Institution
Broad Institute
Nonprofit•Cambridge, Massachusetts, United States•
About: Broad Institute is a nonprofit organization based out in Cambridge, Massachusetts, United States. It is known for research contribution in the topics: Population & Genome-wide association study. The organization has 6584 authors who have published 11618 publications receiving 1522743 citations. The organization is also known as: Eli and Edythe L. Broad Institute of MIT and Harvard.
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TL;DR: New perspective is gained on the roles played by adipocyte in a variety of homeostatic processes and on the mechanisms used by adipocytes to communicate with other tissues and how these relationships are altered during metabolic disease and how they might be manipulated to restore metabolic health.
1,746 citations
TL;DR: The Alzheimer Disease Genetics Consortium performed a genome-wide association study of late-onset Alzheimer disease using a three-stage design consisting of a discovery stage (stage 1), two replication stages (stages 2 and 3), and both joint analysis and meta-analysis approaches were used.
Abstract: The Alzheimer Disease Genetics Consortium (ADGC) performed a genome-wide association study of late-onset Alzheimer disease using a three-stage design consisting of a discovery stage (stage 1) and two replication stages (stages 2 and 3). Both joint analysis and meta-analysis approaches were used. We obtained genome-wide significant results at MS4A4A (rs4938933; stages 1 and 2, meta-analysis P (P(M)) = 1.7 × 10(-9), joint analysis P (P(J)) = 1.7 × 10(-9); stages 1, 2 and 3, P(M) = 8.2 × 10(-12)), CD2AP (rs9349407; stages 1, 2 and 3, P(M) = 8.6 × 10(-9)), EPHA1 (rs11767557; stages 1, 2 and 3, P(M) = 6.0 × 10(-10)) and CD33 (rs3865444; stages 1, 2 and 3, P(M) = 1.6 × 10(-9)). We also replicated previous associations at CR1 (rs6701713; P(M) = 4.6 × 10(-10), P(J) = 5.2 × 10(-11)), CLU (rs1532278; P(M) = 8.3 × 10(-8), P(J) = 1.9 × 10(-8)), BIN1 (rs7561528; P(M) = 4.0 × 10(-14), P(J) = 5.2 × 10(-14)) and PICALM (rs561655; P(M) = 7.0 × 10(-11), P(J) = 1.0 × 10(-10)), but not at EXOC3L2, to late-onset Alzheimer's disease susceptibility.
1,743 citations
TL;DR: A computational method that infers tumor purity and malignant cell ploidy directly from analysis of somatic DNA alterations is described, revealing that genome-doubling events are common in human cancer, likely occur in cells that are already aneuploid, and influence pathways of tumor progression.
Abstract: Tumors vary in their ratio of normal to cancerous cells and in their genomic copy number. Carter et al. describe an analytic method for inferring the purity and ploidy of a tumor sample, enabling longitudinal studies of subclonal mutations and tumor evolution.
1,726 citations
Harvard University1, University of Washington2, University of California, San Francisco3, University of California, San Diego4, Baylor College of Medicine5, Broad Institute6, University of British Columbia7, Salk Institute for Biological Studies8, University of California, Davis9, University of Wisconsin-Madison10
TL;DR: The NIH Roadmap Epigenomics Mapping Consortium aims to produce a public resource of epigenomic maps for stem cells and primary ex vivo tissues selected to represent the normal counterparts of tissues and organ systems frequently involved in human disease.
Abstract: The NIH Roadmap Epigenomics Mapping Consortium aims to produce a public resource of epigenomic maps for stem cells and primary ex vivo tissues selected to represent the normal counterparts of tissues and organ systems frequently involved in human disease.
1,724 citations
Cristen J. Willer, Elizabeth K. Speliotes1, Elizabeth K. Speliotes2, Ruth J. F. Loos +163 more•Institutions (36)
TL;DR: Several of the likely causal genes are highly expressed or known to act in the central nervous system (CNS), emphasizing, as in rare monogenic forms of obesity, the role of the CNS in predisposition to obesity.
Abstract: Common variants at only two loci, FTO and MC4R, have been reproducibly associated with body mass index (BMI) in humans. To identify additional loci, we conducted meta-analysis of 15 genome-wide association studies for BMI (n > 32,000) and followed up top signals in 14 additional cohorts (n > 59,000). We strongly confirm FTO and MC4R and identify six additional loci (P < 5 x 10(-8)): TMEM18, KCTD15, GNPDA2, SH2B1, MTCH2 and NEGR1 (where a 45-kb deletion polymorphism is a candidate causal variant). Several of the likely causal genes are highly expressed or known to act in the central nervous system (CNS), emphasizing, as in rare monogenic forms of obesity, the role of the CNS in predisposition to obesity.
1,710 citations
Authors
Showing all 7146 results
| Name | H-index | Papers | Citations |
|---|---|---|---|
| Eric S. Lander | 301 | 826 | 525976 |
| Albert Hofman | 267 | 2530 | 321405 |
| Frank B. Hu | 250 | 1675 | 253464 |
| David J. Hunter | 213 | 1836 | 207050 |
| Kari Stefansson | 206 | 794 | 174819 |
| Mark J. Daly | 204 | 763 | 304452 |
| Lewis C. Cantley | 196 | 748 | 169037 |
| Matthew Meyerson | 194 | 553 | 243726 |
| Gad Getz | 189 | 520 | 247560 |
| Stacey Gabriel | 187 | 383 | 294284 |
| Stuart H. Orkin | 186 | 715 | 112182 |
| Ralph Weissleder | 184 | 1160 | 142508 |
| Chris Sander | 178 | 713 | 233287 |
| Michael I. Jordan | 176 | 1016 | 216204 |
| Richard A. Young | 173 | 520 | 126642 |