Institution
Astellas Pharma
Company•Tokyo, Japan•
About: Astellas Pharma is a company organization based out in Tokyo, Japan. It is known for research contribution in the topics: Overactive bladder & Population. The organization has 3717 authors who have published 3635 publications receiving 85863 citations. The organization is also known as: Asuterasu Seiyaku Kabushiki-gaisha.
Topics: Overactive bladder, Population, Mirabegron, Solifenacin, Enzalutamide
Papers published on a yearly basis
Papers
More filters
••
Oregon Health & Science University1, Duke University2, Memorial Sloan Kettering Cancer Center3, University of Paris-Sud4, University of Washington5, Guy's and St Thomas' NHS Foundation Trust6, Institute of Cancer Research7, University of California, Berkeley8, University Health Network9, Nippon Medical School10, Charité11, Astellas Pharma12, Université de Montréal13, Harvard University14, University of Alberta15, Cliniques Universitaires Saint-Luc16
TL;DR: Enzalutamide significantly decreased the risk of radiographic progression and death and delayed the initiation of chemotherapy in men with metastatic prostate cancer.
Abstract: BACKGROUND: Enzalutamide is an oral androgen-receptor inhibitor that prolongs survival in men with metastatic castration-resistant prostate cancer in whom the disease has progressed after chemotherapy. New treatment options are needed for patients with metastatic prostate cancer who have not received chemotherapy, in whom the disease has progressed despite androgen-deprivation therapy. METHODS: In this double-blind, phase 3 study, we randomly assigned 1717 patients to receive either enzalutamide (at a dose of 160 mg) or placebo once daily. The coprimary end points were radiographic progression-free survival and overall survival. RESULTS: The study was stopped after a planned interim analysis, conducted when 540 deaths had been reported, showed a benefit of the active treatment. The rate of radiographic progression-free survival at 12 months was 65% among patients treated with enzalutamide, as compared with 14% among patients receiving placebo (81% risk reduction; hazard ratio in the enzalutamide group, 0.19; 95% confidence interval [CI], 0.15 to 0.23; P<0.001). A total of 626 patients (72%) in the enzalutamide group, as compared with 532 patients (63%) in the placebo group, were alive at the data-cutoff date (29% reduction in the risk of death; hazard ratio, 0.71; 95% CI, 0.60 to 0.84; P<0.001). The benefit of enzalutamide was shown with respect to all secondary end points, including the time until the initiation of cytotoxic chemotherapy (hazard ratio, 0.35), the time until the first skeletal-related event (hazard ratio, 0.72), a complete or partial soft-tissue response (59% vs. 5%), the time until prostate-specific antigen (PSA) progression (hazard ratio, 0.17), and a rate of decline of at least 50% in PSA (78% vs. 3%) (P<0.001 for all comparisons). Fatigue and hypertension were the most common clinically relevant adverse events associated with enzalutamide treatment. CONCLUSIONS: Enzalutamide significantly decreased the risk of radiographic progression and death and delayed the initiation of chemotherapy in men with metastatic prostate cancer. (Funded by Medivation and Astellas Pharma; PREVAIL ClinicalTrials.gov number, NCT01212991.).
2,426 citations
••
TL;DR: A basis for thalidomide teratogenicity is revealed and may contribute to the development of new thalidmide derivatives without teratogenic activity.
Abstract: Half a century ago, thalidomide was widely prescribed to pregnant women as a sedative but was found to be teratogenic, causing multiple birth defects. Today, thalidomide is still used in the treatment of leprosy and multiple myeloma, although how it causes limb malformation and other developmental defects is unknown. Here, we identified cereblon (CRBN) as a thalidomide-binding protein. CRBN forms an E3 ubiquitin ligase complex with damaged DNA binding protein 1 (DDB1) and Cul4A that is important for limb outgrowth and expression of the fibroblast growth factor Fgf8 in zebrafish and chicks. Thalidomide initiates its teratogenic effects by binding to CRBN and inhibiting the associated ubiquitin ligase activity. This study reveals a basis for thalidomide teratogenicity and may contribute to the development of new thalidomide derivatives without teratogenic activity.
1,510 citations
••
TL;DR: It is shown that reprogramming factors can activate the p53 (also known as Trp53 in mice, TP53 in humans) pathway and silencing of p53 significantly increased the reprograming efficiency of human somatic cells.
Abstract: Reprogramming somatic cells to induced pluripotent stem (iPS) cells has been accomplished by expressing pluripotency factors and oncogenes, but the low frequency and tendency to induce malignant transformation compromise the clinical utility of this powerful approach. We address both issues by investigating the mechanisms limiting reprogramming efficiency in somatic cells. Here we show that reprogramming factors can activate the p53 (also known as Trp53 in mice, TP53 in humans) pathway. Reducing signalling to p53 by expressing a mutated version of one of its negative regulators, by deleting or knocking down p53 or its target gene, p21 (also known as Cdkn1a), or by antagonizing reprogramming-induced apoptosis in mouse fibroblasts increases reprogramming efficiency. Notably, decreasing p53 protein levels enabled fibroblasts to give rise to iPS cells capable of generating germline-transmitting chimaeric mice using only Oct4 (also known as Pou5f1) and Sox2. Furthermore, silencing of p53 significantly increased the reprogramming efficiency of human somatic cells. These results provide insights into reprogramming mechanisms and suggest new routes to more efficient reprogramming while minimizing the use of oncogenes.
1,111 citations
••
TL;DR: Among men with nonmetastatic, castration‐resistant prostate cancer with a rapidly rising PSA level, enzalutamide treatment led to a clinically meaningful and significant 71% lower risk of metastasis or death than placebo.
Abstract: Background Men with nonmetastatic, castration-resistant prostate cancer and a rapidly rising prostate-specific antigen (PSA) level are at high risk for metastasis. We hypothesized that enz...
711 citations
••
University of Pennsylvania1, University of Texas MD Anderson Cancer Center2, University of Marburg3, Memorial Sloan Kettering Cancer Center4, University of Bologna5, Carlos III Health Institute6, University of Maryland, Baltimore7, University of Chicago8, University of Minnesota9, University of Alabama at Birmingham10, Medical University of South Carolina11, University of California, San Francisco12, Thomas Jefferson University13, National Taiwan University14, Yale University15, Centre Hospitalier Universitaire de Toulouse16, University of Fukui17, Seoul National University18, University of Ulsan19, Wake Forest University20, Harvard University21, Astellas Pharma22, Johns Hopkins University23
TL;DR: Gilteritinib resulted in significantly longer survival and higher percentages of patients with remission than salvage chemotherapy among patients with relapsed or refractory FLT3-mutated AML.
Abstract: Background Patients with relapsed or refractory acute myeloid leukemia (AML) with mutations in the FMS-like tyrosine kinase 3 gene (FLT3) infrequently have a response to salvage chemothera...
687 citations
Authors
Showing all 3718 results
Name | H-index | Papers | Citations |
---|---|---|---|
Ronald M. Evans | 199 | 708 | 166722 |
Shuh Narumiya | 137 | 595 | 70183 |
Minoru Yoshida | 111 | 783 | 55767 |
Yuichi Sugiyama | 107 | 799 | 46197 |
Shuji Ogino | 106 | 549 | 43073 |
Toshio Suda | 104 | 580 | 41069 |
Michael J.E. Sternberg | 93 | 327 | 39429 |
Joel E. Kleinman | 92 | 436 | 29593 |
X. Shirley Liu | 86 | 230 | 47987 |
Nobutaka Fujii | 83 | 695 | 28626 |
Nancy L. Ascher | 75 | 431 | 23244 |
Mitsuo Oshimura | 75 | 426 | 21860 |
George G. Nomikos | 70 | 202 | 13581 |
Haruki Nakamura | 69 | 513 | 19792 |
Lynne S. Taylor | 68 | 407 | 17489 |