Institution
Charles University in Prague
Education•Prague, Czechia•
About: Charles University in Prague is a education organization based out in Prague, Czechia. It is known for research contribution in the topics: Population & Large Hadron Collider. The organization has 32392 authors who have published 74435 publications receiving 1804208 citations.
Topics: Population, Large Hadron Collider, Czech, Magnetization, Transplantation
Papers published on a yearly basis
Papers
More filters
••
Instituto Português de Oncologia Francisco Gentil1, National Autonomous University of Mexico2, University of Valencia3, National Cheng Kung University4, University of Buenos Aires5, Universidad Nacional de Asunción6, Makerere University7, University of Chile8, American University of Beirut9, Hacettepe University10, Hospital General San Juan de Dios11, Lagos University Teaching Hospital12, University of Barcelona13, University of the Philippines14, Bangabandhu Sheikh Mujib Medical University15, Prince of Songkla University16, Peking Union Medical College17, Royal Women's Hospital18, Kanazawa University19, Charles University in Prague20, Harvard University21, VU University Amsterdam22, Kuwait University23, Columbia University Medical Center24, University of Crete25, Aristotle University of Thessaloniki26, Central University of Venezuela27, University of Las Palmas de Gran Canaria28, University of Antioquia29, Medical University of Lublin30, Western Galilee Hospital31
TL;DR: HPV types 16, 18, 31, 33, 35, 45, 52, and 58 should be given priority when the cross-protective effects of current vaccines are assessed, and for formulation of recommendations for the use of second-generation polyvalent HPV vaccines, according to this largest assessment of HPV genotypes to date.
Abstract: Summary Background Knowledge about the distribution of human papillomavirus (HPV) genotypes in invasive cervical cancer is crucial to guide the introduction of prophylactic vaccines. We aimed to provide novel and comprehensive data about the worldwide genotype distribution in patients with invasive cervical cancer. Methods Paraffin-embedded samples of histologically confirmed cases of invasive cervical cancer were collected from 38 countries in Europe, North America, central South America, Africa, Asia, and Oceania. Inclusion criteria were a pathological confirmation of a primary invasive cervical cancer of epithelial origin in the tissue sample selected for analysis of HPV DNA, and information about the year of diagnosis. HPV detection was done by use of PCR with SPF-10 broad-spectrum primers followed by DNA enzyme immunoassay and genotyping with a reverse hybridisation line probe assay. Sequence analysis was done to characterise HPV-positive samples with unknown HPV types. Data analyses included algorithms of multiple infections to estimate type-specific relative contributions. Findings 22 661 paraffin-embedded samples were obtained from 14 249 women. 10 575 cases of invasive cervical cancer were included in the study, and 8977 (85%) of these were positive for HPV DNA. The most common HPV types were 16, 18, 31, 33, 35, 45, 52, and 58 with a combined worldwide relative contribution of 8196 of 8977 (91%, 95% CI 90–92). HPV types 16 and 18 were detected in 6357 of 8977 of cases (71%, 70–72) of invasive cervical cancer. HPV types 16, 18, and 45 were detected in 443 of 470 cases (94%, 92–96) of cervical adenocarcinomas. Unknown HPV types that were identified with sequence analysis were 26, 30, 61, 67, 69, 82, and 91 in 103 (1%) of 8977 cases of invasive cervical cancer. Women with invasive cervical cancers related to HPV types 16, 18, or 45 presented at a younger mean age than did those with other HPV types (50·0 years [49·6–50·4], 48·2 years [47·3–49·2], 46·8 years [46·6–48·1], and 55·5 years [54·9–56·1], respectively). Interpretation To our knowledge, this study is the largest assessment of HPV genotypes to date. HPV types 16, 18, 31, 33, 35, 45, 52, and 58 should be given priority when the cross-protective effects of current vaccines are assessed, and for formulation of recommendations for the use of second-generation polyvalent HPV vaccines. Our results also suggest that type-specific high-risk HPV-DNA-based screening tests and protocols should focus on HPV types 16, 18, and 45. Funding Spanish grants from Instituto de Salud Carlos III, Agencia de Gestio d'Ajuts Universitaris i de Recerca, Marato de TV3 Foundation, and unrestricted grants from GlaxoSmithKline Biologicals, Sanofi Pasteur MSD, and Merck.
2,145 citations
••
TL;DR: Dabrafenib plus trametinib, as compared with vemurafenib monotherapy, significantly improved overall survival in previously untreated patients with metastatic melanoma with BRAF V600E or V600K mutations, without increased overall toxicity.
Abstract: Background The BRAF inhibitors vemurafenib and dabrafenib have shown efficacy as monotherapies in patients with previously untreated metastatic melanoma with BRAF V600E or V600K mutations. Combining dabrafenib and the MEK inhibitor trametinib, as compared with dabrafenib alone, enhanced antitumor activity in this population of patients. Methods In this open-label, phase 3 trial, we randomly assigned 704 patients with metastatic melanoma with a BRAF V600 mutation to receive either a combination of dabrafenib (150 mg twice daily) and trametinib (2 mg once daily) or vemurafenib (960 mg twice daily) orally as first-line therapy. The primary end point was overall survival. Results At the preplanned interim overall survival analysis, which was performed after 77% of the total number of expected events occurred, the overall survival rate at 12 months was 72% (95% confidence interval [CI], 67 to 77) in the combination-therapy group and 65% (95% CI, 59 to 70) in the vemurafenib group (hazard ratio for death in the combination-therapy group, 0.69; 95% CI, 0.53 to 0.89; P = 0.005). The prespecified interim stopping boundary was crossed, and the study was stopped for efficacy in July 2014. Median progression-free survival was 11.4 months in the combinationtherapy group and 7.3 months in the vemurafenib group (hazard ratio, 0.56; 95% CI, 0.46 to 0.69; P<0.001). The objective response rate was 64% in the combinationtherapy group and 51% in the vemurafenib group (P<0.001). Rates of severe adverse events and study-drug discontinuations were similar in the two groups. Cutaneous squamous-cell carcinoma and keratoacanthoma occurred in 1% of patients in the combination-therapy group and 18% of those in the vemurafenib group. Conclusions Dabrafenib plus trametinib, as compared with vemurafenib monotherapy, significantly improved overall survival in previously untreated patients with metastatic melanoma with BRAF V600E or V600K mutations, without increased overall toxicity. (Funded by GlaxoSmithKline; ClinicalTrials.gov number, NCT01597908.)
2,144 citations
••
Clinical Trial Service Unit1, University College London2, North Bristol NHS Trust3, University of Würzburg4, The George Institute for Global Health5, Children's Hospital at Westmead6, Peking Union Medical College7, Sultanah Aminah Hospital8, University of British Columbia9, National Institutes of Health10, Brigham and Women's Hospital11, University of Minnesota12, University of Otago13, University of Picardie Jules Verne14, University of Copenhagen15, Chiang Mai University16, Oslo University Hospital17, Charles University in Prague18, Medical University of Silesia19, Utrecht University20, University Medical Center Groningen21, University of Helsinki22, John Radcliffe Hospital23
TL;DR: Reduction of LDL cholesterol with simvastatin 20 mg plus ezetimibe 10 mg daily safely reduced the incidence of major atherosclerotic events in a wide range of patients with advanced chronic kidney disease.
2,123 citations
••
University of California, San Diego1, University of Western Ontario2, Katholieke Universiteit Leuven3, University of Chicago4, Lille University of Science and Technology5, Icahn School of Medicine at Mount Sinai6, Charles University in Prague7, University of Alberta8, University of Washington9, University of British Columbia10, Millennium Pharmaceuticals11
TL;DR: Vedolizumab-treated patients with active Crohn's disease were more likely than patients receiving placebo to have a remission, but not a CDAI-100 response, at week 6; patients with a response to induction therapy who continued to receive vedolIZumab (rather than switching to placebo) were morelikely to be in remission at week 52.
Abstract: BackgroundUstekinumab, a monoclonal antibody to the p40 subunit of interleukin-12 and interleukin-23, was evaluated as an intravenous induction therapy in two populations with moderately to severely active Crohn’s disease. Ustekinumab was also evaluated as subcutaneous maintenance therapy. MethodsWe randomly assigned patients to receive a single intravenous dose of ustekinumab (either 130 mg or approximately 6 mg per kilogram of body weight) or placebo in two induction trials. The UNITI-1 trial included 741 patients who met the criteria for primary or secondary nonresponse to tumor necrosis factor (TNF) antagonists or had unacceptable side effects. The UNITI-2 trial included 628 patients in whom conventional therapy failed or unacceptable side effects occurred. Patients who completed these induction trials then participated in IM-UNITI, in which the 397 patients who had a response to ustekinumab were randomly assigned to receive subcutaneous maintenance injections of 90 mg of ustekinumab (either every 8 w...
2,059 citations
••
15 Apr 2010
TL;DR: Systematic studies of more than 25,000 cancer genomes will reveal the repertoire of oncogenic mutations, uncover traces of the mutagenic influences, define clinically relevant subtypes for prognosis and therapeutic management, and enable the development of new cancer therapies.
Abstract: The International Cancer Genome Consortium (ICGC) was launched to coordinate large-scale cancer genome studies in tumours from 50 different cancer types and/or subtypes that are of clinical and societal importance across the globe. Systematic studies of more than 25,000 cancer genomes at the genomic, epigenomic and transcriptomic levels will reveal the repertoire of oncogenic mutations, uncover traces of the mutagenic influences, define clinically relevant subtypes for prognosis and therapeutic management, and enable the development of new cancer therapies.
2,041 citations
Authors
Showing all 32719 results
Name | H-index | Papers | Citations |
---|---|---|---|
Ronald C. Petersen | 178 | 1091 | 153067 |
P. Chang | 170 | 2154 | 151783 |
Vaclav Vrba | 141 | 1298 | 95671 |
Milos Lokajicek | 139 | 1511 | 98888 |
Christopher D. Manning | 138 | 499 | 147595 |
Yves Sirois | 137 | 1334 | 95714 |
Rupert Leitner | 136 | 1201 | 90597 |
Gerald M. Reaven | 133 | 799 | 80351 |
Roberto Sacchi | 132 | 1186 | 89012 |
S. Errede | 132 | 1481 | 98663 |
Mark Neubauer | 131 | 1252 | 89004 |
Peter Kodys | 131 | 1262 | 85267 |
Panos A Razis | 130 | 1287 | 90704 |
Vit Vorobel | 130 | 919 | 79444 |
Jehad Mousa | 130 | 1226 | 86564 |