Institution
Boston Children's Hospital
Healthcare•Boston, Massachusetts, United States•
About: Boston Children's Hospital is a(n) healthcare organization based out in Boston, Massachusetts, United States. It is known for research contribution in the topic(s): Population & Transplantation. The organization has 165409 authors who have published 215589 publication(s) receiving 6885627 citation(s).
Topics: Population, Transplantation, Poison control, Intensive care, Health care
Papers published on a yearly basis
Papers
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TL;DR: The Mesenchymal and Tissue Stem Cell Committee of the International Society for Cellular Therapy proposes minimal criteria to define human MSC, believing this minimal set of standard criteria will foster a more uniform characterization of MSC and facilitate the exchange of data among investigators.
Abstract: The considerable therapeutic potential of human multipotent mesenchymal stromal cells (MSC) has generated markedly increasing interest in a wide variety of biomedical disciplines. However, investig...
12,805 citations
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TL;DR: Because of the increased complexity of analysis and interpretation of clinical genetic testing described in this report, the ACMG strongly recommends thatclinical molecular genetic testing should be performed in a Clinical Laboratory Improvement Amendments–approved laboratory, with results interpreted by a board-certified clinical molecular geneticist or molecular genetic pathologist or the equivalent.
Abstract: Standards and guidelines for the interpretation of sequence variants: a joint consensus recommendation of the American College of Medical Genetics and Genomics and the Association for Molecular Pathology
11,349 citations
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TL;DR: Think of the switch to the angiogenic phenotype as a net balance of positive and negative regulators of blood vessel growth, which may dictate whether a primary tumour grows rapidly or slowly and whether metastases grow at all.
Abstract: Recent discoveries of endogenous negative regulators of angiogenesis, thrombospondin, angiostatin and glioma-derived angiogenesis inhibitory factor, all associated with neovascularized tumours, suggest a new paradigm of tumorigenesis. It is now helpful to think of the switch to the angiogenic phenotype as a net balance of positive and negative regulators of blood vessel growth. The extent to which the negative regulators are decreased during this switch may dictate whether a primary tumour grows rapidly or slowly and whether metastases grow at all.
7,776 citations
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Harvard University1, Broad Institute2, Boston Children's Hospital3, University of Washington4, University of Arizona5, Cardiff University6, Google7, Icahn School of Medicine at Mount Sinai8, Samsung Medical Center9, Vertex Pharmaceuticals10, University of Michigan11, University of Cambridge12, State University of New York Upstate Medical University13, Karolinska Institutet14, University of Eastern Finland15, University of Oxford16, Wellcome Trust Centre for Human Genetics17, Cedars-Sinai Medical Center18, University of Ottawa19, University of Pennsylvania20, University of North Carolina at Chapel Hill21, University of Helsinki22, University of California, San Diego23, University of Mississippi Medical Center24
TL;DR: The aggregation and analysis of high-quality exome (protein-coding region) DNA sequence data for 60,706 individuals of diverse ancestries generated as part of the Exome Aggregation Consortium (ExAC) provides direct evidence for the presence of widespread mutational recurrence.
Abstract: Large-scale reference data sets of human genetic variation are critical for the medical and functional interpretation of DNA sequence changes. Here we describe the aggregation and analysis of high-quality exome (protein-coding region) DNA sequence data for 60,706 individuals of diverse ancestries generated as part of the Exome Aggregation Consortium (ExAC). This catalogue of human genetic diversity contains an average of one variant every eight bases of the exome, and provides direct evidence for the presence of widespread mutational recurrence. We have used this catalogue to calculate objective metrics of pathogenicity for sequence variants, and to identify genes subject to strong selection against various classes of mutation; identifying 3,230 genes with near-complete depletion of predicted protein-truncating variants, with 72% of these genes having no currently established human disease phenotype. Finally, we demonstrate that these data can be used for the efficient filtering of candidate disease-causing variants, and for the discovery of human 'knockout' variants in protein-coding genes.
7,679 citations
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TL;DR: The work from the authors' laboratories reviewed herein was supported by grants from the National Cancer Institute.
Abstract: We wish to thank Jeff Arbeit, Karen Smith-McCune, Noel Weidner, Ella Bossy-Wetzel, and Christine Jolicoeur for providing the tissue sections used to prepare Figure 3Figure 3; Noel Bouck, Karen Smith-McCune, David Olson, Dowdy Jackson, and Jeff Arbeit for comments on the manuscript; and Wendy Gee and Terry Schoop of BioMed Arts (San Francisco) for artwork The work from the authors' laboratories reviewed herein was supported by grants from the National Cancer Institute
6,762 citations
Authors
Showing all 165409 results
| Name | H-index | Papers | Citations |
|---|---|---|---|
| Walter C. Willett | 334 | 2399 | 413322 |
| Frederick E. Shelton | 327 | 1485 | 295883 |
| Robert Langer | 281 | 2324 | 326306 |
| Graham A. Colditz | 261 | 1542 | 256034 |
| Frank B. Hu | 250 | 1675 | 253464 |
| George M. Whitesides | 240 | 1739 | 269833 |
| Eugene Braunwald | 230 | 1711 | 264576 |
| Ralph B. D'Agostino | 226 | 1287 | 229636 |
| Mark J. Daly | 204 | 763 | 304452 |
| Eric B. Rimm | 196 | 988 | 147119 |
| Virginia M.-Y. Lee | 194 | 993 | 148820 |
| Bernard Rosner | 190 | 1162 | 147661 |
| Stuart H. Orkin | 186 | 715 | 112182 |
| Mark Hallett | 186 | 1170 | 123741 |
| Ralph Weissleder | 184 | 1160 | 142508 |