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, Radiation therapy, Prostate cancer
Papers published on a yearly basis
Papers
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Broad Institute1, Buck Institute for Research on Aging2, Harvard University3, National Institute of Standards and Technology4, Texas A&M University5, Vanderbilt University6, University of California, San Francisco7, University of Victoria8, Purdue University9, New York University10, National Institutes of Health11, University of North Carolina at Chapel Hill12, Indiana University13, Fred Hutchinson Cancer Research Center14, Memorial Sloan Kettering Cancer Center15
TL;DR: A multilaboratory study to assess reproducibility, recovery, linear dynamic range and limits of detection and quantification of multiplexed, MRM-based assays, conducted by NCI-CPTAC demonstrates that these assays can be highly reproducible within and across laboratories and instrument platforms.
Abstract: Verification of candidate biomarkers relies upon specific, quantitative assays optimized for selective detection of target proteins, and is increasingly viewed as a critical step in the discovery pipeline that bridges unbiased biomarker discovery to preclinical validation. Although individual laboratories have demonstrated that multiple reaction monitoring (MRM) coupled with isotope dilution mass spectrometry can quantify candidate protein biomarkers in plasma, reproducibility and transferability of these assays between laboratories have not been demonstrated. We describe a multilaboratory study to assess reproducibility, recovery, linear dynamic range and limits of detection and quantification of multiplexed, MRM-based assays, conducted by NCI-CPTAC. Using common materials and standardized protocols, we demonstrate that these assays can be highly reproducible within and across laboratories and instrument platforms, and are sensitive to low mug/ml protein concentrations in unfractionated plasma. We provide data and benchmarks against which individual laboratories can compare their performance and evaluate new technologies for biomarker verification in plasma.
997 citations
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Institut Gustave Roussy1, Aix-Marseille University2, University of Zurich3, Memorial Sloan Kettering Cancer Center4, Aarhus University Hospital5, Saint Louis University6, Cross Cancer Institute7, Bristol-Myers Squibb8, European Organisation for Research and Treatment of Cancer9, European Institute of Oncology10
TL;DR: Adjuvant ipilimumab significantly improved recurrence-free survival for patients with completely resected high-risk stage III melanoma and the adverse event profile was consistent with that observed in advanced melanoma, but at higher incidences in particular for endocrinopathies.
Abstract: Summary Background Ipilimumab is an approved treatment for patients with advanced melanoma. We aimed to assess ipilimumab as adjuvant therapy for patients with completely resected stage III melanoma at high risk of recurrence. Methods We did a double-blind, phase 3 trial in patients with stage III cutaneous melanoma (excluding lymph node metastasis ≤1 mm or in-transit metastasis) with adequate resection of lymph nodes (ie, the primary cutaneous melanoma must have been completely excised with adequate surgical margins) who had not received previous systemic therapy for melanoma from 91 hospitals located in 19 countries. Patients were randomly assigned (1:1), centrally by an interactive voice response system, to receive intravenous infusions of 10 mg/kg ipilimumab or placebo every 3 weeks for four doses, then every 3 months for up to 3 years. Using a minimisation technique, randomisation was stratified by disease stage and geographical region. The primary endpoint was recurrence-free survival, assessed by an independent review committee, and analysed by intention to treat. Enrollment is complete but the study is ongoing for follow-up for analysis of secondary endpoints. This trial is registered with EudraCT, number 2007-001974-10, and ClinicalTrials.gov, number NCT00636168. Findings Between July 10, 2008, and Aug 1, 2011, 951 patients were randomly assigned to ipilimumab (n=475) or placebo (n=476), all of whom were included in the intention-to-treat analyses. At a median follow-up of 2·74 years (IQR 2·28–3·22), there were 528 recurrence-free survival events (234 in the ipilimumab group vs 294 in the placebo group). Median recurrence-free survival was 26·1 months (95% CI 19·3–39·3) in the ipilimumab group versus 17·1 months (95% CI 13·4–21·6) in the placebo group (hazard ratio 0·75; 95% CI 0·64–0·90; p=0·0013); 3-year recurrence-free survival was 46·5% (95% CI 41·5–51·3) in the ipilimumab group versus 34·8% (30·1–39·5) in the placebo group. The most common grade 3–4 immune-related adverse events in the ipilimumab group were gastrointestinal (75 [16%] vs four [ vs one [ vs none). Adverse events led to discontinuation of treatment in 245 (52%) of 471 patients who started ipilimumab (182 [39%] during the initial treatment period of four doses). Five patients (1%) died due to drug-related adverse events. Five (1%) participants died because of drug-related adverse events in the ipilimumab group; three patients died because of colitis (two with gastrointestinal perforation), one patient because of myocarditis, and one patient because of multiorgan failure with Guillain-Barre syndrome. Interpretation Adjuvant ipilimumab significantly improved recurrence-free survival for patients with completely resected high-risk stage III melanoma. The adverse event profile was consistent with that observed in advanced melanoma, but at higher incidences in particular for endocrinopathies. The risk–benefit ratio of adjuvant ipilimumab at this dose and schedule requires additional assessment based on distant metastasis-free survival and overall survival endpoints to define its definitive value. Funding Bristol-Myers Squibb.
996 citations
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Roswell Park Cancer Institute1, Duke University2, Ohio State University3, Wake Forest University4, Memorial Sloan Kettering Cancer Center5, Harvard University6, University of Pennsylvania7, University of Minnesota8, Washington University in St. Louis9, University of Florida10, University of Wisconsin-Madison11, University of Chicago12, State University of New York Upstate Medical University13, Icahn School of Medicine at Mount Sinai14, Oregon Health & Science University15, University of North Carolina at Chapel Hill16, University of California, San Francisco17, University of Texas MD Anderson Cancer Center18, Medical College of Wisconsin19
TL;DR: Lenalidomide maintenance therapy, initiated at day 100 after hematopoietic stem-cell transplantation, was associated with more toxicity and second cancers but a significantly longer time to disease progression and significantly improved overall survival among patients with myeloma.
Abstract: Background Data are lacking on whether lenalidomide maintenance therapy prolongs the time to disease progression after autologous hematopoietic stem-cell transplantation in patients with multiple myeloma. Methods Between April 2005 and July 2009, we randomly assigned 460 patients who were younger than 71 years of age and had stable disease or a marginal, partial, or complete response 100 days after undergoing stem-cell transplantation to lenalidomide or placebo, which was administered until disease progression. The starting dose of lenalidomide was 10 mg per day (range, 5 to 15). Results The study-drug assignments were unblinded in 2009, when a planned interim analysis showed a significantly longer time to disease progression in the lenalidomide group. At unblinding, 20% of patients who received lenalidomide and 44% of patients who received placebo had progressive disease or had died (P<0.001); of the remaining 128 patients who received placebo and who did not have progressive disease, 86 crossed over to ...
996 citations
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Vita-Salute San Raffaele University1, National University of Singapore2, University of Buenos Aires3, University of California, San Francisco4, University of Miami5, Wake Forest Institute for Regenerative Medicine6, University of Western Ontario7, Mayo Clinic8, Johns Hopkins University9, Duke University10, Karolinska University Hospital11, Aristotle University of Thessaloniki12, Tulane University13, Erasmus University Rotterdam14, London Bridge Hospital15, Istanbul University16, Rush University Medical Center17, Georgia Regents University18, University of Florence19, Deakin University20, Cleveland Clinic21, University of Milan22, Memorial Sloan Kettering Cancer Center23, Concordia University Wisconsin24, Valparaiso University25, University of Medicine and Dentistry of New Jersey26, Maimonides Medical Center27, Ludwig Maximilian University of Munich28, Rambam Health Care Campus29, Emory University30
TL;DR: Specific evaluation, treatment guidelines, and algorithms were developed for every sexual dysfunction in men, including erectile dysfunction; disorders of libido, orgasm, and ejaculation; Peyronie's disease; and priapism.
993 citations
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TL;DR: The discovery of microRNAs almost two decades ago established a new paradigm of gene regulation, and during the past ten years these tiny non-coding RNAs have been linked to virtually all known physiological and pathological processes, including cancer.
Abstract: MicroRNAs (miRNAs) are small, evolutionarily conserved, non-coding RNAs of 18–25 nucleotides in length that have an important function in gene regulation. Mature miRNA products are generated from a longer primary miRNA (pri-miRNA) transcript through sequential processing by the ribonucleases Drosha and Dicer1 (ref. 1). The first description of miRNAs was made in 1993 in Caenorhabditis elegans as regulators of developmental timing 2,3 . Later, miRNAs were shown to inhibit their target genes through sequences that are complementary to the target messenger RNA, leading to decreased expression of the target protein 1 (Box 1). This discovery resulted in a pattern shift in our understanding of gene regulation because miRNAs are now known to repress thousands of target genes and coordinate normal processes, including cellular proliferation, differentiation and apoptosis. The aberrant expression or alteration of miRNAs also contributes to a range of human pathologies, including cancer. The control of gene expression by miRNAs is a process seen in virtually all cancer cells. These cells show alterations in their miRNA expression profiles, and emerging data indicate that these patterns could be useful in improving the classification of cancers and predicting their behaviour. In addition, miRNAs have now been shown to behave as cancer ‘drivers’ in the same way as protein-coding genes whose alterations actively and profoundly contribute to malignant transformation and cancer progression. Owing to the capacity of miRNAs to modulate tens to hundreds of target genes, they are emerging as important factors in the control of the ‘hallmarks’ of cancer 4 . In this Review, we summarize the findings that provide evidence for the central role of miRNAs in controlling cellular transformation and tumour progression. We also highlight the potential uses of miRNAs and miRNA-based drugs in cancer therapy and discuss the obstacles that will need to be overcome. miRNAs are cancer genes In 2002, Croce and colleagues first demonstrated that an miRNA cluster was frequently deleted or downregulated in chronic lymphocytic leukaemia 5 . This discovery suggested that non-coding genes were contributing to the development of cancer, and paved the way for the closer investigation of miRNA loss or amplification in tumours. Subsequently, miRNAs were shown to be differentially expressed in cancer cells, in which they formed distinct and unique miRNA expression patterns 6 , and whole classes of miRNAs could be controlled directly by key oncogenic transcription factors 7 . In parallel, studies with mouse models established that miRNAs were actively involved in tumorigenesis
992 citations
Authors
Showing all 30708 results
Name | H-index | Papers | Citations |
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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 |