Matthijs Moed

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Small insertions and deletions (indels) and large structural variations (SVs) are major contributors to human genetic diversity and disease. However, mutation rates and characteristics of de novo indels and SVs in the general population have remained largely unexplored. We report 332 validated de novo structural changes identified in whole genomes of 250(More)
Complex insertions and deletions (indels) are formed by simultaneously deleting and inserting DNA fragments of different sizes at a common genomic location. Here we present a systematic analysis of somatic complex indels in the coding sequences of samples from over 8,000 cancer cases using Pindel-C. We discovered 285 complex indels in cancer-associated(More)
Epigenetic change is a hallmark of ageing but its link to ageing mechanisms in humans remains poorly understood. While DNA methylation at many CpG sites closely tracks chronological age, DNA methylation changes relevant to biological age are expected to gradually dissociate from chronological age, mirroring the increased heterogeneity in health status at(More)
Most disease-associated genetic variants are noncoding, making it challenging to design experiments to understand their functional consequences. Identification of expression quantitative trait loci (eQTLs) has been a powerful approach to infer the downstream effects of disease-associated variants, but most of these variants remain unexplained. The analysis(More)
It has been postulated that aging is the consequence of an accelerated accumulation of somatic DNA mutations and that subsequent errors in the primary structure of proteins ultimately reach levels sufficient to affect organismal functions. The technical limitations of detecting somatic changes and the lack of insight about the minimum level of erroneous(More)
Daria V. Zhernakova1*, Patrick Deelen1,2*, Martijn Vermaat3*, Maarten van Iterson4*, Michiel van Galen3, Wibowo Arindrarto5, Peter van ’t Hof5, Hailiang Mei5, Freerk van Dijk1,2, Harm-Jan Westra6,7,8, Marc Jan Bonder1, Jeroen van Rooij9, Marijn Verkerk9, P. Mila Jhamai9, Matthijs Moed4, Szymon M. Kielbasa4 , Jan Bot10, Irene Nooren10, René Pool11, Jenny van(More)
Genetic risk factors often localize to noncoding regions of the genome with unknown effects on disease etiology. Expression quantitative trait loci (eQTLs) help to explain the regulatory mechanisms underlying these genetic associations. Knowledge of the context that determines the nature and strength of eQTLs may help identify cell types relevant to(More)
Cells can be primed by external stimuli to obtain a long-term epigenetic memory. We hypothesize that long-term exposure to elevated blood lipids can prime circulating immune cells through changes in DNA methylation, a process that may contribute to the development of atherosclerosis. To interrogate the causal relationship between triglyceride, low-density(More)
Erik B. van den Akker, Steven J. Pitts, Joris Deelen, Matthijs H. Moed, Shobha Potluri, Jeroen van Rooij, H. Eka D. Suchiman, Nico Lakenberg, Wesley J. de Dijcker, André G. Uitterlinden, Robert Kraaij, Albert Hofman, Anton J. M. de Craen, Jeanine J. Houwing-Duistermaat, Gert-Jan B. van Ommen on behalf of the Genome of The Netherlands Consortium, David R.(More)
Emerging evidence suggests that the basis for variation in late-life mobility is attributable, in part, to genetic factors, which may become increasingly important with age. Our objective was to systematically assess the contribution of genetic variation to gait speed in older individuals. We conducted a meta-analysis of gait speed GWASs in 31,478 older(More)