Institution
Sunnybrook Health Sciences Centre
Healthcare•Toronto, Ontario, Canada•
About: Sunnybrook Health Sciences Centre is a healthcare organization based out in Toronto, Ontario, Canada. It is known for research contribution in the topics: Population & Breast cancer. The organization has 7689 authors who have published 15236 publications receiving 523019 citations. The organization is also known as: Sunnybrook.
Papers published on a yearly basis
Papers
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TL;DR: A number of oral mucositis scoring systems that are commonly used are reviewed and the biological basis of its development and management is discussed.
156 citations
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TL;DR: AHS is an adverse drug reaction associated with the aromatic antiepileptic drugs (AEDs) phenytoin (PHT), carbamazepine (CBZ), phenobarbital (PB), and primidone, defined by the triad of fever, skin rash, and internal organ involvement.
Abstract: The antiepileptic drug hypersensitivity syndrome (AHS) is an adverse drug reaction associated with the aromatic antiepileptic drugs (AEDs) phenytoin (PHT), carbamazepine (CBZ), phenobarbital (PB), and primidone. The syndrome is defined by the triad of fever, skin rash, and internal organ involvement. It can also be caused by other drugs, such as sulfonamides, dapsone, minocycline, terbinafine, azathioprine, and allopurinol. Diagnosis of AHS may be difficult because of the variety of clinical and laboratory abnormalities and manifestations and because the syndrome may mimic infectious, neoplastic, or collagen vascular disorders. The incidence is approximately 1 in 3,000 exposures. AHS starts with fever, rash, and lymphadenopathy, within the first 2-8 weeks after initiation of therapy. Internal manifestations include, among others, agranulocytosis, hepatitis, nephritis, and myostitis. AHS is associated with a relative excess of reactive oxidative metabolites of the AED. Insufficient detoxification may lead to cell death or contribute to the formation of antigen that triggers an immune reaction. Crossreactivity among PHT, CBZ, and PB is as high as 70-80%.
156 citations
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TL;DR: There are several nonpharmacological interventions that may be effective for NPS in LTC, although there are a limited number of large-scale, high-quality studies in this area.
155 citations
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Memorial Sloan Kettering Cancer Center1, Indiana University2, Sarah Cannon Research Institute3, Baylor University4, Hebron University5, Mater Misericordiae University Hospital6, Sunnybrook Health Sciences Centre7, University of Sussex8, Vita-Salute San Raffaele University9, University of Chicago10, Washington University in St. Louis11, University of Nottingham12, Astellas Pharma13, Medivation14
TL;DR: The primary endpoint was clinical benefit (CR, PR or SD) at 16 wks (CBR16) in ‘Evaluable’ pts defined as having both AR IHC ≥10% and a response assessment.
Abstract: 1003 Background: The AR may be a therapeutic target for pts with androgen-driven TNBC. ENZA, a potent AR inhibitor, is approved in men with metastatic castration-resistant prostate cancer (mCRPC) and improves median PFS compared to bicalutamide in men with mCRPC (15.7 vs 5.8 mos; HR 0.44; p 0% by IHC; NCT01889238). Pts could be prescreened for AR, and have non-measurable bone disease and unlimited prior regimens; CNS metastases or seizure history were exclusionary. The primary endpoint was clinical benefit (CR, PR or SD) at 16 wks (CBR16) in ‘Evaluable’ pts defined as having both AR IHC ≥10% and a response assessment. CBR24, PFS, response rate, and safety were assessed. An androgen-driven gene signature (Dx) was created from gene profiling and outcomes were assessed accordingly. Stage 2 enrolled if CBR16 was ≥3 of 26 Evaluable pts; H0 was rejected if CBR16 was ≥9 in 62 yielding 85% po...
155 citations
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TL;DR: Gene expression changes in rat asbestos-induced malignant mesothelioma (MM) cells were investigated by differential mRNA display and data suggest that down-regulation of GPC3 is a common occurrence in MM and that G PC3, an X-linked recessive overgrowth gene, may encode a negative regulator of mesothelial cell growth.
Abstract: Gene expression changes in rat asbestos-induced malignant mesothelioma (MM) cells were investigated by differential mRNA display. A mRNA transcript identified by this approach was abundant in normal rat mesothelial cells but not expressed in rat MM cell lines. Northern blot analysis confirmed that this transcript is uniformly silenced in rat MM cell lines and primary tumors. Nucleotide sequence analysis revealed that this transcript is encoded by the rat glypican 3 gene (GPC3), whose human homolog is mutated in the Simpson-Golabi-Behmel overgrowth syndrome. Allelic loss at the GPC3 locus was infrequent (6.9%) in MM cell lines, and no mutations were found. GPC3 transcript levels were markedly decreased in 16 of 18 primary tumors and 17 of 22 human MM cell lines. Most of the cell lines were shown to have aberrant methylation of the GPC3 promoter region. In two of four human MM cell lines tested, GPC3 expression was restored after 2-deoxy 5-azacytidine (DAC)-mediated demethylation of its promoter region. Ectopic expression of GPC3 inhibited in vitro colony formation of human MM cells. Collectively, these data suggest that down-regulation of GPC3 is a common occurrence in MM and that GPC3, an X-linked recessive overgrowth gene, may encode a negative regulator of mesothelial cell growth.
155 citations
Authors
Showing all 7765 results
Name | H-index | Papers | Citations |
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Gordon B. Mills | 187 | 1273 | 186451 |
David A. Bennett | 167 | 1142 | 109844 |
Bruce R. Rosen | 148 | 684 | 97507 |
Robert Tibshirani | 147 | 593 | 326580 |
Steven A. Narod | 134 | 970 | 84638 |
Peter Palese | 132 | 526 | 57882 |
Gideon Koren | 129 | 1994 | 81718 |
John B. Holcomb | 120 | 733 | 53760 |
Julie A. Schneider | 118 | 492 | 56843 |
Patrick Maisonneuve | 118 | 582 | 53363 |
Mitch Dowsett | 114 | 478 | 62453 |
Ian D. Graham | 113 | 700 | 87848 |
Peter C. Austin | 112 | 657 | 60156 |
Sandra E. Black | 104 | 681 | 51755 |
Michael B. Yaffe | 102 | 379 | 41663 |