Institution
Memorial Sloan Kettering Cancer Center
Healthcare•New York, New York, United States•
About: Memorial Sloan Kettering Cancer Center is a healthcare organization based out in New York, New York, United States. It is known for research contribution in the topics: Cancer & Population. The organization has 30293 authors who have published 65381 publications receiving 4462534 citations. The organization is also known as: MSKCC & New York Cancer Hospital.
Topics: Cancer, Population, Breast cancer, Prostate cancer, Radiation therapy
Papers published on a yearly basis
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Université libre de Bruxelles1, Charité2, New York University3, University of Milan4, University of Antwerp5, University of California, San Francisco6, University of Auvergne7, Mayo Clinic8, University of Texas MD Anderson Cancer Center9, Harvard University10, Katholieke Universiteit Leuven11, Yeshiva University12, University of Toronto13, University of British Columbia14, Yale University15, Stanford University16, Memorial Sloan Kettering Cancer Center17, Indiana University – Purdue University Indianapolis18, University of Melbourne19
TL;DR: Current data on the clinical validity and utility of TILs in BC are reviewed in an effort to foster better knowledge and insight in this rapidly evolving field, and to develop a standardized methodology for visual assessment on H&E sections.
1,971 citations
Boston University1, Cornell University2, Johns Hopkins University3, University of Miami4, University of California, San Francisco5, Texas A&M Health Science Center College of Medicine6, Centers for Disease Control and Prevention7, University of Washington8, Case Western Reserve University9, University of Pennsylvania10, Denver Health Medical Center11, University of Michigan12, University of California, Davis13, University of California, Los Angeles14, United States Department of Veterans Affairs15, Washington University in St. Louis16, Wake Forest University17, University of Utah18, Memorial Sloan Kettering Cancer Center19
TL;DR: These recommendations address the best approaches for antibiotic stewardship programs to influence the optimal use of antibiotics.
Abstract: Evidence-based guidelines for implementation and measurement of antibiotic stewardship interventions in inpatient populations including long-term care were prepared by a multidisciplinary expert panel of the Infectious Diseases Society of America and the Society for Healthcare Epidemiology of America. The panel included clinicians and investigators representing internal medicine, emergency medicine, microbiology, critical care, surgery, epidemiology, pharmacy, and adult and pediatric infectious diseases specialties. These recommendations address the best approaches for antibiotic stewardship programs to influence the optimal use of antibiotics.
1,969 citations
TL;DR: It is demonstrated that recruitment of VEGF-responsive BM-derived precursors is necessary and sufficient for tumor angiogenesis and suggested new clinical strategies to block tumor growth are suggested.
Abstract: The role of bone marrow (BM)-derived precursor cells in tumor angiogenesis is not known. We demonstrate here that tumor angiogenesis is associated with recruitment of hematopoietic and circulating endothelial precursor cells (CEPs). We used the angiogenic defective, tumor resistant Id-mutant mice to show that transplantation of wild-type BM or vascular endothelial growth factor (VEGF)-mobilized stem cells restore tumor angiogenesis and growth. We detected donor-derived CEPs throughout the neovessels of tumors and Matrigel-plugs in an Id1+/-Id3-/- host, which were associated with VEGF-receptor-1-positive (VEGFR1+) myeloid cells. The angiogenic defect in Id-mutant mice was due to impaired VEGF-driven mobilization of VEGFR2+ CEPs and impaired proliferation and incorporation of VEGFR1+ cells. Although targeting of either VEGFR1 or VEGFR2 alone partially blocks the growth of tumors, inhibition of both VEGFR1 and VEGFR2 was necessary to completely ablate tumor growth. These data demonstrate that recruitment of VEGF-responsive BM-derived precursors is necessary and sufficient for tumor angiogenesis and suggest new clinical strategies to block tumor growth.
1,945 citations
TL;DR: Cyclin D2-Cdk4 complexes bind competitively to and down-regulate the activity of p27 and may thereby act in a pathway that reverses Cdk2 inhibition and enables G1 progression.
Abstract: Cell-cell contact and TGF-beta can arrest the cell cycle in G1. Mv1Lu mink epithelial cells arrested by either mechanism are incapable of assembling active complexes containing the G1 cyclin, cyclin E, and its catalytic subunit, Cdk2. These growth inhibitory signals block Cdk2 activation by raising the threshold level of cyclin E necessary to activate Cdk2. In arrested cells the threshold is set higher than physiological cyclin E levels and is determined by an inhibitor that binds to cyclin E-Cdk2 complexes. A 27-kD protein that binds to and prevents the activation of cyclin E-Cdk2 complexes can be purified from arrested cells but not from proliferating cells, using cyclin E-Cdk2 affinity chromatography. p27 is present in proliferating cells, but it is sequestered and unavailable to interact with cyclin E-Cdk2 complexes. Cyclin D2-Cdk4 complexes bind competitively to and down-regulate the activity of p27 and may thereby act in a pathway that reverses Cdk2 inhibition and enables G1 progression.
1,934 citations
TL;DR: Among patients with HER2‐negative metastatic breast cancer and a germline BRCA mutation, Olaparib monotherapy provided a significant benefit over standard therapy; median progression‐free survival was 2.8 months longer and the risk of disease progression or death was 42% lower with olaparIB monotherapy than with standard therapy.
Abstract: BackgroundOlaparib is an oral poly(adenosine diphosphate–ribose) polymerase inhibitor that has promising antitumor activity in patients with metastatic breast cancer and a germline BRCA mutation. MethodsWe conducted a randomized, open-label, phase 3 trial in which olaparib monotherapy was compared with standard therapy in patients with a germline BRCA mutation and human epidermal growth factor receptor type 2 (HER2)–negative metastatic breast cancer who had received no more than two previous chemotherapy regimens for metastatic disease. Patients were randomly assigned, in a 2:1 ratio, to receive olaparib tablets (300 mg twice daily) or standard therapy with single-agent chemotherapy of the physician’s choice (capecitabine, eribulin, or vinorelbine in 21-day cycles). The primary end point was progression-free survival, which was assessed by blinded independent central review and was analyzed on an intention-to-treat basis. ResultsOf the 302 patients who underwent randomization, 205 were assigned to receive...
1,927 citations
Authors
Showing all 30708 results
| Name | H-index | Papers | Citations |
|---|---|---|---|
| Gordon H. Guyatt | 231 | 1620 | 228631 |
| Edward Giovannucci | 206 | 1671 | 179875 |
| Irving L. Weissman | 201 | 1141 | 172504 |
| Craig B. Thompson | 195 | 557 | 173172 |
| Joan Massagué | 189 | 408 | 149951 |
| Gad Getz | 189 | 520 | 247560 |
| Chris Sander | 178 | 713 | 233287 |
| Richard B. Lipton | 176 | 2110 | 140776 |
| Richard K. Wilson | 173 | 463 | 260000 |
| George P. Chrousos | 169 | 1612 | 120752 |
| Stephen J. Elledge | 162 | 406 | 112878 |
| Murray F. Brennan | 161 | 925 | 97087 |
| Lewis L. Lanier | 159 | 554 | 86677 |
| David W. Bates | 159 | 1239 | 116698 |
| Dan R. Littman | 157 | 426 | 107164 |