (GR) protein, but fail to kill MM1R cells which lack GR protein. Given recent demonstrations of altered microRNA profiles in a diverse range of haematological malignancies and drug resistance, we characterized GC inducible mRNA and microRNA transcription profiles in GC sensitive MM1S as compared to GC resistant MM1R cells. Transcriptome analysis revealed that GCs regulate expression of multiple genes involved in cell cycle control, cell organization, cell death and immunological disease in MM1S cells, which remain unaffected in MM1R cells. With respect to microRNAs, mir-150-5p was identified as the most time persistent GC regulated microRNA, out of 5 QPCR validated microRNAs (mir-26b, mir-125a-5p, mir-146-5p, mir-150-5p, and mir-184), which are GC inducible in MM1S but not in MM1R cells. Functional studies further revealed that ectopic transfection of a synthetic mir-150-5p mimics GR dependent gene expression changes involved in cell death and cell proliferation pathways. Remarkably, despite the gene expression changes observed, overexpression of mir-150-5p in absence of GCs did not trigger significant cytotoxicity in MM1S or MM1R cells. This suggests the requirement of additional steps in GC induced cell death, which can not be mimicked by mir-150-5p overexpression alone. Interestingly, a combination of mir-150-5p transfection with low doses GC in MM1S cells was found to sensitize therapy response, whereas opposite effects could be observed with a mir-150-5p specific antagomir. Although mir-150-5p overexpression did not substantially change GR expression levels, it was found that mir-150-5p evokes GR specific effects through indirect mRNA regulation of GR interacting transcription factors and hormone receptors, GR chaperones, as well as various effectors of unfolded protein stress and chemokine signalling. Altogether GC-inducible mir-150-5p adds another level of regulation to GC specific therapeutic responses in multiple myeloma.
    PLoS ONE 12/2014; 9(12):e113842. DOI:10.1371/journal.pone.0113842
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    ABSTRACT: The analytical methods which are often used for the determination of cocaine in complex biological matrices are a prescreening immunoassay and confirmation by chromatography combined with mass spectrometry. We suggest an ultra-high-pressure liquid chromatography combined with a potentiometric detector, as a fast and practical method to detect and quantify cocaine in biological samples. An adsorption/desorption model was used to investigate the usefulness of the potentiometric detector to determine cocaine in complex matrices. Detection limits of 6.3 ng mL−1 were obtained in plasma and urine, which is below the maximum residue limit (MRL) of 25 ng mL−1. A set of seven plasma samples and 10 urine samples were classified identically by both methods as exceeding the MRL or being inferior to it. The results obtained with the UPLC/potentiometric detection method were compared with the results obtained with the UPLC/MS method for samples spiked with varying cocaine concentrations. The intraclass correlation coefficient was 0.997 for serum (n =7) and 0.977 for urine (n =8). As liquid chromatography is an established technique, and as potentiometry is very simple and cost-effective in terms of equipment, we believe that this method is potentially easy, inexpensive, fast and reliable. Copyright © 2014 John Wiley & Sons, Ltd.
    Biomedical Chromatography 12/2014; 29(7). DOI:10.1002/bmc.3400
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    ABSTRACT: Anti-EGFR therapy in metastatic colorectal cancer (mCRC) has improved survival outcome. However, many patients do not respond to this therapy and almost all patients develop resistance after a few months of treatment. Since 2008, the therapy has been restricted to patients without mutations in KRAS, an important target in the EGFR pathway, as these patients do not benefit from anti-EGFR therapy. Recently, this has been changed to an all-RAS wild-type strategy. Despite these restrictions, still 40 to 60 % of mCRC patients are resistant. New biomarkers need to be identified in order to improve patient selection. Another problem is tumor heterogeneity, which impedes the detection of mutations in resistance genes and can consequently lead to wrong treatment decisions. A possible solution for this problem may be found in liquid biopsies. In this review, known and promising upcoming biomarkers associated with resistance to anti-EGFR therapy will be summarized. Moreover, the potential added value of liquid biopsies in patient selection and follow-up will be discussed.
    Current Colorectal Cancer Reports 12/2014; 10(4). DOI:10.1007/s11888-014-0242-5
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    ABSTRACT: In the present article, the utility of a special potentiometric titration approach for recognition and calculation of biomolecule/small molecule interactions is reported. This approach is fast, sensitive, reproducible and inexpensive in comparison to the other methods for the determination of the association constant values (Ka) and the interaction energies (ΔG). The potentiometric titration measurement is based on the use of a classical polymeric membrane indicator electrode in a solution of the small molecule ligand. The biomolecule is used as a titrant. The potential is measured versus a reference electrode and transformed to a concentration related signal over the entire concentration interval, also at low concentrations, where the mV (y-axis) versus logcanalyte (x-axis) potentiometric calibration curve is not linear. In the procedure, the Ka is calculated for the interaction of cocaine with a cocaine binding aptamer and with an anti-cocaine antibody. To study the selectivity and cross-reactivity, other oligonucleotides and aptamers are tested, as well as other small ligand molecules such as tetrakis (4-chlorophenyl)borate, metergoline, lidocaine, and bromhexine. The calculated Ka compared favorably to the value reported in the literature using SPR. The potentiometric titration approach called "Concentration related Response Potentiometry", is used to study molecular interaction for 7 macromolecular target molecules and 4 small molecule ligands.
    Analytical Chemistry 11/2014; DOI:10.1021/ac503385x
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    ABSTRACT: The MDM2 promoter SNP285C is located on the SNP309G allele. While SNP309G enhances Sp1 transcription factor binding and MDM2 transcription, SNP285C antagonizes Sp1 binding and reduces the risk of breast-, ovary- and endometrial cancer. Assessing SNP285 and 309 genotypes across 25 different ethnic populations (>10.000 individuals), the incidence of SNP285C was 6-8% across European populations except for Finns (1.2%) and Saami (0.3%). The incidence decreased towards the Middle-East and Eastern Russia, and SNP285C was absent among Han Chinese, Mongolians and African Americans. Interhaplotype variation analyses estimated SNP285C to have originated about 14,700 years ago (95% CI: 8,300 - 33,300). Both this estimate and the geographical distribution suggest SNP285C to have arisen after the separation between Caucasians and modern day East Asians (17,000 - 40,000 years ago). We observed a strong inverse correlation (r = -0.805; p < 0.001) between the percentage of SNP309G alleles harboring SNP285C and the MAF for SNP309G itself across different populations suggesting selection and environmental adaptation with respect to MDM2 expression in recent human evolution. In conclusion, we found SNP285C to be a pan-Caucasian variant. Ethnic variation regarding distribution of SNP285C needs to be taken into account when assessing the impact of MDM2 SNPs on cancer risk.
    Oncotarget 09/2014; 5(18):8223-34.
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    ABSTRACT: Unraveling the underlying mechanisms of cetuximab resistance in head and neck squamous cell carcinoma (HNSCC) is of major importance as many tumors remain non-responsive or become resistant. Our microarray results suggest that "resistant" cells still exhibit RAS-MAPK pathway signaling contributing to drug resistance, as witnessed by low expression of DUSP5 and DUSP6, negative regulators of ERK1/2, and increased expression of AURKB, a key regulator of mitosis. Therefore, interrupting the RAS-MAPK pathway by an ERK1/2 inhibitor (apigenin) or an AURKB inhibitor (barasertib) might be a new strategy for overcoming cetuximab resistance in HNSCC.
    Cancer Letters 09/2014; 354(2). DOI:10.1016/j.canlet.2014.08.039
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    ABSTRACT: We performed a genome-wide association study (GWAS) to identify the genes responsible for age-related hearing impairment (ARHI), the most common form of hearing impairment in the elderly. Analysis of common variants, with and without adjustment for stratification and environmental covariates, rare variants and interactions, as well as gene-set enrichment analysis, showed no variants with genome-wide significance. No evidence for replication of any previously reported genes was found. A study of the genetic architecture indicates for the first time that ARHI is highly polygenic in nature, with probably no major genes involved. The phenotype depends on the aggregated effect of a large number of SNPs, of which the individual effects are undetectable in a modestly powered GWAS. We estimated that 22% of the variance in our data set can be explained by the collective effect of all genotyped SNPs. A score analysis showed a modest enrichment in causative SNPs among the SNPs with a P-value below 0.01.European Journal of Human Genetics advance online publication, 18 June 2014; doi:10.1038/ejhg.2014.56.
    European journal of human genetics: EJHG 06/2014; DOI:10.1038/ejhg.2014.56
  • Annals of Oncology 05/2014; 25 Suppl 1:i15. DOI:10.1093/annonc/mdu066.27
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    ABSTRACT: Focal sclerosis of one or more semicircular canals on computed tomographic (CT) scans and a corresponding signal loss on magnetic resonance (MR) imaging are radiologic lesions that are linked to patients who are suffering from advanced otovestibular impairment caused by hereditary DFNA9 hearing loss. DFNA9 is a hereditary hearing loss that is characterized by late-onset progressive imbalance and hearing deterioration, caused by mutations in the COCH gene. To date, no radiologic lesions have been associated with this condition. A retrospective chart review SETTING: Tertiary referral center SUBJECTS: The radiologic data of 9 patients who presented between 2007 and 2012 with otovestibular deterioration caused by a mutation in the COCH gene were reviewed. All 9 subjects were carriers of the same c.151C > T, p.Pro51Ser (P51S) - missense mutation in the COCH gene. In 8 of them similar sclerotic lesions and/or narrowing were demonstrated in one or more semicircular canals on computed tomography CT scan, with a signal loss at corresponding areas on T2-weighted magnetic resonance (MR) images. In 1 patient, the posterior part of the vestibule was also affected. The posterior canals were affected in most cases (58%), compared with the superior (21%) and lateral canals (16%) or the vestibule (5%). Only 68.4% of the lesions on MR images were also visible on CT scans, suggesting a fibrotic process without calcification. Ears presenting radiologic lesions showed significantly more severe hearing loss (median PTA 104 dB HL) compared with unaffected ears (58 dB HL). Eight of 9 subjects with the same P51S mutation in the COCH gene showed similar radiologic lesions, affecting the PSCC in the majority of the cases. These radiologic abnormalities occurred in more advanced stages of the otovestibular deterioration, supporting the hypothesis that these lesions might represent the end phase of a low-grade chronic inflammation or protein deposition. A new phenotypic and characteristic radiologic feature of DFNA9 has been discovered.
    Otology & neurotology: official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology 03/2014; DOI:10.1097/MAO.0000000000000283
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    ABSTRACT: Otosclerosis is a frequent cause of hearing impairment characterized by abnormal resorption and deposition of bone in the human otic capsule. It is a disease of complex etiopathogenesis that is caused by both environmental and genetic factors. The goal of this study is to replicate association for genes that were previously reported to be associated with otosclerosis. However, in this study, patients were used in which the presence of otosclerotic foci was confirmed by histologic investigation, in contrast to previous studies, that did not use histologic confirmation. Case-control association study using 153 cases and 300 controls. Thirteen single nucleotide polymorphisms (SNPs) in 6 genes (COL1A1, TGFB1, BMP2, BMP4, AGT, and RELN) were genotyped. An association between TGFB1 (rs1800472) and otosclerosis was detected, confirming several previous reports. It is surprising that no association was found between RELN and otosclerosis because the current analysis had very reasonable power and the RELN association has been published before in different articles using several independent populations. Our findings strengthen the association of TGFB1 (rs1800472) with otosclerosis. The fact that other genes did not replicate could be due to different reasons like lack of power (BMP2 and BMP4) and possible false-positive initial association (COL1A1 and AGT). A plausible explanation for the lack of association for RELN is that RELN could be associated with a specific otosclerosis-like phenotype that is different from the histologically confirmed phenotype of the patients in this study, and that is clinically not distinguishable.
    Otology & neurotology: official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology 03/2014; DOI:10.1097/MAO.0000000000000334
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    ABSTRACT: Withaferin A (WA) isolated from Withania somnifera (Ashwagandha) has recently become an attractive phytochemical under investigation in various preclinical studies for treatment of different cancer types. In the present study, a comparative pathway-based transcriptome analysis was applied in epithelial-like MCF-7 and triple negative mesenchymal MDA-MB-231 breast cancer cells exposed to different concentrations of WA which can be detected systemically in in vivo experiments. Whereas WA treatment demonstrated attenuation of multiple cancer hallmarks, the withanolide analogue Withanone (WN) did not exert any of the described effects at comparable concentrations. Pathway enrichment analysis revealed that WA targets specific cancer processes related to cell death, cell cycle and proliferation, which could be functionally validated by flow cytometry and real-time cell proliferation assays. WA also strongly decreased MDA-MB-231 invasion as determined by single-cell collagen invasion assay. This was further supported by decreased gene expression of extracellular matrix-degrading proteases (uPA, PLAT, ADAM8), cell adhesion molecules (integrins, laminins), pro-inflammatory mediators of the metastasis-promoting tumor microenvironment (TNFSF12, IL6, ANGPTL2, CSF1R) and concomitant increased expression of the validated breast cancer metastasis suppressor gene (BRMS1). In line with the transcriptional changes, nanomolar concentrations of WA significantly decreased protein levels and corresponding activity of uPA in MDA-MB-231 cell supernatant, further supporting its anti-metastatic properties. Finally, hierarchical clustering analysis of 84 chromatin writer-reader-eraser enzymes revealed that WA treatment of invasive mesenchymal MDA-MB-231 cells reprogrammed their transcription levels more similarly towards the pattern observed in non-invasive MCF-7 cells. In conclusion, taking into account that sub-cytotoxic concentrations of WA target multiple metastatic effectors in therapy-resistant triple negative breast cancer, WA-based therapeutic strategies targeting the uPA pathway hold promise for further (pre)clinical development to defeat aggressive metastatic breast cancer.
    PLoS ONE 02/2014; 9(2):e87850. DOI:10.1371/journal.pone.0087850
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    ABSTRACT: Genetic variation in BMP2 and BMP4 found in otosclerosis patients result in altered Smad signaling. Otosclerosis is a common form of adult-onset conductive hearing loss resulting from abnormal bone remodeling of the bony labyrinth that surrounds the inner ear. Both genetic and environmental factors are implicated in the disease, yet very little is known about its pathogenesis. The evidence for a genetic component has been established through family-based linkage and population-based association studies. Previously, members of the TGF-β superfamily of genes have been associated with otosclerosis. Sequencing of BMP2 and BMP4 coding regions was performed to identify common and rare variation in German otosclerosis patients compared with controls. Functional analyses of rare variation in the patient cohort were conducted by exposing an osteosarcoma cell line to conditioned media containing either wild type or variant forms of BMP2 or BMP4 and analyzing Smad1/5/8 phosphorylation. Although no significant association with common variation in these 2 genes was detected, there were 8 singleton variants identified in the German population. Of the 4 coding variants found solely in otosclerosis patients, two-BMP4 and BMP2-were found to decrease Smad1/5/8 signaling. Rare variants in BMP2 and BMP4 are not a major genetic component in the otosclerosis population. However, those with functional affect showed decreased Smad signaling. Further analysis of Smad signaling molecules should be performed to determine if these pathways in combination are a major contributor to otosclerosis, which could lead to additional treatment options for otosclerosis patients.
    Otology & neurotology: official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology 01/2014; 35(3). DOI:10.1097/MAO.0000000000000244
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    ABSTRACT: Cell motility and invasion initiate metastasis. However, only a subpopulation of cancer cells within a tumor will ultimately become invasive. Due to this stochastic and transient nature, in an experimental setting, migrating and invading cells need to be isolated from the general population in order to study the gene expression profiles linked to these processes. This report describes microarray analysis on RNA derived from migrated or invaded subpopulations of triple negative breast cancer cells in a Transwell set-up, at two different time points during motility and invasion, pre-determined as "early" and "late" in real-time kinetic assessments. Invasion- and migration-related gene expression signatures were generated through comparison with non-invasive cells, remaining at the upper side of the Transwell membranes. Late-phase signatures of both invasion and migration indicated poor prognosis in a series of breast cancer data sets. Furthermore, evaluation of the genes constituting the prognostic invasion-related gene signature revealed Krüppel-like factor 9 (KLF9) as a putative suppressor of invasive growth in breast cancer. Next to loss in invasive vs non-invasive cell lines, KLF9 also showed significantly lower expression levels in the "early" invasive cell population, in several public expression data sets and in clinical breast cancer samples when compared to normal tissue. Overexpression of EGFP-KLF9 fusion protein significantly altered morphology and blocked invasion and growth of MDA-MB-231 cells in vitro. In addition, KLF9 expression correlated inversely with mitotic activity in clinical samples, indicating anti-proliferative effects.
  • 11th Annual ENETS Conference for the Diagnosis and Treatment of; 01/2014
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    ABSTRACT: The gray platelet syndrome is a hereditary, usually autosomal recessive bleeding disorder caused by a deficiency of alpha granules in platelets. We detected a nonsense mutation in the gene encoding the transcription factor GFI1B (growth factor independent 1B) that causes autosomal dominant gray platelet syndrome. Both gray platelets and megakaryocytes had abnormal marker expression. In addition, the megakaryocytes had dysplastic features, and they were abnormally distributed in the bone marrow. The GFI1B mutant protein inhibited nonmutant GFI1B transcriptional activity in a dominant-negative manner. Our studies show that GFI1B, in addition to being causally related to the gray platelet syndrome, is key to megakaryocyte and platelet development.
    New England Journal of Medicine 12/2013; 370(3). DOI:10.1056/NEJMoa1308130
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    ABSTRACT: The most successful binding kinetics analysis systems at this moment include surface plasmon resonance (SPR), quartz microcrystal balance (QMB) and surface acoustic wave (SAW). Although these are powerful methods, they generally are complex, expensive and require the use of monolayers. Here, we report on potentiometric sensors as an inexpensive and simple alternative to do binding kinetics analysis between small molecules in solution and biomolecules (covalently) attached in a biopolymer sensor coating layer. As an example, dopamine and an anti-dopamine aptamer were used as the small molecule and the biomolecule respectively. Binding between both follows a Langmuir adsorption type model and creates a surface potential. The system operates in Flow Injection Analysis mode (FIA). Besides being an interesting new binding kinetics tool, the approach allows systematic design of potentiometric biosensors (in the present study a dopamine sensor), and gives new insights into the functioning of ion-selective electrodes (ISE's).
    Biosensors & Bioelectronics 11/2013; 54C:515-520. DOI:10.1016/j.bios.2013.11.045
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    ABSTRACT: Two siblings, from a consanguineous Iraqi family, were investigated to identify the underlying genetic cause of their high myopia, esotropia, vitreous changes and cataract. Subsequent investigation identified low molecular weight proteinuria as part of their syndrome. Exome sequencing of one of the probands revealed a new non-synonymous variant in the LRP2 gene. Sanger sequencing confirmed the mutation and segregation in the family. No mutation was identified in COL9A1/2, COL11A1/2, or COL2A1 genes. The variant (c.11483A>G; p.Asp3828Gly), is predicted to be damaging and is conserved among vertebrate species. Mutations in LRP2 have been shown to cause the Donnai-Barrow syndrome or Facio-oculo-acoustico-renal (FOAR) syndrome, a syndrome associated with facial dysmorphism, ocular anomalies, sensorineural hearing loss, low molecular weight proteinuria, and diaphragmatic hernia and absent corpus callosum, although there is variability in the expression of some features. This family shows a milder phenotype with a predominant eye phenotype similar to the Stickler syndrome and only a few features of the Donnai-Barrow syndrome, including microglobulinuria. The presence of microglobulinuria was only detected after molecular results were known. In conclusion, with the identification of a new mutation in LRP2 associated with a predominant eye phenotype similar to the Stickler syndrome, we have broadened the phenotypic spectrum of LRP2 mutations.
    Clinical Genetics 08/2013; 86(3). DOI:10.1111/cge.12265

Publication Stats

9k Citations
1,550.19 Total Impact Points


  • 1989–2015
    • University of Antwerp
      • • Centre of Medical Genetics
      • • Department of medical genetics
      • • VIB Department of Molecular Genetics
      Antwerpen, Flemish, Belgium
  • 2013
    • University of Tuebingen
      Tübingen, Baden-Württemberg, Germany
  • 2010
    • Centre of Biotechnology of Sfax (CBS)
      Şafāqis, Şafāqis, Tunisia
  • 2009
    • University Medical Center Utrecht
      • Department of Otorhinolaryngology - Head and Neck Surgery
      Utrecht, Provincie Utrecht, Netherlands
    • University-Hospital of Padova
      Padua, Veneto, Italy
  • 2007
    • Cedars-Sinai Medical Center
      Los Ángeles, California, United States
  • 2006
    • Radboud University Nijmegen
      Nymegen, Gelderland, Netherlands
  • 1995–2006
    • Vrije Universiteit Brussel
      Bruxelles, Brussels Capital, Belgium
    • Maastricht University
      Maestricht, Limburg, Netherlands
  • 1995–2004
    • University of Iowa
      • Department of Otolaryngology-Head and Neck Surgery
      Iowa City, Iowa, United States
  • 2002–2003
    • Radboud University Medical Centre (Radboudumc)
      • Department of Human Genetics
      Nymegen, Gelderland, Netherlands
  • 2000–2002
    • Canisius-Wilhelmina Ziekenhuis
      Nymegen, Gelderland, Netherlands
  • 1998
    • The University of Manchester
      Manchester, England, United Kingdom
  • 1993
    • Johns Hopkins University
      Baltimore, Maryland, United States