Institution
University of Tübingen
Education•Tübingen, Germany•
About: University of Tübingen is a education organization based out in Tübingen, Germany. It is known for research contribution in the topics: Population & Transplantation. The organization has 40555 authors who have published 84108 publications receiving 3015320 citations. The organization is also known as: Eberhard Karls University & Eberhard-Karls-Universität Tübingen.
Topics: Population, Transplantation, Immune system, Antigen, T cell
Papers published on a yearly basis
Papers
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Rolf C. Hagen Group1, University of Tübingen2, University of Hamburg3, Lund University4, Karolinska Institutet5, University of Copenhagen6, Radboud University Nijmegen7, Erasmus University Rotterdam8, Charité9, Institut Gustave Roussy10, University of Duisburg-Essen11, University of Cologne12, The Royal Marsden NHS Foundation Trust13, Norwegian University of Science and Technology14, University of British Columbia15, Hannover Medical School16, University of Amsterdam17, Hochschule Hannover18, Southampton General Hospital19, Oregon Health & Science University20, St Bartholomew's Hospital21, Maastricht University22, University of Mainz23, Martin Luther University of Halle-Wittenberg24, Aarhus University25
TL;DR: F refinements in the treatment of early- and advanced-stage testicular cancer have emerged from clinical trials, and expert clinical skills will continue to be one of the major determinants for the prognosis of patients with germ cell cancer.
569 citations
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TL;DR: In this paper, a class of finite-dimensional integrable systems that may be viewed as relativistic generalizations of the Calogero-Moser systems were studied.
568 citations
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TL;DR: In this article, the authors present a simplified model of the phagocytic synapse and discuss the role of lysophosphatidylcholine as soluble attraction signal in the removal of apoptotic cells.
568 citations
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University of Tübingen1, German Cancer Research Center2, University Hospital Heidelberg3, Geneva College4, Leiden University Medical Center5, Herlev Hospital6, University of Copenhagen7, Hebron University8, University of California, San Francisco9, Technion – Israel Institute of Technology10, University of Southampton11, University of Texas MD Anderson Cancer Center12, GlaxoSmithKline13, Charité14, University of Mainz15
TL;DR: In a phase I trial, highly individualized peptide vaccines against unmutated tumour antigens and neoepitopes elicited sustained responses in CD8+ and CD4+ T cells, respectively, in patients with newly diagnosed glioblastoma.
Abstract: Patients with glioblastoma currently do not sufficiently benefit from recent breakthroughs in cancer treatment that use checkpoint inhibitors1,2. For treatments using checkpoint inhibitors to be successful, a high mutational load and responses to neoepitopes are thought to be essential3. There is limited intratumoural infiltration of immune cells4 in glioblastoma and these tumours contain only 30–50 non-synonymous mutations5. Exploitation of the full repertoire of tumour antigens—that is, both unmutated antigens and neoepitopes—may offer more effective immunotherapies, especially for tumours with a low mutational load. Here, in the phase I trial GAPVAC-101 of the Glioma Actively Personalized Vaccine Consortium (GAPVAC), we integrated highly individualized vaccinations with both types of tumour antigens into standard care to optimally exploit the limited target space for patients with newly diagnosed glioblastoma. Fifteen patients with glioblastomas positive for human leukocyte antigen (HLA)-A*02:01 or HLA-A*24:02 were treated with a vaccine (APVAC1) derived from a premanufactured library of unmutated antigens followed by treatment with APVAC2, which preferentially targeted neoepitopes. Personalization was based on mutations and analyses of the transcriptomes and immunopeptidomes of the individual tumours. The GAPVAC approach was feasible and vaccines that had poly-ICLC (polyriboinosinic-polyribocytidylic acid-poly-l-lysine carboxymethylcellulose) and granulocyte–macrophage colony-stimulating factor as adjuvants displayed favourable safety and strong immunogenicity. Unmutated APVAC1 antigens elicited sustained responses of central memory CD8+ T cells. APVAC2 induced predominantly CD4+ T cell responses of T helper 1 type against predicted neoepitopes.
568 citations
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University of Sheffield1, University of Cambridge2, National Institutes of Health3, Curie Institute4, Nofer Institute of Occupational Medicine5, University of Melbourne6, University of Otago7, Cancer Council Victoria8, University of London9, University of Copenhagen10, German Cancer Research Center11, University of Tübingen12, Bosch13, University of Ulm14, Hannover Medical School15, University of Helsinki16, International Agency for Research on Cancer17, QIMR Berghofer Medical Research Institute18, University of Eastern Finland19, Mayo Clinic20, Netherlands Cancer Institute21, Seoul National University22, University of Ulsan23, Karolinska Institutet24, Agency for Science, Technology and Research25, Carlos III Health Institute26, University of Minnesota27
TL;DR: It is demonstrated that common breast cancer susceptibility alleles with small effects on risk can be identified, given sufficiently powerful studies, as well as the need for further studies to confirm putative genetic associations with breast cancer.
Abstract: The Breast Cancer Association Consortium (BCAC) has been established to conduct combined case-control analyses with augmented statistical power to try to confirm putative genetic associations with breast cancer. We genotyped nine SNPs for which there was some prior evidence of an association with breast cancer: CASP8 D302H (rs1045485), IGFBP3 -202 C --> A (rs2854744), SOD2 V16A (rs1799725), TGFB1 L10P (rs1982073), ATM S49C (rs1800054), ADH1B 3' UTR A --> G (rs1042026), CDKN1A S31R (rs1801270), ICAM5 V301I (rs1056538) and NUMA1 A794G (rs3750913). We included data from 9-15 studies, comprising 11,391-18,290 cases and 14,753-22,670 controls. We found evidence of an association with breast cancer for CASP8 D302H (with odds ratios (OR) of 0.89 (95% confidence interval (c.i.): 0.85-0.94) and 0.74 (95% c.i.: 0.62-0.87) for heterozygotes and rare homozygotes, respectively, compared with common homozygotes; P(trend) = 1.1 x 10(-7)) and weaker evidence for TGFB1 L10P (OR = 1.07 (95% c.i.: 1.02-1.13) and 1.16 (95% c.i.: 1.08-1.25), respectively; P(trend) = 2.8 x 10(-5)). These results demonstrate that common breast cancer susceptibility alleles with small effects on risk can be identified, given sufficiently powerful studies.
567 citations
Authors
Showing all 41039 results
Name | H-index | Papers | Citations |
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John Q. Trojanowski | 226 | 1467 | 213948 |
Lily Yeh Jan | 162 | 467 | 73655 |
Monique M.B. Breteler | 159 | 546 | 93762 |
Wolfgang Wagner | 156 | 2342 | 123391 |
Thomas Meitinger | 155 | 716 | 108491 |
Hermann Brenner | 151 | 1765 | 145655 |
Amartya Sen | 149 | 689 | 141907 |
Bernhard Schölkopf | 148 | 1092 | 149492 |
Niels Birbaumer | 142 | 835 | 77853 |
Detlef Weigel | 142 | 516 | 84670 |
Peter Lang | 140 | 1136 | 98592 |
Marco Colonna | 139 | 512 | 71166 |
António Amorim | 136 | 1477 | 96519 |
Alexis Brice | 135 | 870 | 83466 |
Elias Campo | 135 | 761 | 85160 |