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
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TL;DR: In this article, the authors evaluated the relationship between efficacy and in vitro neutralizing and binding antibodies of 7 vaccines for which sufficient data have been generated, and they found a robust correlation was seen between neutralizing titer and efficacy.
600 citations
University of Southern California1, National Institutes of Health2, Memorial Sloan Kettering Cancer Center3, University of Massachusetts Amherst4, Yale University5, Karolinska Institutet6, University of Washington7, Maastricht University8, University of Pennsylvania9, QIMR Berghofer Medical Research Institute10, Vanderbilt University11, University of Minnesota12, Roswell Park Cancer Institute13, University of Toronto14, American Cancer Society15, University of South Florida16, Curie Institute17, City of Hope National Medical Center18, Alberta Health Services19, University at Buffalo20, Dartmouth College21, Harvard University22, University of Alberta23, University of New Mexico24, Fred Hutchinson Cancer Research Center25, University of California, Irvine26, Cancer Prevention Institute of California27
TL;DR: The results of this pooled analysis suggest that the two endometrial cancer types share many common etiologic factors, and the etiology of type II tumors may, therefore, not be completely estrogen independent, as previously believed.
Abstract: Purpose Endometrial cancers have long been divided into estrogen-dependent type I and the less common clinically aggressive estrogen-independent type II. Little is known about risk factors for type II tumors because most studies lack sufficient cases to study these much less common tumors separately. We examined whether so-called classical endometrial cancer risk factors also influence the risk of type II tumors. Patients and Methods Individual-level data from 10 cohort and 14 case-control studies from the Epidemiology of Endometrial Cancer Consortium were pooled. A total of 14,069 endometrial cancer cases and 35,312 controls were included. We classified endometrioid (n = 7,246), adenocarcinoma not otherwise specified (n = 4,830), and adenocarcinoma with squamous differentiation (n = 777) as type I tumors and serous (n = 508) and mixed cell (n = 346) as type II tumors. Results Parity, oral contraceptive use, cigarette smoking, age at menarche, and diabetes were associated with type I and type II tumors to...
599 citations
TL;DR: This article showed that a common stop codon polymorphism in the ligand-binding domain of TLR5 (TLR5392STOP) is associated with susceptibility to pneumonia caused by Legionella pneumophila.
Abstract: Although Toll-like receptors (TLRs) are critical mediators of the immune response to pathogens, the influence of polymorphisms in this gene family on human susceptibility to infection is poorly understood. We demonstrated recently that TLR5 recognizes flagellin, a potent inflammatory stimulus present in the flagellar structure of many bacteria. Here, we show that a common stop codon polymorphism in the ligand-binding domain of TLR5 (TLR5392STOP) is unable to mediate flagellin signaling, acts in a dominant fashion, and is associated with susceptibility to pneumonia caused by Legionella pneumophila, a flagellated bacterium. We also show that flagellin is a principal stimulant of proinflammatory cytokine production in lung epithelial cells. Together, these observations suggest that TLR5392STOP increases human susceptibility to infection through an unusual dominant mechanism that compromises TLR5's essential role as a regulator of the lung epithelial innate immune response.
599 citations
TL;DR: It is suggested that Mad-Max represses transcription by tethering mSin3 to DNA as corepressors and that a transcriptional repression mechanism is conserved from yeast to mammals.
598 citations
TL;DR: It is conceivable that transplantation of G-CSF-stimulated PBSC does not result in overwhelming acute GVHD because the graft contains predominantly Th2-inducing DC, and adoptive transfer of purified DC2 may be exploited to induce immune deviation after transplanting of hematopoietic stem cells or organ allografts.
598 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 |