Thomas J Hudson

University of Toronto, Toronto, Ontario, Canada

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Publications (295)3240.72 Total impact

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    ABSTRACT: We propose an extension to quantile normalization that removes unwanted technical variation using control probes. We adapt our algorithm, functional normalization, to the Illumina 450k methylation array and address the open problem of normalizing methylation data with global epigenetic changes, such as human cancers. Using data sets from The Cancer Genome Atlas and a large case–control study, we show that our algorithm outperforms all existing normalization methods with respect to replication of results between experiments, and yields robust results even in the presence of batch effects. Functional normalization can be applied to any microarray platform, provided suitable control probes are available.
    Genome Biology 12/2014; 15(11). · 10.30 Impact Factor
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    ABSTRACT: Background: Calcium intake may reduce risk of colorectal cancer (CRC), but the mechanisms remain unclear. Studies of interaction between calcium intake and single nucleotide polymorphisms (SNPs) in calcium-related pathways have yielded inconsistent results. Methods: To identify gene-calcium interactions, we tested interactions between ~2.7 million SNPs across the genome with self-reported calcium intake (from dietary or supplemental sources) in 9,006 CRC cases and 9,503 controls of European ancestry. To test for multiplicative interactions, we used multivariable logistic regression and defined statistical significance using the conventional genome-wide α=5E-08. Results: After accounting for multiple comparisons, there were no statistically significant SNP-interactions with total, dietary, or supplemental calcium intake. Conclusions: We found no evidence of SNP-interactions with calcium intake for CRC risk in a large population of 18,509 individuals. Impact: These results suggest that in genome-wide analysis common genetic variants do not strongly modify the association between calcium intake and CRC in European populations.
    Cancer Epidemiology Biomarkers &amp Prevention 09/2014; · 4.56 Impact Factor
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    Thomas J Hudson
    Human Genetics 03/2014; · 4.63 Impact Factor
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    ABSTRACT: Less than 10% of pancreatic cancer cases survive 5 years, yet its etiology is not well understood. Studies suggest allergies are associated with reduced pancreatic cancer risk. Our study collected additional information on allergies (including skin prick test results and differentiation of allergic/nonallergic asthma), and is the first to assess possible confounding by allergy medications. A population-based case-control study was designed to comprehensively assess the association between allergy and pancreatic cancer risk. Pancreas cancer cases were diagnosed during 2011 to 2012, and identified through the Ontario Cancer Registry (345 cases). Population-based controls were identified using random digit dialing and age/sex frequency matched to cases (1,285 controls). Questionnaires collected lifetime allergy history (type of allergy, age at onset, skin prick testing results), allergy medications, and established pancreas cancer risk factors. Logistic regression was used to estimate odd ratios and test potential confounders, including allergy medications. Hay fever was associated with a significant reduction in pancreatic cancer risk [AOR = 0.68; 95% confidence intervals (CI), 0.52-0.89], and reduction was greatest for those whose skin prick test was positive for hay fever allergens. No particular patterns were observed as regards age at onset and duration of allergy. Positive dust/mold allergy skin prick test and animal allergies were associated with a statistically significant reduced pancreatic cancer risk; AOR = 0.49; 95% CI, 0.31-0.78 and AOR = 0.68; 95% CI, 0.46-0.99, respectively. Asthma was not associated with pancreatic cancer risk. These findings support the growing body of evidence that suggests certain allergies are associated with reduced pancreatic cancer risk. Cancer Epidemiol Biomarkers Prev; 23(3); 1-12. ©2014 AACR.
    Cancer Epidemiology Biomarkers &amp Prevention 02/2014; · 4.56 Impact Factor
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    ABSTRACT: In acute myeloid leukaemia (AML), the cell of origin, nature and biological consequences of initiating lesions, and order of subsequent mutations remain poorly understood, as AML is typically diagnosed without observation of a pre-leukaemic phase. Here, highly purified haematopoietic stem cells (HSCs), progenitor and mature cell fractions from the blood of AML patients were found to contain recurrent DNMT3A mutations (DNMT3A(mut)) at high allele frequency, but without coincident NPM1 mutations (NPM1c) present in AML blasts. DNMT3A(mut)-bearing HSCs showed a multilineage repopulation advantage over non-mutated HSCs in xenografts, establishing their identity as pre-leukaemic HSCs. Pre-leukaemic HSCs were found in remission samples, indicating that they survive chemotherapy. Therefore DNMT3A(mut) arises early in AML evolution, probably in HSCs, leading to a clonally expanded pool of pre-leukaemic HSCs from which AML evolves. Our findings provide a paradigm for the detection and treatment of pre-leukaemic clones before the acquisition of additional genetic lesions engenders greater therapeutic resistance.
    Nature 02/2014; · 38.60 Impact Factor
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    ABSTRACT: Inherited variation in genes that regulate innate immunity and inflammation may contribute to colorectal neoplasia risk. To evaluate this association, we conducted a nested case-control study of 451 colorectal cancer cases, 694 colorectal advanced adenoma cases and 696 controls of European descent within the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. A total of 935 tag single-nucleotide polymorphisms (SNPs) in 98 genes were evaluated. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the association with colorectal neoplasia. Sixteen SNPs were associated with colorectal neoplasia risk at P < 0.01, but after adjustment for multiple testing, only rs2838732 (ITGB2) remained suggestively associated with colorectal neoplasia (OR(per T allele) = 0.68, 95% CI: 0.57-0.83, P = 7.7 × 10(-5), adjusted P = 0.07). ITGB2 codes for the CD18 protein in the integrin beta chain family. The ITGB2 association was stronger for colorectal cancer (OR(per T allele) = 0.41, 95% CI: 0.30-0.55, P = 2.4 × 10(-) (9)) than for adenoma (OR(per T allele) = 0.84, 95%CI: 0.69-1.03, P = 0.08), but it did not replicate in the validation study. The ITGB2 rs2838732 association was significantly modified by smoking status (P value for interaction = 0.003). Among never and former smokers, it was inversely associated with colorectal neoplasia (OR(per T allele) = 0.5, 95% CI: 0.37-0.69 and OR(per T allele) = 0.72, 95% CI: 0.54-0.95, respectively), but no association was seen among current smokers. Other notable findings were observed for SNPs in BPI/LBP and MYD88. Although the results need to be replicated, our findings suggest that genetic variation in inflammation-related genes may be related to the risk of colorectal neoplasia.
    Carcinogenesis 11/2013; 34(11):2512-20. · 5.64 Impact Factor
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    ABSTRACT: A locus on human chromosome 11q23 tagged by marker rs3802842 was associated with colorectal cancer in a genome-wide association study; this finding has been replicated in case-control studies worldwide. In order to identify biologic factors at this locus that are related to the etiopathology of colorectal cancer, we used microarray-based target selection methods, coupled to next-generation sequencing, to study 103 kb at the 11q23 locus. We genotyped 369 putative variants from 1030 patients with colorectal cancer (cases) and 1061 individuals without colorectal cancer (controls) from the Ontario Familial Colorectal Cancer Registry. Two previously uncharacterized genes, COLCA1 and COLCA2, were found to be co-regulated genes that are transcribed from opposite strands. Expression levels of COLCA1 and COLCA2 transcripts correlate with rs3802842 genotypes. In colon tissues, COLCA1 co-localizes with crystalloid granules of eosinophils and granular organelles of mast cells, neutrophils, macrophages, dendritic cells, and differentiated myeloid-derived cell lines. COLCA2 is present in the cytoplasm of normal epithelial, immune, and other cell lineages, as well as tumor cells. Tissue microarray analysis demonstrates the association of rs3802842 with lymphocyte density in the lamina propria (P=.014) and levels of COLCA1 in the lamina propria (P=.00016) and COLCA2 (tumor cells, P=.0041 and lamina propria, P = 6x10(-5) ). In conclusion, genetic, expression, and immunohistochemical data implicate COLCA1 and COLCA2 in the pathogenesis of colon cancer. Histologic analyses indicate the involvement of immune pathways. © 2013 Wiley Periodicals, Inc.
    International Journal of Cancer 10/2013; · 6.20 Impact Factor
  • Alan Ashworth, Thomas J Hudson
    Nature 10/2013; 502(7471):306-7. · 38.60 Impact Factor
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    ABSTRACT: Background: Experimental evidence has demonstrated an anti-neoplastic role for vitamin D in the colon and higher circulating 25-hydroxyvitamin D (25[OH]D) levels are consistently associated with a lower risk of colorectal cancer (CRC). Genome-wide association studies have identified loci associated with levels of circulating 25(OH)D. The identified SNPs from four gene regions, collectively explain approximately 5% of the variance in circulating 25(OH)D. Methods: We investigated whether six polymorphisms in GC, CYP2R1, CYP24A1 and DHCR7/NADSYN1, genes previously shown to be associated with circulating 25(OH)D levels, were associated with CRC risk in 10,061 cases and 12,768 controls drawn from 13 studies included in the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO) and Colon Cancer Family Registry (CCFR). We performed a meta-analysis of crude and multivariate-adjusted logistic regression models to calculate odds ratios and associated confidence intervals for SNPs individually, SNPs simultaneously, and for a vitamin D additive genetic risk score (GRS). Results: We did not observe a statistically significant association between the 25(OH)D associated SNPs and CRC marginally, conditionally, or as a GRS, or for colon or rectal cancer separately or combined. Conclusions: Our findings do not support an association between SNPs associated with circulating 25(OH)D and risk of CRC. Additional work is warranted to investigate the complex relationship between 25(OH)D and CRC risk. Impact: There was no association observed between genetic markers of circulating 25(OH)D and CRC. These genetic markers account for a small proportion of the variance in 25(OH)D.
    Cancer Epidemiology Biomarkers &amp Prevention 08/2013; · 4.56 Impact Factor
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    ABSTRACT: Genome-wide association studies have identified a large number of single nucleotide polymorphisms (SNPs) associated with a wide array of cancer sites. Several of these variants demonstrate associations with multiple cancers, suggesting pleiotropic effects and shared biological mechanisms across some cancers. We hypothesised that SNPs previously associated with other cancers may additionally be associated with colorectal cancer. In a large-scale study, we examined 171 SNPs previously associated with 18 different cancers for their associations with colorectal cancer. We examined 13 338 colorectal cancer cases and 40 967 controls from three consortia: Population Architecture using Genomics and Epidemiology (PAGE), Genetic Epidemiology of Colorectal Cancer (GECCO), and the Colon Cancer Family Registry (CCFR). Study-specific logistic regression results, adjusted for age, sex, principal components of genetic ancestry, and/or study specific factors (as relevant) were combined using fixed-effect meta-analyses to evaluate the association between each SNP and colorectal cancer risk. A Bonferroni-corrected p value of 2.92×10(-4) was used to determine statistical significance of the associations. Two correlated SNPs-rs10090154 and rs4242382-in Region 1 of chromosome 8q24, a prostate cancer susceptibility region, demonstrated statistically significant associations with colorectal cancer risk. The most significant association was observed with rs4242382 (meta-analysis OR=1.12; 95% CI 1.07 to 1.18; p=1.74×10(-5)), which also demonstrated similar associations across racial/ethnic populations and anatomical sub-sites. This is the first study to clearly demonstrate Region 1 of chromosome 8q24 as a susceptibility locus for colorectal cancer; thus, adding colorectal cancer to the list of cancer sites linked to this particular multicancer risk region at 8q24.
    Gut 08/2013; · 10.73 Impact Factor
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    ABSTRACT: This study used an integrated analysis of copy number, gene expression, and RNA interference screens for identification of putative driver genes harbored in somatic copy number gains in pancreatic ductal adenocarcinoma (PDAC). Somatic copy number gain data on 60 PDAC genomes were extracted from public data sets to identify genomic loci that are recurrently gained. Array-based data from a panel of 29 human PDAC cell lines were used to quantify associations between copy number and gene expression for the set of genes found in somatic copy number gains. The most highly correlated genes were assessed in a compendium of pooled short hairpin RNA screens on 27 of the same human PDAC cell lines. A catalog of 710 protein-coding and 46 RNA genes mapping to 20 recurrently gained genomic loci were identified. The gene set was further refined through stringent integration of copy number, gene expression, and RNA interference screening data to uncover 34 candidate driver genes. Among the candidate genes from the integrative analysis, ECT2 was found to have significantly higher essentiality in specific PDAC cell lines with genomic gains at the 3q26.3 locus, which harbors this gene, suggesting that ECT2 may play an oncogenic role in the PDAC neoplastic process.
    Pancreas 08/2013; 42(6):1016-1026. · 2.95 Impact Factor
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    ABSTRACT: The search for expression quantitative trait loci has traditionally centred entirely on the process of transcription, whereas variants with effects on messenger RNA translation have not been systematically studied. Here we present a high-throughput approach for measuring translational cis-regulation in the human genome. Using ribosomal association as proxy for translational efficiency of polymorphic messenger RNAs, we test the ratio of polysomal/non-polysomal messenger RNA level as a quantitative trait for association with single nucleotide polymorphisms on the same messenger RNA transcript. We identify one important ribosomal distribution effect, from rs1131017 in the 5'-untranslated region of RPS26, that is in high linkage disequilibrium with the 12q13 locus for susceptibility to type 1 diabetes. The effect on translation is confirmed at the protein level by quantitative western blots, both ex vivo and after in vitro translation. Our results are a proof-of-principle that allelic effects on translation can be detected at a transcriptome-wide scale.
    Nature Communications 07/2013; 4:2260. · 10.74 Impact Factor
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    Thomas J Hudson
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    ABSTRACT: Genomic variation, through effects on gene structure and expression, plays an important role in understanding disease predisposition, biology and clinical response to therapy. Transforming this knowledge into clinically relevant information that tailors interventions to an individual's specific genetic, physical, social and environmental profile is challenging. To illustrate how research initiatives at preclinical phases of development are attempting to address clinically important issues in oncology, six clinical problems related to cancers of the colon, prostate, breast, pancreas and brain (medulloblastoma) as well as metastatic disease of different origins are described. A unifying theme across applications is that healthy individuals previously indistinguishable in regards to cancer risk and cancer patients previously categorised as similar with regard to prognosis or drug response are being stratified into more refined subgroups with different clinical profiles. Effective matching of a broad range of tests with more tailored strategies for prevention and/or treatment will require well-designed clinical studies to evaluate benefits and costs. This article is protected by copyright. All rights reserved.
    Journal of Internal Medicine 06/2013; · 6.46 Impact Factor
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    ABSTRACT: Using sequencing information to guide clinical decision-making requires coordination of a diverse set of people and activities. In clinical genomics, the process typically includes sample acquisition, template preparation, genome data generation, analysis to identify and confirm variant alleles, interpretation of clinical significance, and reporting to clinicians. We describe a software application developed within a clinical genomics study, to support this entire process. The software application tracks patients, samples, genomic results, decisions and reports across the cohort, monitors progress and sends reminders, and works alongside an electronic data capture system for the trial's clinical and genomic data. It incorporates systems to read, store, analyze and consolidate sequencing results from multiple technologies, and provides a curated knowledge base of tumor mutation frequency (from the COSMIC database) annotated with clinical significance and drug sensitivity to generate reports for clinicians. By supporting the entire process, the application provides deep support for clinical decision making, enabling the generation of relevant guidance in reports for verification by an expert panel prior to forwarding to the treating physician.
    Genomics 04/2013; · 3.01 Impact Factor
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    ABSTRACT: Leukemia stem cells (LSCs) play a pivotal role in the resistance of chronic myeloid leukemia (CML) to tyrosine kinase inhibitors (TKIs) and its progression to blast crisis (BC), in part, through the alternative splicing of self-renewal and survival genes. To elucidate splice-isoform regulators of human BC LSC maintenance, we performed whole-transcriptome RNA sequencing, splice-isoform-specific quantitative RT-PCR (qRT-PCR), nanoproteomics, stromal coculture, and BC LSC xenotransplantation analyses. Cumulatively, these studies show that the alternative splicing of multiple prosurvival BCL2 family genes promotes malignant transformation of myeloid progenitors into BC LSCS that are quiescent in the marrow niche and that contribute to therapeutic resistance. Notably, sabutoclax, a pan-BCL2 inhibitor, renders marrow-niche-resident BC LSCs sensitive to TKIs at doses that spare normal progenitors. These findings underscore the importance of alternative BCL2 family splice-isoform expression in BC LSC maintenance and suggest that the combinatorial inhibition of prosurvival BCL2 family proteins and BCR-ABL may eliminate dormant LSCs and obviate resistance.
    Cell stem cell 01/2013; · 23.56 Impact Factor
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    ABSTRACT: To identify new genetic factors for colorectal cancer (CRC), we conducted a genome-wide association study in east Asians. By analyzing genome-wide data in 2,098 cases and 5,749 controls, we selected 64 promising SNPs for replication in an independent set of samples, including up to 5,358 cases and 5,922 controls. We identified four SNPs with association P values of 8.58 × 10(-7) to 3.77 × 10(-10) in the combined analysis of all east Asian samples. Three of the four were replicated in a study conducted in 26,060 individuals of European descent, with combined P values of 1.22 × 10(-10) for rs647161 (5q31.1), 6.64 × 10(-9) for rs2423279 (20p12.3) and 3.06 × 10(-8) for rs10774214 (12p13.32 near the CCND2 gene), derived from meta-analysis of data from both east Asian and European-ancestry populations. This study identified three new CRC susceptibility loci and provides additional insight into the genetics and biology of CRC.
    Nature Genetics 12/2012; 45(2):191-196. · 35.21 Impact Factor
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    ABSTRACT: BACKGROUND & AIMS: Heritable factors contribute to development of colorectal cancer (CRC). Identifying the genetic loci associated with colorectal tumor formation could elucidate the mechanisms of pathogenesis. METHODS: We conducted a genome-wide association study (GWAS) that included 14 studies, 12,696 cases of colorectal tumors (11,870 cancer, 826 adenoma), and 15,113 controls of European descent. The 10 most statistically significant, previously unreported findings were followed up in 6 studies; these included 3056 colorectal tumor cases (2098 cancer, 958 adenoma) and 6658 controls of European and Asian descent. RESULTS: Based on the combined analysis we identified a locus that reached the conventional genome-wide significance level at <5.0 x 10-8: an intergenic region on chromosome 2q32.3, close toNABP1 (most significant single nucleotide polymorphism: rs11903757; odds ratio [OR]=1.15 per risk allele;P =3.7 x 10-8). We also found evidence for 3 additional loci with P values <5.0 x 10-7: a locus within theLAMC1gene on chromosome 1q25.3 (rs10911251; OR=1.10 per risk allele;P =9.5 x 10-8), a locus within theCCND2gene on chromosome 12p13.32 (rs3217810 per risk allele; OR=0.84;P =5.9 x 10-8), and a locus in theTBX3gene on chromosome 12q24.21 (rs59336, OR=0.91 per risk allele;P =3.7 x 10-7). CONCLUSIONS: In a large GWAS, we associated polymorphisms close toNABP (which encodes a DNA-binding protein involved in DNA repair) with colorectal tumor risk. We also provided evidence for an association between colorectal tumor risk and polymorphisms inLAMC1 (this is the second gene in the laminin family to be associated with CRCs),CCND2 (which encodes for cyclin D2), andTBX3 (which encodes a T-box transcription factor and is a target of Wnt signaling to -catenin). The roles of these genes and their products in cancer pathogenesis warrant further investigation.
    Gastroenterology 12/2012; · 12.82 Impact Factor
  • Nardin Samuel, Thomas J Hudson
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    ABSTRACT: BACKGROUND:Sequencing of cancer genomes has become a pivotal method for uncovering and understanding the deregulated cellular processes driving tumor initiation and progression. Whole-genome sequencing is evolving toward becoming less costly and more feasible on a large scale; consequently, thousands of tumors are being analyzed with these technologies. Interpreting these data in the context of tumor complexity poses a challenge for cancer genomics.CONTENT:The sequencing of large numbers of tumors has revealed novel insights into oncogenic mechanisms. In particular, we highlight the remarkable insight into the pathogenesis of breast cancers that has been gained through comprehensive and integrated sequencing analysis. The analysis and interpretation of sequencing data, however, must be considered in the context of heterogeneity within and among tumor samples. Only by adequately accounting for the underlying complexity of cancer genomes will the potential of genome sequencing be understood and subsequently translated into improved management of patients.SUMMARY:The paradigm of personalized medicine holds promise if patient tumors are thoroughly studied as unique and heterogeneous entities and clinical decisions are made accordingly. Associated challenges will be ameliorated by continued collaborative efforts among research centers that coordinate the sharing of mutation, intervention, and outcomes data to assist in the interpretation of genomic data and to support clinical decision-making.
    Clinical Chemistry 11/2012; · 7.15 Impact Factor
  • Jennifer Jennings, Thomas J Hudson
    Clinical Chemistry 11/2012; · 7.15 Impact Factor

Publication Stats

23k Citations
3,240.72 Total Impact Points


  • 2014
    • University of Toronto
      Toronto, Ontario, Canada
  • 2013
    • Cancer Prevention Institute of California
      Fremont, California, United States
  • 2012
    • Fred Hutchinson Cancer Research Center
      • Division of Public Health Sciences
      Seattle, WA, United States
  • 2007–2012
    • Ontario Institute for Cancer Research
      Toronto, Ontario, Canada
    • The Scripps Research Institute
      La Jolla, California, United States
    • Broad Institute of MIT and Harvard
      Cambridge, Massachusetts, United States
  • 2011
    • Garvan Institute of Medical Research
      • Cancer Research Program
      Darlinghurst, New South Wales, Australia
  • 1998–2011
    • McGill University
      • • Department of Human Genetics
      • • Centre for the Study of Host Resistance
      Montréal, Quebec, Canada
  • 2010
    • Montreal Heart Institute
      • Research Centre
      Montréal, Quebec, Canada
    • University of Waterloo
      • Department of Applied Mathematics
      Waterloo, Ontario, Canada
  • 2009
    • Institute of Cancer Research
      • Division of Genetics and Epidemiology
      Londinium, England, United Kingdom
    • University of British Columbia - Vancouver
      Vancouver, British Columbia, Canada
    • Institut universitaire de cardiologie et de pneumologie de Québec
      Québec, Quebec, Canada
    • University of British Columbia - Okanagan
      Kelowna, British Columbia, Canada
    • McMaster University
      • Population Health Research Institute (PHRI)
      Hamilton, Ontario, Canada
  • 2002–2009
    • Université de Montréal
      • School of Speech Pathology and Audiology
      Montréal, Quebec, Canada
  • 2000–2009
    • Laval University
      • Département de Médecine
      Québec, Quebec, Canada
    • McGill University Health Centre
      Montréal, Quebec, Canada
  • 2008
    • Imperial College London
      • Faculty of Medicine
      London, ENG, United Kingdom
    • The University of Edinburgh
      • MRC Human Genetics Unit
      Edinburgh, SCT, United Kingdom
  • 2007–2008
    • Samuel Lunenfeld Research Institute
      Toronto, Ontario, Canada
  • 2001–2007
    • University of Québec in Chicoutimi
      • Department of Sciences Fondamentales
      Saguenay, Quebec, Canada
    • Singapore-MIT Alliance
      Cambridge, Massachusetts, United States
    • Providence University
      臺中市, Taiwan, Taiwan
  • 1996–2007
    • Brigham and Women's Hospital
      • • Department of Medicine
      • • Department of Pathology
      Boston, MA, United States
    • Harvard Medical School
      • Department of Genetics
      Boston, MA, United States
  • 2005
    • Lund University
      • Department of Endocrinology
      Lund, Skane, Sweden
    • University of Oxford
      • Nuffield Department of Clinical Neurosciences
      Oxford, ENG, United Kingdom
  • 1995–2002
    • Whitehead Institute for Biomedical Research
      Cambridge, Massachusetts, United States
    • Boston Children's Hospital
      • Department of Pathology
      Boston, MA, United States
    • The Children's Hospital of Philadelphia
      • Division of Human Genetics and Molecular Biology
      Philadelphia, PA, United States
  • 1992–2001
    • Massachusetts Institute of Technology
      • • Center for Genome Research
      • • Department of Biology
      Cambridge, MA, United States
  • 1999
    • University of California, Los Angeles
      • Department of Human Genetics
      Los Angeles, CA, United States