Institution
Fred Hutchinson Cancer Research Center
Nonprofit•Cape Town, South Africa•
About: Fred Hutchinson Cancer Research Center is a nonprofit organization based out in Cape Town, South Africa. It is known for research contribution in the topics: Population & Transplantation. The organization has 12322 authors who have published 30954 publications receiving 2288772 citations. The organization is also known as: Fred Hutch & The Hutch.
Topics: Population, Transplantation, Cancer, Breast cancer, Prostate cancer
Papers published on a yearly basis
Papers
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TL;DR: The HLH domain can mediate heterodimer formation between either daughterless, E12, or E47 and achaete-scute T3 or MyoD to form proteins with high affinity for the kappa E2 site in the immunoglobulin kappa chain enhancer.
1,736 citations
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University of Cambridge1, Harvard University2, Peking University3, National Institutes of Health4, University of Oxford5, Curtin University6, Australian National University7, Imperial College London8, American Cancer Society9, University of Southern California10, Johns Hopkins University11, University of Sydney12, Vanderbilt University13, Chinese Center for Disease Control and Prevention14, University of Bristol15, Capital Medical University16, Erasmus University Rotterdam17, Yonsei University18, Fred Hutchinson Cancer Research Center19, University of Turin20, University of Glasgow21, University of North Carolina at Chapel Hill22, Shiga University of Medical Science23, Innsbruck Medical University24, International Agency for Research on Cancer25, University of Hong Kong26, Massey University27
TL;DR: The associations of both overweight and obesity with higher all-cause mortality were broadly consistent in four continents and supports strategies to combat the entire spectrum of excess adiposity in many populations.
1,731 citations
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University of California, Los Angeles1, Wayne State University2, University of California, San Diego3, Stanford University4, University of Cincinnati5, Stony Brook University6, Fred Hutchinson Cancer Research Center7, Medical College of Wisconsin8, Brown University9, NorthShore University HealthSystem10, University of Hawaii at Manoa11
TL;DR: Relatively short-term combined estrogen plus progestin use increases incident breast cancers, which are diagnosed at a more advanced stage compared with placebo use, and also substantially increases the percentage of women with abnormal mammograms, a pattern which continued for the study duration.
Abstract: ContextThe Women's Health Initiative trial of combined estrogen plus progestin
was stopped early when overall health risks, including invasive breast cancer,
exceeded benefits. Outstanding issues not previously addressed include characteristics
of breast cancers observed among women using hormones and whether diagnosis
may be influenced by hormone effects on mammography.ObjectiveTo determine the relationship among estrogen plus progestin use, breast
cancer characteristics, and mammography recommendations.Design, Setting, and ParticipantsFollowing a comprehensive breast cancer risk assessment, 16 608
postmenopausal women aged 50 to 79 years with an intact uterus were randomly
assigned to receive combined conjugated equine estrogens (0.625 mg/d) plus
medroxyprogesterone acetate (2.5 mg/d) or placebo from 1993 to 1998 at 40
clinical centers. Screening mammography and clinical breast examinations were
performed at baseline and yearly thereafter.Main Outcome MeasuresBreast cancer number and characteristics, and frequency of abnormal
mammograms by estrogen plus progestin exposure.ResultsIn intent-to-treat analyses, estrogen plus progestin increased total
(245 vs 185 cases; hazard ratio [HR], 1.24; weighted P<.001)
and invasive (199 vs 150 cases; HR, 1.24; weighted P =
.003) breast cancers compared with placebo. The invasive breast cancers diagnosed
in the estrogen plus progestin group were similar in histology and grade but
were larger (mean [SD], 1.7 cm [1.1] vs 1.5 cm [0.9], respectively; P = .04) and were at more advanced stage (regional/metastatic
25.4% vs 16.0%, respectively; P = .04) compared with
those diagnosed in the placebo group. After 1 year, the percentage of women
with abnormal mammograms was substantially greater in the estrogen plus progestin
group (716 [9.4%] of 7656) compared with placebo group (398 [5.4%] of 7310; P<.001), a pattern which continued for the study duration.ConclusionsRelatively short-term combined estrogen plus progestin use increases
incident breast cancers, which are diagnosed at a more advanced stage compared
with placebo use, and also substantially increases the percentage of women
with abnormal mammograms. These results suggest estrogen plus progestin may
stimulate breast cancer growth and hinder breast cancer diagnosis.
1,707 citations
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TL;DR: Long-term exposure to fine particulate air pollution is associated with the incidence of cardiovascular disease and death among postmenopausal women and the between-city effect appeared to be smaller than the within- city effect.
Abstract: A total of 1816 women had one or more fatal or nonfatal cardiovascular events, as confirmed by a review of medical records, including death from coronary heart disease or cerebrovascular disease, coronary revascularization, myocardial infarction, and stroke. In 2000, levels of PM2.5 exposure varied from 3.4 to 28.3 μg per cubic meter (mean, 13.5). Each increase of 10 μg per cubic meter was associated with a 24% increase in the risk of a cardiovascular event (hazard ratio, 1.24; 95% confidence interval [CI], 1.09 to 1.41) and a 76% increase in the risk of death from cardiovascular disease (hazard ratio, 1.76; 95% CI, 1.25 to 2.47). For cardiovascular events, the between-city effect appeared to be smaller than the within-city effect. The risk of cerebrovascular events was also associated with increased levels of PM2.5 (hazard ratio, 1.35; 95% CI, 1.08 to 1.68). Conclusions Long-term exposure to fine particulate air pollution is associated with the incidence of cardiovascular disease and death among postmenopausal women. Exposure differences within cities are associated with the risk of cardiovascular disease.
1,704 citations
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University of Bologna1, University of Utah2, University of Jena3, Imperial College London4, University of Barcelona5, Royal Liverpool and Broadgreen University Hospital NHS Trust6, University of Texas MD Anderson Cancer Center7, University of Poitiers8, Norwegian University of Science and Technology9, University of Adelaide10, Catholic University of Korea11, University of Chicago12, University of Toronto13, University of Bordeaux14, Masaryk University15, Heidelberg University16, Leipzig University17, University of Naples Federico II18, Fred Hutchinson Cancer Research Center19, University of Turin20, Wayne State University21, Cornell University22, Uppsala University23
TL;DR: Optimal responders to chronic myeloid leukemia treatment should continue therapy indefinitely, with careful surveillance, or they can be enrolled in controlled studies of treatment discontinuation once a deeper molecular response is achieved.
1,679 citations
Authors
Showing all 12368 results
Name | H-index | Papers | Citations |
---|---|---|---|
Walter C. Willett | 334 | 2399 | 413322 |
Robert Langer | 281 | 2324 | 326306 |
Meir J. Stampfer | 277 | 1414 | 283776 |
JoAnn E. Manson | 270 | 1819 | 258509 |
David J. Hunter | 213 | 1836 | 207050 |
Peer Bork | 206 | 697 | 245427 |
Eric Boerwinkle | 183 | 1321 | 170971 |
Ruedi Aebersold | 182 | 879 | 141881 |
Bruce M. Psaty | 181 | 1205 | 138244 |
Aaron R. Folsom | 181 | 1118 | 134044 |
David Baker | 173 | 1226 | 109377 |
Frederick W. Alt | 171 | 577 | 95573 |
Lily Yeh Jan | 162 | 467 | 73655 |
Yuh Nung Jan | 162 | 460 | 74818 |
Charles N. Serhan | 158 | 728 | 84810 |