Institution
Lund University
Education•Lund, Sweden•
About: Lund University is a education organization based out in Lund, Sweden. It is known for research contribution in the topics: Population & Cancer. The organization has 42345 authors who have published 124676 publications receiving 5016438 citations. The organization is also known as: Lunds Universitet & University of Lund.
Topics: Population, Cancer, Insulin, Breast cancer, Diabetes mellitus
Papers published on a yearly basis
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TL;DR: Sufficient evidence exists to recommend HPV testing in triage of women with atypical cytology and in surveillance after treatment of CIN lesions, and the European screening policy will be reviewed based on the longitudinal results of randomised population trials which are currently underway.
533 citations
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TL;DR: In this paper, the authors explored the prevalence of cells with different CD44/CD24 phenotypes within breast cancer subtypes and demonstrated an association between basal-like and particularly BRCA1 hereditary breast cancer and the presence of CD44+/cd24- cells.
Abstract: Human breast tumors are heterogeneous and consist of phenotypically diverse cells. Breast cancer cells with a CD44+/CD24- phenotype have been suggested to have tumor-initiating properties with stem cell-like and invasive features, although it is unclear whether their presence within a tumor has clinical implications. There is also a large heterogeneity between tumors, illustrated by reproducible stratification into various subtypes based on gene expression profiles or histopathological features. We have explored the prevalence of cells with different CD44/CD24 phenotypes within breast cancer subtypes. Double-staining immunohistochemistry was used to quantify CD44 and CD24 expression in 240 human breast tumors for which information on other tumor markers and clinical characteristics was available. Gene expression data were also accessible for a cohort of the material. A considerable heterogeneity in CD44 and CD24 expression was seen both between and within tumors. A complete lack of both proteins was evident in 35% of the tumors, while 13% contained cells of more than one of the CD44+/CD24-, CD44-/CD24+ and CD44+/CD24+ phenotypes. CD44+/CD24- cells were detected in 31% of the tumors, ranging in proportion from only a few to close to 100% of tumor cells. The CD44+/CD24- phenotype was most common in the basal-like subgroup – characterized as negative for the estrogen and progesterone receptors as well as for HER2, and as positive for cytokeratin 5/14 and/or epidermal growth factor receptor, and particularly common in BRCA1 hereditary tumors, of which 94% contained CD44+/CD24- cells. The CD44+/CD24- phenotype was surprisingly scarce in HER2+ tumors, which had a predominantly CD24+ status. A CD44+/CD24- gene expression signature was generated, which included CD44 and α6-integrin (CD49f) among the top-ranked overexpressed genes. We demonstrate an association between basal-like and particularly BRCA1 hereditary breast cancer and the presence of CD44+/CD24- cells. Not all basal-like tumors and very few HER2+ tumors, however, contain CD44+/CD24- cells, emphasizing that a putative tumorigenic ability may not be confined to cells of this phenotype and that other breast cancer stem cell markers remain to be identified.
533 citations
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TL;DR: The determination of methane potentials is a biological method subject to relatively large variation due to the use of non-standardized inoculum and waste heterogeneity, therefore, procedures for addressing repeatability and reproducibility are suggested.
532 citations
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TL;DR: A novel population-based approach to identify metastases from both death certificates and national inpatient data to describe metastatic pathways in lung cancer patients found liver metastases conferred the worst prognosis, especially for large cell histology.
530 citations
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National Institute for Health Research1, University of Leicester2, Wellcome Trust Centre for Human Genetics3, University of Oxford4, University of Cambridge5, Queen Mary University of London6, Technische Universität München7, Stanford University8, Icahn School of Medicine at Mount Sinai9, Imperial College London10, Imperial College Healthcare11, London North West Healthcare NHS Trust12, University of Dundee13, University of Leeds14, Massachusetts Institute of Technology15, Tartu University Hospital16, University of Ioannina17, Harvard University18, Umeå University19, Lund University20, Peking Union Medical College21, University College London22, University of Tampere23, Vanderbilt University24, Medical University of Graz25, Synlab Group26, Heidelberg University27, University of Ottawa28, University of Tartu29, Lebanese American University30, King Abdulaziz University31, University of Manchester32, Central Manchester University Hospitals NHS Foundation Trust33, National Institutes of Health34, St Bartholomew's Hospital35, Manchester Academic Health Science Centre36, Wellcome Trust Sanger Institute37, University of Lübeck38, Harokopio University39, Karolinska University Hospital40
TL;DR: This approach identified 13 new loci at genome-wide significance, 12 of which were on the previous list of loci meeting the 5% FDR threshold, thus providing strong support that the remaining loci identified by FDR represent genuine signals.
Abstract: Genome-wide association studies (GWAS) in coronary artery disease (CAD) had identified 66 loci at 'genome-wide significance' (P < 5 × 10-8) at the time of this analysis, but a much larger number of putative loci at a false discovery rate (FDR) of 5% (refs. 1,2,3,4). Here we leverage an interim release of UK Biobank (UKBB) data to evaluate the validity of the FDR approach. We tested a CAD phenotype inclusive of angina (SOFT; ncases = 10,801) as well as a stricter definition without angina (HARD; ncases = 6,482) and selected cases with the former phenotype to conduct a meta-analysis using the two most recent CAD GWAS. This approach identified 13 new loci at genome-wide significance, 12 of which were on our previous list of loci meeting the 5% FDR threshold, thus providing strong support that the remaining loci identified by FDR represent genuine signals. The 304 independent variants associated at 5% FDR in this study explain 21.2% of CAD heritability and identify 243 loci that implicate pathways in blood vessel morphogenesis as well as lipid metabolism, nitric oxide signaling and inflammation.
529 citations
Authors
Showing all 42777 results
Name | H-index | Papers | Citations |
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Yi Chen | 217 | 4342 | 293080 |
Fred H. Gage | 216 | 967 | 185732 |
Kari Stefansson | 206 | 794 | 174819 |
Mark I. McCarthy | 200 | 1028 | 187898 |
Ruedi Aebersold | 182 | 879 | 141881 |
Jie Zhang | 178 | 4857 | 221720 |
Feng Zhang | 172 | 1278 | 181865 |
Martin G. Larson | 171 | 620 | 117708 |
Michael Snyder | 169 | 840 | 130225 |
Unnur Thorsteinsdottir | 167 | 444 | 121009 |
Anders Björklund | 165 | 769 | 84268 |
Carl W. Cotman | 165 | 809 | 105323 |
Dennis R. Burton | 164 | 683 | 90959 |
Jaakko Kaprio | 163 | 1532 | 126320 |
Panos Deloukas | 162 | 410 | 154018 |