Guy Van Camp

University of Antwerp, Antwerpen, Flanders, Belgium

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Publications (316)1538.93 Total impact

  • [Show abstract] [Hide abstract]
    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; · 1.95 Impact Factor
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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).
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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;
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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. · 6.64 Impact Factor
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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;
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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; · 3.56 Impact Factor
  • Annals of Oncology 05/2014; 25 Suppl 1:i15. · 7.38 Impact Factor
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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; · 1.44 Impact Factor
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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; · 1.44 Impact Factor
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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; · 1.44 Impact Factor
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    Oncoscience. 01/2014; 1(1):69.
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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 01/2014; 9(2):e87850. · 3.53 Impact Factor
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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 01/2014; 9(12):e113842. · 3.53 Impact Factor
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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; · 54.42 Impact Factor
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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. · 6.45 Impact Factor
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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; · 4.25 Impact Factor
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    Manou Sommen, Guy van Camp, An Boudewyns
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    ABSTRACT: Once a diagnosis of unilateral or bilateral congenital hearing loss is established in an infant by age-specific auditory testing, a search for an underlying aetiological diagnosis is required. A rational and cost-efficient aetiological work-up requires a basic knowledge about risk factors and the most common reasons for congenital hearing loss. Both genetic and environmental factors each account for about half of the causes. Among the environmental factors, perinatal insults and congenital infections, especially congenital cytomegalovirus infection, should be considered. Imaging is required to exclude structural inner ear anomalies that may occur as an isolated entity, be part of a syndrome and/or may have therapeutic implications when a surgical intervention for the hearing loss by means of cochlear implantation is envisaged. Genetic testing is an integral part of the aetiological work-up. Although more than 47 causative genes have been identified for the non-syndromic forms of hearing loss alone, diagnostic application of the scientific progress has lagged behind, because screening all the known causative genes for hearing loss in one patient with current technology would be extremely expensive. Consequently, current routine DNA diagnostic testing for non-syndromic hearing loss is restricted to one or two of the most common causative genes, which identifies the responsible gene in only 10–20% of cases. However, on the basis of audiometric information (frequencies affected, thresholds), age of onset, imaging results or other clinical information, specific genes should be analysed. The aims of the present paper are to propose a rational and scientifically valid diagnostic strategy for an aetiological work-up of congenital hearing loss including an overview of the current DNA diagnostics as well as a brief look into the future.
    Hearing, Balance and Communication. 08/2013; 11(3).
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    ABSTRACT: OBJECTIVE: To investigate the familial correlations and intraclass correlation of age-related hearing impairment (ARHI) in specific frequencies. In addition, heritability estimates were calculated. STUDY DESIGN: Multicenter survey in 8 European centers. SUBJECTS: One hundred ninety-eight families consisting of 952 family members, screened by otologic examination and structured interviews. Subjects with general conditions, known to affect hearing thresholds or known otologic cause were excluded from the study. RESULTS: We detected familial correlation coefficients of 0.36, 0.37, 0.36, and 0.30 for 0.25, 0.5, 1, and 2 kHz, respectively, and correlation coefficients of 0.20 and 0.18 for 4 and 8 kHz, respectively. Variance components analyses showed that the proportion of the total variance attributable to family differences was between 0.32 and 0.40 for 0.25, 0.5, 1, and 2 kHz and below 0.20 for 4 and 8 kHz. When testing for homogeneity between sib pair types, we observed a larger familial correlation between female than male subjects. Heritability estimates ranged between 0.79 and 0.36 across the frequencies. DISCUSSION: Our results indicate that there is a substantial shared familial effect in ARHI. We found that familial aggregation of ARHI is markedly higher in the low frequencies and that there is a trend toward higher familial aggregation in female compared with male subjects.
    Otology & neurotology: official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology 06/2013; · 1.44 Impact Factor
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    ABSTRACT: Observation of a potentiometric sensor's response behaviour after injection in flow injection analysis at different concentrations allowed studying "on" and "off" kinetics of the analyte's adsorption/diffusion behaviour. The alkaloid metergoline was mostly used as an example. kon and koff rate constant values were measured, and the association constant Kass, and ΔG values of the analyte-surface interaction were calculated with an adsorption-based model which proved to be fully applicable. kon increased by decreasing the sensor dimensions, while koff was unaffected by miniaturization. Increasing acetonitrile concentrations in the running buffer increased koff, while kon was unaffected. The experimentally determined ΔG values of the analyte-surface interaction showed a linear relation to the response of the sensor, in mV. This knowledge was applied to optimize the potentiometric detection of plant alkaloids in (U)HPLC. Sub-micromolar detection limits were obtained with the potentiometric detector/(U)HPLC combination. This is the first time that the response rates and the response itself can be modelled accurately for coated wire potentiometric sensors, and it is the first application of a potentiometric detector in UPLC.
    Analytica chimica acta 05/2013; 777:25-31. · 4.31 Impact Factor
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    ABSTRACT: Recently, mutations in the SMAD3 gene were found to cause a new autosomal dominant aneurysm condition similar to Loeys-Dietz syndrome (LDS), mostly with osteoarthritis, called aneurysms-osteoarthritis syndrome (AOS). Our 3-year-old propositus underwent correction of an inguinal hernia at 3 months and substitution of the ascending aorta for pathologic dilation at 12 months of age. Family history reveals aortic dilation in his mother at 30 years, death due to aortic dissection of an 18-year-old maternal aunt, surgical replacement of the ascending aorta because of aneurysm in a maternal uncle at 19 years, postpartum death of the maternal grandmother at 24 years and surgical intervention because of thoracic aortic aneurysm in a brother of the propositus' grandmother at 54 years. The affected individuals present with several other signs of connective tissue disease, but the two adult patients evaluated revealed no radiologic evidence of osteoarthritis. Molecular testing of the TGFBR1 and TGFBR2 genes, involved in LDS, resulted negative, but analysis of SMAD3 disclosed the novel heterozygous loss-of-function mutation c.1170_1179del (p.Ser391AlafsX7) in exon 9 in all affected family members, confirming the diagnosis of AOS. SMAD3 mutations should be considered in patients of all ages with LDS-like phenotypes and negative TGFBR1/2 molecular tests, especially in the presence of aortic root or ascending aortic aneurysms, even though signs of early onset osteoarthritis are absent. © 2013 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part A 03/2013; · 2.30 Impact Factor

Publication Stats

7k Citations
1,538.93 Total Impact Points


  • 1989–2014
    • University of Antwerp
      • • Centre of Medical Genetics
      • • Medische Genetica (MEDGEN)
      • • VIB Department of Molecular Genetics
      Antwerpen, Flanders, Belgium
  • 2012
    • University of Sfax
      • Faculty of Medicine of Sfax
      Şafāqis, Şafāqis, Tunisia
  • 2010–2012
    • Universidad Peruana Cayetano Heredia
      • Instituto de Medicina Tropical Alexander von Humboldt
      Lima, LMA, Peru
    • Centre of Biotechnology of Sfax (CBS)
      Şafāqis, Şafāqis, Tunisia
  • 2009
    • University-Hospital of Padova
      Padua, Veneto, Italy
    • House Research Institute
      Los Angeles, California, United States
    • University Medical Center Utrecht
      • Department of Otorhinolaryngology - Head and Neck Surgery
      Utrecht, Provincie Utrecht, Netherlands
  • 1995–2009
    • University of Iowa
      • • Department of Otolaryngology-Head and Neck Surgery
      • • Department of Pediatrics
      Iowa City, IA, United States
  • 2007–2008
    • Faculty of Medecine of Tunis
      Tunis-Ville, Tūnis, Tunisia
  • 2000–2007
    • Radboud University Nijmegen
      • Institute of Otorhinolaryngology
      Nijmegen, Provincie Gelderland, Netherlands
  • 2006
    • Rijnstate Hospital
      Arnheim, Gelderland, Netherlands
    • Universitair Ziekenhuis Antwerpen
      Antwerpen, Flanders, Belgium
  • 2005
    • The Postgraduate Dental Education Center Örebro
      Örebro, Örebro, Sweden
  • 2002–2004
    • Radboud University Medical Centre (Radboudumc)
      • Department of Human Genetics
      Nymegen, Gelderland, Netherlands
  • 2003
    • Shinshu University
      • Department of Otorhinolaryngology
      Shonai, Nagano, Japan
  • 2000–2002
    • Canisius-Wilhelmina Ziekenhuis
      Nymegen, Gelderland, Netherlands
  • 1998
    • St. James University
      Saint James, New York, United States