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: Sentinel lymph node biopsy in early cervical cancer is a more sensitive procedure in detecting pelvic lymph node metastases compared to complete lymphadenectomy.
122 citations
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TL;DR: Long-term exposure to testosterone replacement therapy was associated with reduced risks of mortality, cardiovascular events, and prostate cancer, however, testosterone replacement Therapy increased the risk of mortality and cardiovascular events with short durations of therapy.
122 citations
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TL;DR: It is demonstrated that alpha 2 beta 1 integrin activation can result in the specific stimulation of tyrosine phosphorylation of 47-52-kDa proteins, as well as activation of a signaling pathway involving p21ras.
122 citations
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TL;DR: Among older adults with COPD, particularly those with asthma and those not receiving a long-acting anticholinergic medication, newly prescribed LABA and inhaled corticosteroid combination therapy, compared with newly prescribed LABAs alone, was associated with a significantly lower risk of the composite outcome of death or COPD hospitalization.
Abstract: RESULTS The main outcome was observed among 5594 new users of LABAs and inhaled corticosteroids (3174 deaths [36.4%]; 2420 COPD hospitalizations [27.8%]) and 2129 new users of LABAs alone (1179 deaths [37.3%]; 950 COPD hospitalizations [30.1%]). New use of LABAs and inhaled corticosteroids was associated with a modestly reduced risk of death or COPD hospitalization compared with new use of LABAs alone (difference in composite outcome at 5 years, −3.7%; 95% CI, −5.7% to −1.7%; hazard ratio [HR], 0.92; 95% CI, 0.88-0.96). The greatest difference was among COPD patients with a codiagnosis of asthma (difference in composite at 5 years, −6.5%; 95% CI, −10.3% to −2.7%; HR, 0.84; 95% CI, 0.77-0.91) and those who were not receiving inhaled long-acting anticholinergic medication (difference in composite at 5 years, −8.4%; 95% CI, −11.9% to −4.9%; HR, 0.79; 95% CI, 0.73-0.86). CONCLUSIONS AND RELEVANCE Among older adults with COPD, particularly those with asthma and those not receiving a long-acting anticholinergic medication, newly prescribed LABA and inhaled corticosteroid combination therapy, compared with newly prescribed LABAs alone, was associated with a significantly lower risk of the composite outcome of death or COPD hospitalization.
122 citations
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TL;DR: It is concluded that versican can stimulate cell proliferation via two mechanisms: through two EGF‐like motifs in the G3 domain which play a role in stimulating cell growth, and through the G1 domain, which destabilizes cell adhesion and facilitates cell growth.
Abstract: We have demonstrated previously that versican stimulated cell proliferation through the G3 domain. In these experiments, we show that versican mini-gene-transfected cell lines exhibited decreased cell-substratum interaction and increased cell proliferation. Exogenous addition of growth medium containing the versican gene product produced the same results. Because the G1 domain of versican is structurally similar to the G1 domain of aggrecan and to link protein, both of which play role in cell adhesion, we hypothesized that versican's proliferative effects may be a consequence of its ability to reduce cell adhesion, and may be mediated through the G1 domain. To investigate this, we expressed a G1 construct in NIH3T3 cells and showed that it reduced cell adhesion and enhanced cell proliferation. We then demonstrated that deletion of the G1 domain from versican greatly, but not completely, reversed the effects of versican: G1-deletion mutants of versican show slightly reduced amounts of cell adhesion and slightly increased rates of proliferation. We concluded that versican can stimulate cell proliferation via two mechanisms: through two EGF-like motifs in the G3 domain which play a role in stimulating cell growth, and through the G1 domain, which destabilizes cell adhesion and facilitates cell growth. We purified the G1 product with an affinity column and demonstrated that it reduced cell adhesion and enhanced cell proliferation.
122 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 |