Institution
Poznan University of Medical Sciences
Education•Poznań, Poland•
About: Poznan University of Medical Sciences is a education organization based out in Poznań, Poland. It is known for research contribution in the topics: Population & Cancer. The organization has 5021 authors who have published 10098 publications receiving 145607 citations.
Topics: Population, Cancer, Diabetes mellitus, Bipolar disorder, Pregnancy
Papers published on a yearly basis
Papers
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TL;DR: The current status of TCGA Research Network structure, purpose, and achievements are discussed, to provide publicly available datasets to help improve diagnostic methods, treatment standards, and finally to prevent cancer.
Abstract: The Cancer Genome Atlas (TCGA) is a public funded project that aims to catalogue and discover major cancer-causing genomic alterations to create a comprehensive "atlas" of cancer genomic profiles. So far, TCGA researchers have analysed large cohorts of over 30 human tumours through large-scale genome sequencing and integrated multi-dimensional analyses. Studies of individual cancer types, as well as comprehensive pan-cancer analyses have extended current knowledge of tumorigenesis. A major goal of the project was to provide publicly available datasets to help improve diagnostic methods, treatment standards, and finally to prevent cancer. This review discusses the current status of TCGA Research Network structure, purpose, and achievements.
2,530 citations
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University of Arizona1, Ludwig Maximilian University of Munich2, Technische Universität München3, Hospital Universitario La Paz4, Katholieke Universiteit Leuven5, Hebrew University of Jerusalem6, Innsbruck Medical University7, Poznan University of Medical Sciences8, Stanford University9, Oslo University Hospital10, University of Oslo11, BC Cancer Agency12, University of Texas MD Anderson Cancer Center13, Linköping University14, McGill University15, Cedars-Sinai Medical Center16, VA Boston Healthcare System17, Harvard University18
TL;DR: Among patients with platinum-sensitive, recurrent ovarian cancer, the median duration of progression-free survival was significantly longer amongThose receiving niraparib than among those receiving placebo, regardless of the presence or absence of gBRCA mutations or HRD status, with moderate bone marrow toxicity.
Abstract: Tesaro; Amgen; Genentech; Roche; AstraZeneca; Myriad Genetics; Merck; Gradalis; Cerulean; Vermillion; ImmunoGen; Pfizer; Bayer; Nu-Cana BioMed; INSYS Therapeutics; GlaxoSmithKline; Verastem; Mateon Therapeutics; Pharmaceutical Product Development; Clovis Oncology; Janssen/Johnson Johnson; Eli Lilly; Merck Sharp Dohme
1,686 citations
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TL;DR: The flagship paper of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes Consortium describes the generation of the integrative analyses of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types, the structures for international data sharing and standardized analyses, and the main scientific findings from across the consortium studies.
Abstract: Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale1,2,3. Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4–5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter4; identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation5,6; analyses timings and patterns of tumour evolution7; describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity8,9; and evaluates a range of more-specialized features of cancer genomes8,10,11,12,13,14,15,16,17,18.
1,600 citations
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TL;DR: Molecular similarities among histologically or anatomically related cancer types provide a basis for focused pan-cancer analyses, such as pan-gastrointestinal, Pan-gynecological, pan-kidney, and pan-squamous cancers, and those related by stemness features, which may inform strategies for future therapeutic development.
1,535 citations
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Verneri Anttila1, Verneri Anttila2, Brendan Bulik-Sullivan1, Brendan Bulik-Sullivan2 +717 more•Institutions (270)
TL;DR: It is demonstrated that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine, and it is shown that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures.
Abstract: Disorders of the brain can exhibit considerable epidemiological comorbidity and often share symptoms, provoking debate about their etiologic overlap. We quantified the genetic sharing of 25 brain disorders from genome-wide association studies of 265,218 patients and 784,643 control participants and assessed their relationship to 17 phenotypes from 1,191,588 individuals. Psychiatric disorders share common variant risk, whereas neurological disorders appear more distinct from one another and from the psychiatric disorders. We also identified significant sharing between disorders and a number of brain phenotypes, including cognitive measures. Further, we conducted simulations to explore how statistical power, diagnostic misclassification, and phenotypic heterogeneity affect genetic correlations. These results highlight the importance of common genetic variation as a risk factor for brain disorders and the value of heritability-based methods in understanding their etiology.
1,357 citations
Authors
Showing all 5055 results
Name | H-index | Papers | Citations |
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Thorkild I. A. Sørensen | 114 | 747 | 60060 |
Ingrid E. Scheffer | 113 | 585 | 53463 |
Kim A. Papp | 82 | 361 | 28368 |
Carle Paul | 72 | 437 | 21426 |
Sirkka Keinänen-Kiukaanniemi | 69 | 372 | 29268 |
George R. Blumenschein | 64 | 358 | 21605 |
Janusz K. Rybakowski | 59 | 485 | 14097 |
Marie-Claude Morice | 58 | 279 | 22264 |
Joerg Lahann | 56 | 262 | 13872 |
Roman Kaliszan | 54 | 282 | 9089 |
Karl-Heinz Herzig | 54 | 321 | 12623 |
Matti Uusitupa | 54 | 123 | 34387 |
Joanna Hauser | 53 | 196 | 9860 |
Maria Siemionow | 47 | 350 | 8055 |
Sakari Reitamo | 46 | 148 | 7381 |