@article{StoelzelMohrKrameretal.2016,
  author    = {St{\"o}lzel, F. and Mohr, B. and Kramer, M. and Oelschl{\"a}gel, U. and Bochtler, T. and Berdel, W. E. and Kaufmann, M. and Baldus, C. D. and Sch{\"a}fer-Eckart, K. and Stuhlmann, R. and Einsele, H. and Krause, S. W. and Serve, H. and H{\"a}nel, M. and Herbst, R. and Neubauer, A. and Sohlbach, K. and Mayer, J. and Middeke, J. M. and Platzbecker, U. and Schaich, M. and Kr{\"a}mer, A. and R{\"o}llig, C. and Schetelig, J. and Bornh{\"a}user, M. and Ehninger, G.},
  title     = {Karyotype complexity and prognosis in acute myeloid leukemia},
  series = {Blood Cancer Journal},
  volume    = {6},
  journal   = {Blood Cancer Journal},
  doi       = {10.1038/bcj.2015.114},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-164530},
  pages     = {e386},
  year      = {2016},
  abstract  = {A complex aberrant karyotype consisting of multiple unrelated cytogenetic abnormalities is associated with poor prognosis in patients with acute myeloid leukemia (AML). The European Leukemia Net classification and the UK Medical Research Council recommendation provide prognostic categories that differ in the definition of unbalanced aberrations as well as the number of single aberrations. The aim of this study on 3526 AML patients was to redefine and validate a cutoff for karyotype complexity in AML with regard to adverse prognosis. Our study demonstrated that (1) patients with a pure hyperdiploid karyotype have an adverse risk irrespective of the number of chromosomal gains, (2) patients with translocation t(9;11)(p21∼22;q23) have an intermediate risk independent of the number of additional aberrations, (3) patients with 4 abnormalities have an adverse risk per se and (4) patients with three aberrations in the absence of abnormalities of strong influence (hyperdiploid karyotype, t(9;11)(p21∼22;q23), CBF-AML, unique adverse-risk aberrations) have borderline intermediate/adverse risk with a reduced overall survival compared with patients with a normal karyotype.},
  language  = {en}
}
@article{MambrettiKistnerMayeretal.2016,
  author    = {Mambretti, Egle M. and Kistner, Katrin and Mayer, Stefanie and Massotte, Dominique and Kieffer, Brigitte L. and Hoffmann, Carsten and Reeh, Peter W. and Brack, Alexander and Asan, Esther and Rittner, Heike L.},
  title     = {Functional and structural characterization of axonal opioid receptors as targets for analgesia},
  series = {Molecular Pain},
  journal   = {Molecular Pain},
  number    = {12},
  doi       = {10.1177/1744806916628734},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-145917},
  pages     = {1-17},
  year      = {2016},
  abstract  = {Background Opioids are the gold standard for the treatment of acute pain despite serious side effects in the central and enteric nervous system. µ-opioid receptors (MOPs) are expressed and functional at the terminals of sensory axons, when activated by exogenous or endogenous ligands. However, the presence and function of MOP along nociceptive axons remains controversial particularly in na{\"i}ve animals. Here, we characterized axonal MOPs by immunofluorescence, ultrastructural, and functional analyses. Furthermore, we evaluated hypertonic saline as a possible enhancer of opioid receptor function. Results Comparative immunolabeling showed that, among several tested antibodies, which all provided specific MOP detection in the rat central nervous system (CNS), only one monoclonal MOP-antibody yielded specificity and reproducibility for MOP detection in the rat peripheral nervous system including the sciatic nerve. Double immunolabeling documented that MOP immunoreactivity was confined to calcitonin gene-related peptide (CGRP) positive fibers and fiber bundles. Almost identical labeling and double labeling patterns were found using mcherry-immunolabeling on sciatic nerves of mice producing a MOP-mcherry fusion protein (MOP-mcherry knock-in mice). Preembedding immunogold electron microscopy on MOP-mcherry knock-in sciatic nerves indicated presence of MOP in cytoplasm and at membranes of unmyelinated axons. Application of [D-Ala\(^2\), N-MePhe\(^4\), Gly-ol]-enkephalin (DAMGO) or fentanyl dose-dependently inhibited depolarization-induced CGRP release from rat sciatic nerve axons ex vivo, which was blocked by naloxone. When the lipophilic opioid fentanyl was applied perisciatically in na{\"i}ve Wistar rats, mechanical nociceptive thresholds increased. Subthreshold doses of fentanyl or the hydrophilic opioid DAMGO were only effective if injected together with hypertonic saline. In vitro, using β-arrestin-2/MOP double-transfected human embryonic kidney cells, DAMGO as well as fentanyl lead to a recruitment of β-arrestin-2 to the membrane followed by a β-arrestin-2 reappearance in the cytosol and MOP internalization. Pretreatment with hypertonic saline prevented MOP internalization. Conclusion MOPs are present and functional in the axonal membrane from na{\"i}ve animals. Hypertonic saline acutely decreases ligand-induced internalization of MOP and thereby might improve MOP function. Further studies should explore potential clinical applications of opioids together with enhancers for regional analgesia.},
  language  = {en}
}
@article{WilhelmMayer1975,
  author    = {Wilhelm, Gernot and Mayer, W.},
  title     = {Altassyrische Texte aus Privatsammlungen},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-82740},
  year      = {1975},
  abstract  = {No abstract available},
  subject      = {Ugarit},
  language  = {de}
}
@article{OehlerKistnerMartinetal.2017,
  author    = {Oehler, Beatrice and Kistner, Katrin and Martin, Corinna and Schiller, J{\"u}rgen and Mayer, Rafaela and Mohammadi, Milad and Sauer, Reine-Solange and Filipovic, Milos R. and Nieto, Francisco R. and Kloka, Jan and Pfl{\"u}cke, Diana and Hill, Kerstin and Schaefer, Michael and Malcangio, Marzia and Reeh, Peter W. and Brack, Alexander and Blum, Robert and Rittner, Heike L.},
  title     = {Inflammatory pain control by blocking oxidized phospholipid-mediated TRP channel activation},
  series = {Scientific Reports},
  volume    = {7},
  journal   = {Scientific Reports},
  number    = {5447},
  doi       = {10.1038/s41598-017-05348-3},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-158536},
  year      = {2017},
  abstract  = {Phospholipids occurring in cell membranes and lipoproteins are converted into oxidized phospholipids (OxPL) by oxidative stress promoting atherosclerotic plaque formation. Here, OxPL were characterized as novel targets in acute and chronic inflammatory pain. Oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (OxPAPC) and its derivatives were identified in inflamed tissue by mass spectrometry and binding assays. They elicited calcium influx, hyperalgesia and induced pro-nociceptive peptide release. Genetic, pharmacological and mass spectrometric evidence in vivo as well as in vitro confirmed the role of transient receptor potential channels (TRPA1 and TRPV1) as OxPAPC targets. Treatment with the monoclonal antibody E06 or with apolipoprotein A-I mimetic peptide D-4F, capturing OxPAPC in atherosclerosis, prevented inflammatory hyperalgesia, and in vitro TRPA1 activation. Administration of D-4F or E06 to rats profoundly ameliorated mechanical hyperalgesia and inflammation in collagen-induced arthritis. These data reveal a clinically relevant role for OxPAPC in inflammation offering therapy for acute and chronic inflammatory pain treatment by scavenging OxPAPC.},
  language  = {en}
}
@article{RiegerLissMellinghoffetal.2018,
  author    = {Rieger, C. T. and Liss, B. and Mellinghoff, S. and Buchheidt, D. and Cornely, O. A. and Egerer, G. and Heinz, W. J. and Hentrich, M. and Maschmeyer, G. and Mayer, K. and Sandherr, M. and Silling, G. and Ullmann, A. and Vehreschild, M. J. G. T. and von Lilienfeld-Toal, M. and Wolf, H. H. and Lehners, N.},
  title     = {Anti-infective vaccination strategies in patients with hematologic malignancies or solid tumors-Guideline of the Infectious Diseases Working Party (AGIHO) of the German Society for Hematology and Medical Oncology (DGHO)},
  series = {Annals of Oncology},
  volume    = {29},
  journal   = {Annals of Oncology},
  number    = {6},
  doi       = {10.1093/annonc/mdy117},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-226196},
  pages     = {1354-1365},
  year      = {2018},
  abstract  = {Infectious complications are a significant cause of morbidity and mortality in patients with malignancies specifically when receiving anticancer treatments. Prevention of infection through vaccines is an important aspect of clinical care of cancer patients. Immunocompromising effects of the underlying disease as well as of antineoplastic therapies need to be considered when devising vaccination strategies. This guideline provides clinical recommendations on vaccine use in cancer patients including autologous stem cell transplant recipients, while allogeneic stem cell transplantation is subject of a separate guideline. The document was prepared by the Infectious Diseases Working Party (AGIHO) of the German Society for Hematology and Medical Oncology (DGHO) by reviewing currently available data and applying evidence-based medicine criteria.},
  language  = {en}
}
@article{EckardtStasikKrameretal.2021,
  author    = {Eckardt, Jan-Niklas and Stasik, Sebastian and Kramer, Michael and R{\"o}llig, Christoph and Kr{\"a}mer, Alwin and Scholl, Sebastian and Hochhaus, Andreas and Crysandt, Martina and Br{\"u}mmendorf, Tim H. and Naumann, Ralph and Steffen, Bj{\"o}rn and Kunzmann, Volker and Einsele, Hermann and Schaich, Markus and Burchert, Andreas and Neubauer, Andreas and Sch{\"a}fer-Eckart, Kerstin and Schliemann, Christoph and Krause, Stefan W. and Herbst, Regina and H{\"a}nel, Mathias and Frickhofen, Norbert and Noppeney, Richard and Kaiser, Ulrich and Baldus, Claudia D. and Kaufmann, Martin and R{\´a}cil, Zdenek and Platzbecker, Uwe and Berdel, Wolfgang E. and Mayer, Jiř{\´i} and Serve, Hubert and M{\"u}ller-Tidow, Carsten and Ehninger, Gerhard and St{\"o}lzel, Friedrich and Kroschinsky, Frank and Schetelig, Johannes and Bornh{\"a}user, Martin and Thiede, Christian and Middeke, Jan Moritz},
  title     = {Loss-of-function mutations of BCOR are an independent marker of adverse outcomes in intensively treated patients with acute myeloid leukemia},
  series = {Cancers},
  volume    = {13},
  journal   = {Cancers},
  number    = {9},
  issn      = {2072-6694},
  doi       = {10.3390/cancers13092095},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-236735},
  year      = {2021},
  abstract  = {Acute myeloid leukemia (AML) is characterized by recurrent genetic events. The BCL6 corepressor (BCOR) and its homolog, the BCL6 corepressor-like 1 (BCORL1), have been reported to be rare but recurrent mutations in AML. Previously, smaller studies have reported conflicting results regarding impacts on outcomes. Here, we retrospectively analyzed a large cohort of 1529 patients with newly diagnosed and intensively treated AML. BCOR and BCORL1 mutations were found in 71 (4.6\%) and 53 patients (3.5\%), respectively. Frequently co-mutated genes were DNTM3A, TET2 and RUNX1. Mutated BCORL1 and loss-of-function mutations of BCOR were significantly more common in the ELN2017 intermediate-risk group. Patients harboring loss-of-function mutations of BCOR had a significantly reduced median event-free survival (HR = 1.464 (95\%-Confidence Interval (CI): 1.005-2.134), p = 0.047), relapse-free survival (HR = 1.904 (95\%-CI: 1.163-3.117), p = 0.01), and trend for reduced overall survival (HR = 1.495 (95\%-CI: 0.990-2.258), p = 0.056) in multivariable analysis. Our study establishes a novel role for loss-of-function mutations of BCOR regarding risk stratification in AML, which may influence treatment allocation.},
  language  = {en}
}