This Fellowship is awarded for a period of up to two years to early career clinician scientists undergoing medical specialist training with a strong interest in molecular medicine research topics. The fellows are integrated within the clinical setting of the Medical Faculty and aim at doing research at the interface of medicine and basic molecular biology and have the opportunity to work at a laboratory at the medical campus (e.g. OMZ) or at the EMBL. The fellows conduct their research in collaboration with a matching EMBL group.
CDF awardees Fall 2017:
Isabella Haberbosch, MD
Isabella is a physician scientist in the Department of Hematology, Oncology and Rheumatology of Heidelberg University Hospital.
License to practice medicine/approbation; Frankfurt University 2015
Residency in Hematology/Oncology at the Department of Hematology/Oncology and Rheumatology at Heidelberg University; since 2016
HRCMM Career Development Fellowship since 2017
Clinical host: Prof. Dr. med. Alwin Krämer, Department of Hematology, Oncology and Rheumatology, University Hospital Heidelberg
EMBL host: Dr. Yannick Schwab, Cell Biology and Biophysics
Disease studied: Acute myeloid leukemia
Acute myeloid leukemia (AML) is the most common acute leukemia in adults. Although much progress has been achieved in the treatment and understanding of AML, the mortality in AML patients remains relatively high. Hence further insights into tumorigenesis are crucial in the process of identifying new therapeutic targets. Centrosome aberrations are a hallmark of cancer and can be detected in all kind of malignancies. Previous studies found that centrosome aberrations represent an early event in the evolution of malignant phenotypes, which makes them a potential driver of tumorigenesis. So far in contrast to experimentally induced centrosome aberrations nothing is known in regards to composition and consequences of centrosome abnormalities in primary cancer cells.
This project aims to identify the nature of centrosome aberrations in acute myeloid leukemia and further malignancies. Isabella wants to analyze the ultrastructure of centrosome aberrations in primary AML cells using different electron microscopy techniques, in order to obtain a high resolution image of the centrosomes. A better understanding of the ultrastructure and number of centrosome aberrations in primary cancer cells may provide important information of their role in tumorigenesis.
Matthias Zielonka, MD
Matthias is a physician scientist in the Division for Neuropediatrics and Metabolic Medicine at the Center for Child and Adolescent Medicine of Heidelberg University.
Medical licensing exam, approbation; 2012
Residency in General Pediatrics at the Center for Child and Adolescent Medicine, Heidelberg University; since 2012
MD thesis, Max-Planck-Institute for Heart and Lung Research, Bad Nauheim & Heidelberg University; 2014
Fellow of the Physician-Scientist-Program, Medical Faculty of Heidelberg University; 2015-2017
HRCMM Career Development Fellowship; since 2017
Clinical host: Prof. Dr. med. Georg F. Hoffmann, Center for Child and Adolescent Medicine, University Hospital Heidelberg
EMBL host: Prof. Dr. Matthias Hentze, Directors' Research, RNA Biology, Metabolism and Molecular Medicine
Disease studied: Inborn Errors of Metabolism
Inborn errors of metabolism constitute a heterogeneous group of various enzyme deficiencies. Although inborn errors of metabolism are individually rare, their cumulative prevalence is estimated to be around 1:500, defining them as highly common and relevant causes of morbidity and mortality in children and adolescents. In the current concepts for inborn errors of metabolism, specific diseases are caused by mutations leading to a dysfunction of the catalytic site of a respective enzyme, thereby blocking intermediary metabolic pathways. In general, this enzymatic dysfunction results in the accumulation of toxic or complex metabolites and/or depletion of essential end products, ultimately causing a specific dysfunction and, subsequently, a mono- or multisystemic clinical phenotype. However, clear genotype-phenotype correlations are often poor and treatment options predominantly limited, which emphasizes that the understanding of the pathophysiological bases of this group of inherited diseases still remains restricted.
This project aims at elucidating the underlying pathomechanisms of selected inherited metabolic diseases to ultimately improve current and develop new diagnostic and therapeutic strategies. By combining both biochemical and system level approaches, Matthias wants to define genotype-phenotype-correlations of specific mutations in vitro and establish a zebrafish model to study morphological, biochemical as well as genetic alterations contributing to the phenotypic presentation of defined inborn errors of metabolism in vivo. Since several enzymes of intermediary metabolism have been shown to be involved in RNA-binding, one major aim of this project is the exact characterization of RNA-binding enzymes, the investigation of the role of RNA-binding in the context of intermediary metabolism and their pathomechanistic relevance for the respective diseases.
CDF awardee Summer 2015:
Jakob Gierten, MD
Jakob is a resident in the Department of Pediatric Cardiology and Congenital Heart Disease at the Hospital for Children and Adolescents of Heidelberg University.
MD/PhD Program of the Faculty of Medicine and the Faculty of Biosciences incorporated into HBIGS, since 2008
Residency in General Pediatrics at the Hospital for Children and Adolescents in Heidelberg, 2012-2015Residency in Pediatric Cardiology at the Hospital for Children and Adolescents in Heidelberg, since 2015
HRCMM Career Development Fellowship 2015 - 2017
Clinical host: Prof. Dr. med. Matthias Gorenflo, Department of Pediatric Cardiology and Congenital Heart Disease at the Hospital for Children and Adolescents in Heidelberg
EMBL host: Dr. Lars Hufnagel, Cell Biology and Biophysics
Disease studied:Congenital heart disease
Congenital heart disease (CHD) is one of the most common human birth defect and a leading cause of perinatal morbidity and mortality. The most frequently occurring non-syndromic CHD cases are commonly considered as multifactorial disorders resulting from polygenic effects of common DNA sequence variants with low penetrance that are influenced by environmental factors. The aim of this project is to identify DNA variants relevant to quantitative cardiac phenotypes by systematically dissecting genotype-phenotype correlations in fish. Jakob wants to tackle this question by adapting a light sheet fluorescent microscopy platform for large-scale characterization of morphometric and dynamic cardiac phenotypes. Identifying new disease-relevant alleles might help deducing key pathogenic events and ultimately, facilitate the development of novel therapeutic approaches.
CDF awardee Summer 2015:
Susanne Dittrich, MD
Susanne is a physician scientist in the Department of Pneumology and Critical Care Medicine of the Thoraxklinik and the Department of Translational Pulmonology at the University Hospital Heidelberg, both members of the Translational Lung Research Center Heidelberg (TLRC).
2013, approbation/license to practice medicine, Dresden University of Technology.
Research fellow at the Department of Translational Pulmonology, Translational Lung Research Center Heidelberg (TLRC), since 2014.
Physician undertaking specialty training at the Department of Pneumology and Critical Care Medicine, Thoraxklinik at the University Hospital Heidelberg, since 2014.
2015, MD Thesis, Dresden University of Technology.
HRCMM Career Development Fellowship, 2015 - 2017.
Clinical host: Prof. Dr. med. Marcus Mall, Department of Translational Pulmonology and Department of Pediatric Oncology, Hematology, Immunology and Pulmonology
EMBL host: PD Dr. Carsten Schultz, Cell Biology and Biophysics
Disease studied: Chronic Airway Diseases
Airway inflammation is a main characteristic of chronic lung diseases, such as chronic obstructive pulmonary disease (COPD) or cystic fibrosis (CF), the most common lethal inherited disease in western countries. Previous studies indicate that imbalances of protease-antiprotease networks are crucial contributors to structural lung damage and disease progression. Therefore, quantification of protease activity could provide a valuable, non-invasive tool for the monitoring of disease activity, evaluation of anti-inflammatory therapies and a better understanding of the underlying pathophysiology.
In the current project, Susanne studies the role of membrane-associated and free protease activity in airway secretions from patients with CF and COPD. For this purpose, she uses a novel approach based on Foerster resonance energy transfer (FRET).
May 2015: American Thoracic Society Abstract Scholarship Award of the Assembly on Clinical Problems
June 2015: Young Investigator Award of the European Cystic Fibrosis Society, pdf
Chronic but not intermittent infection with Pseudomonas aeruginosa is associated with global changes of the lung microbiome in cystic fibrosis
Sébastien Boutin, Simon Y. Graeber, Mirjam Stahl, A. Susanne Dittrich, Marcus A. Mall, Alexander H. Dalpke
Eur Respir J. 2017 Oct 5;50(4). pii: 1701086. doi: 10.1183/13993003.01086-2017. Print 2017 Oct. PMID:28982777
CDF awardee February 2015:
Johannes Pfeil, MD
Johannes is a physician for Pediatric Rheumatology and Infectious Diseases at the Hospital for Children and Adolescents of Heidelberg University(General Pediatrics).
2007 MD thesis, University Heidelberg
Residency in General Pediatrics, University of Würzburg, Germany (2007-2008)
Physician at the Center for Childhood and Adolescent Medicine (General Pediatrics), University Hospital Heidelberg, since 2008
Board certification in General Pediatrics, 2012
Board certification Pediatric Rheumatology, 2014
Board certification Infectious Diseases, 2015
HRCMM Career Development Fellowship 2015 - 2017.
Clinical host: Dr. Ann-Kristin Müller, Center for Infectious Diseases, Parasitology Unit, University Hospital Heidelberg
EMBL host: Dr. Jeroen Krijgsveld, Genome Biology
Disease studied: Malaria
Malaria, a parasite infection of red blood cells, kills roughly 2000 people per day, most of whom are children in Africa. In experimental immunization trials, intravenous administration of whole attenuated malaria parasites successfully protected humans against wild-type malaria infection. Even though this concept is unfeasible for direct translation towards routine vaccination, it still serves as a model to investigate protective immune responses against malaria.
By applying advanced mass spectrometric analysis, Johannes wants to identify critical targets of protective immunity induced by whole-parasite immunization at the very early and clinically silent malaria liver stage. The successful identification of these targets may provide the basis for future development of highly protective subunit malaria vaccines.
Reverse-transcription loop-mediated isothermal amplification for rapid detection of respiratory syncytial virus directly from nasopharyngeal swabs.
Hoos J, Peters RM, Tabatabai J, Grulich-Henn J, Schnitzler P, Pfeil J.
J Virol Methods. 2017 Jan 16;242:53-57. doi: 10.1016/j.jviromet.2017.01.006. [Epub ahead of print] PMID: 28093275
Evaluation of Alere™ i RSV for rapid detection of respiratory syncytial virus in children hospitalized with acute respiratory tract infection.
Peters RM, Schnee SV, Tabatabai J, Schnitzler P, Pfeil J.
J Clin Microbiol. 2017 Jan 11. pii: JCM.02433-16. doi: 10.1128/JCM.02433-16. [Epub ahead of print] PMID: 28077700
High-Density Peptide Arrays for Malaria Vaccine Development.
Loeffler FF, Pfeil J, Heiss K.
Methods Mol Biol. 2016;1403:569-82. doi: 10.1007/978-1-4939-3387-7_32. PMID: 27076154
CDF awardee 2014:
Sascha Dietrich, MD
Sascha is physician undergoing specialty training for Hematology and Oncology in the Department of Hematology, Oncology and Rheumatology at the University Medical Center for Internal Medicine, Heidelberg.
2007 MD thesis, University of Jena.
Residency in Internal Medicine and Hematology at Heidelberg University Hospital, since 2006.
Emergency medicine board certification, since 2011.
HRCMM Career Development Fellowship, 2014 - 2016.
Clinical hosts: Anthony D. Ho, Department of Internal Medicine V: Hematology, Oncology and Rheumatology, Heidelberg University Hospital
Thorsten Zenz, Department of Translational Oncology, Section Lymphoma Research, National Center for Tumor Diseases (NCT) Heidelberg
EMBL host: Wolfgang Huber, Genome Biology
Disease studied: Hematologic cancers, lympho- proliferative diseases (LPD)
Most cancer patients are treated with chemotherapy irrespective of diverse biology, but the discovery of key pathogenetic mutations has already transformed the treatment of specific cancer types. Successful examples of hematologic cancers include BCR-ABL inhibition of chronic myeloid leukaemia and as recently published by us, BRAF inhibition in hairy cell leukaemia.
We are aiming to understand the functional role of critical signalling pathways in lympho- proliferative diseases (LPD) and to determine the biological basis for differential response to genotype specific treatment. Pathway sensitivity and resistance of primary human tumour cells will be systematically mapped ex vivo using large and diverse compound libraries (up to 2500 compounds) across leukaemia s and lymphoma subtypes (refractory CLL, T-PLL, B-PLL, MCL, LPL, FL) to functionally group patients according to drug sensitivities. Paired with detailed molecular characterization of all tumour samples, and available clinical follow-up of the same patients, this novel and innovative approach provides unique opportunities to identify key pathways that determine sensitivity to specific drugs and drug combinations with the immediate potential for clinical translation.
Post-transplant cyclophosphamide-based haplo-identical transplantation as alternative to matched sibling or unrelated donor transplantation for non-Hodgkin lymphoma: a registry study by the European society for blood and marrow transplantation.
Dietrich S, Finel H, Martinez C, Tischer J, Blaise D, Chevallier P, Castagna L, Milpied N, Bacigalupo A, Corradini P, Mohty M, Sanz M, Hausmann A, Montoto S, Robinson S, Boumendil A, Sureda A, Dreger P.
Leukemia. 2016 Oct;30(10):2086-2089. doi: 10.1038/leu.2016.125
BRAF inhibitor therapy in HCL.
Dietrich S, Zenz T.
Best Pract Res Clin Haematol. 2015 Dec;28(4):246-52. doi: 10.1016/j.beha.2015.10.001. Epub 2015 Oct 20. Review. PMID:26614903
Recurrent CDKN1B (p27) mutations in hairy cell leukemia.
Dietrich S, Hüllein J, Lee SC, Hutter B, Gonzalez D, Jayne S, Dyer MJ, Oleś M, Else M, Liu X, Słabicki M, Wu B, Troussard X, Dürig J, Andrulis M, Dearden C, von Kalle C, Granzow M, Jauch A, Fröhling S, Huber W, Meggendorfer M, Haferlach T, Ho AD, Richter D, Brors B, Glimm H, Matutes E, Abdel Wahab O, Zenz T.
Blood. 2015 Aug 20;126(8):1005-8. doi: 10.1182/blood-2015-04-643361. Epub 2015 Jun 11. PMID: 26065650
CDF awardees 2013:
Joachim Kunz, MD
Joachim is an attending physician for Pediatric Hematology and Oncology in the Department of Pediatric Oncology, Hematology, Immunology and Pulmonology at the Hospital for Children and Adolescents of Heidelberg University.
2002 MD thesis, approbation/license to practice medicine, University of Tübingen.
Medical specialist in pediatric hematology and oncology, University Medical Center for Children and Adolescents, Heidelberg, since 2009.
Attending physician in pediatric hematology and oncology, University Medical Center for Children and Adolescents, Heidelberg, since 2013.
HRCMM Career Development Fellowship 2013 - 2015.
Clinical host: Andreas E. Kulozik, Department of Pediatric Oncology, Hematology, Immunology and Pulmonology
University Medical Center for Children and Adolescents, Heidelberg
EMBL host: Jan Korbel, Genome Biology
Disease studied: T-cell acute lymphoblastic leukemia (T-ALL) in children
Leukemia is the most common malignancy in childhood. T-ALL accounts for approximately 15% of all ALL in children and adolescents. Whereas the primary T-ALL can be cured in more than 80% of patients with current treatment protocols, relapsed T-ALL is almost invariably fatal: during the time between first diagnosis and relapse, T-ALL evolves into a resistant disease by acquiring new mutations induced by chemotherapy and by selection of subclones. Using whole exome sequencing, Joachim hopes to find mechanisms of treatment resistance and understand the evolution of T-ALL during a patient’s course of disease.
Pediatric T-lymphoblastic leukemia evolves into relapse by clonal selection, acquisition of mutations and promoter hypomethylation.
Kunz JB, Rausch T, Bandapalli OR, Eilers J, Pechanska P, Schuessele S, Assenov Y, Stütz AM, Kirschner-Schwabe R, Hof J, Eckert C, von Stackelberg A, Schrappe M, Stanulla M, Koehler R, Avigad S, Elitzur S, Handgretinger R, Benes V, Weischenfeldt J, Korbel JO, Muckenthaler MU, Kulozik AE.
Haematologica. 2015 Aug 20. pii: haematol.2015.129692. Epub 2015 Aug 20. PMID: 26294725
The activating STAT5B N642H mutation is a common abnormality in pediatric T-cell acute lymphoblastic leukemia and confers a higher risk of relapse.
Bandapalli OR, Schuessele S, Kunz JB, Rausch T, Stütz AM, Tal N, Geron I, Gershman N, Izraeli S, Eilers J, Vaezipour N, Kirschner-Schwabe R, Hof J, von Stackelberg A, Schrappe M, Stanulla M, Zimmermann M, Koehler R, Avigad S, Handgretinger R, Frismantas V, Bourquin JP, Bornhauser B, Korbel JO, Muckenthaler MU, Kulozik AE.
Haematologica. 2014 Oct;99(10):e188-92. doi: 10.3324/haematol.2014.104992. Epub 2014 Jun 27.
Pädiatrie 4. Auflage
Kunz J, Kulozik A
Kap 178 Erythrozyten,2014, S 1429-56 Hrsg: Hoffmann, Lentze, Spranger, Zepp: Springer ISBN 978-3-642-41865-5
Lorenz Lehmann, MD
Lorenz is a physician for Cardiology in the Department of Cardiology, Angiology and Pulmonology, at the University Medical Center for Internal Medicine, Heidelberg.
2006 MD thesis, University of Heidelberg.
Physician undertaking specialty training at the Department of Cardiology, Angiology and Pulmonology, University Hospital Heidelberg, since 2007.
Research fellow in experimental cardiology, Johannes Backs lab, University of Heidelberg, since 2007.
HRCMM Career Development Fellowship 2013 - 2015.
Clinical host: Hugo A. Katus, Department of Cardiology, Angiology and Pulmonology, University Hospital Heidelberg
EMBL host: Eileen Furlong, Genome Biology
Disease studied: Heart failure
Research focus: Heart failure is one of the main causes of death in the western world. Previously, histone deacetylase 4 (HDAC4) was identified as a cardioprotective factor. Understanding the molecular basis of its posttranslational modifications enabled the development of potential therapeutic tools for the treatment of heart diseases. For instance, the N-terminal part of HDAC4 inhibits specific transcription factors such as MEF2, which is one of the key regulators for pathological cardiac remodeling which leads ultimately to heart failure.
During the HRCMM project Lorenz aims to comprehensively identify MEF2 and HDAC4 regulated genes via ChIP-seq experiments. Subsequently, he will study their contribution to the transition from a healthy to a diseased heart. It is the overall goal to gain a deep understanding of the epigenetic modifications driven by HDAC4 and to identify epigenetic drug targets for cardioprotection.
Advanced echocardiography in adult zebrafish reveals delayed recovery of heart function after myocardial cryoinjury.
Hein SJ, Lehmann LH, Kossack M, Juergensen L, Fuchs D, Katus HA, Hassel D.
PLoS One. 2015 Apr 8;10(4):e0122665. doi: 10.1371/journal.pone.0122665. eCollection 2015. PMID:25853735
Essential role of sympathetic endothelin A receptors for adverse cardiac remodeling.
Lehmann LH, Rostosky JS, Buss SJ, Kreusser MM, Krebs J, Mier W, Enseleit F, Spiger K, Hardt SE, Wieland T, Haass M, Lüscher TF, Schneider MD, Parlato R, Gröne HJ, Haberkorn U, Yanagisawa M, Katus HA, Backs J. Proc Natl Acad Sci U S A. 2014 Sep 2. pii: 201409026. [Epub ahead of print]
CaM Kinase II mediates maladaptive post-infarct remodeling and pro-inflammatory chemoattractant signaling but not acute myocardial ischemia/reperfusion injury.
Weinreuter M, Kreusser MM, Beckendorf J, Schreiter FC, Leuschner F, Lehmann LH, Hofmann KP, Rostosky JS, Diemert N, Xu C, Volz HC, Jungmann A, Nickel A, Sticht C, Gretz N, Maack C, Schneider MD, Gröne HJ, Müller OJ, Katus HA, Backs J. EMBO Mol Med. 2014 Sep 5. pii: e201403848. doi: 10.15252/emmm.201403848. [Epub ahead of print]
The Cardiac CaMKII Genes δ and γ Contribute Redundantly to Adverse Remodeling but Inhibit Calcineurin-Induced Myocardial Hypertrophy.
Kreusser MM, Lehmann LH, Keranov S, Hoting MO, Kohlhaas M, Reil JC, Neumann K, Schneider MD, Hill JA, Dobrev D, Maack C, Maier LS, Gröne HJ, Katus HA, Olson EN, Backs J.
Circulation. 2014 Aug 14. pii: CIRCULATIONAHA.114.006185. [Epub ahead of print] PMID:25124496
Depletion of globosides and isoglobosides fully reverts the morphologic phenotype of Fabry disease.
Porubsky S, Jennemann R, Lehmann L, Gröne HJ.
Cell Tissue Res. 2014 Jul 4. [Epub ahead of print]
Histone deacetylase signaling in cardioprotection.
Lehmann LH, Worst BC, Stanmore DA, Backs J.
Cell Mol Life Sci. 2013 Dec 6.
The role of endothelin-1 in the sympathetic nervous system in the heart.
Lehmann LH, Stanmore DA, Backs
J. Life Sci. 2014 Mar 13. pii: S0024-3205(14)00317-8. doi: 10.1016/j.lfs.2014.03.005. [Epub ahead of print] Review. PMID: 24632477
April 2013: Lorenz Lehmann receives Rudi Busse - Young Investigator Award for his work in experimental cardiovascular research.
Stephan Singer, MD
Stephan is a physician for Pathology in the Department of General Pathology at the Institute of Pathology Heidelberg, IPH.
2005 MD thesis, University of Heidelberg.
Physician undertaking specialty training at the Institute of Pathology, University Medical Center Heidelberg, since 2005.
2008 Postdoc Columbia University New York City, USA.
2011 Gerok fellowship SFB/TRR77.
HRCMM Career Development Fellowship 2013 - 2015.
Clinical host: Peter Schirmacher, Institute of Pathology Heidelberg
EMBL host: Martin Beck, Structural and Computational Biology
Disease studied: Liver cancer
Research focus: Hepatocellular carcinoma (HCC) is one of the most frequent malignancies world-wide with an increasing incidence and a poor prognosis. Signalling cascades of (hepato-)carcinogenic pathways pass the nuclear envelope through the nuclear pore complex (NPC). The NPC is a multiprotein complex spanning the nuclear envelope and consists of ~30 nucleoporins (Nups). The project investigates compositional changes of the NPC occurring in the process of hepatocarcinogenesis and to what extent NPC remodelling modulates liver cancer-relevant pathways. In collaboration with the Beck lab (EMBL) Stephan will address this in vitro and in vivo by using targeted and non-targeted mass spectrometry, gene expression arrays, cell-based assays, murine HCC models, and human HCC samples. Tumour-specific alterations of the NPC may provide the basis for novel therapeutic approaches.
Cellular apoptosis susceptibility (CAS) is linked to integrin β1 and required for tumor cell migration and invasion in hepatocellular carcinoma (HCC).
Winkler J, Roessler S, Sticht C, DiGuilio AL, Drucker E, Holzer K, Eiteneuer E, Herpel E, Breuhahn K, Gretz N, Schirmacher P, Ori A, Singer S.
Oncotarget. 2016 Mar 23. doi: 10.18632/oncotarget.8256. [Epub ahead of print] PMID: 27015362
Spatiotemporal variation of mammalian protein complex stoichiometries.
Ori A, Iskar M, Buczak K, Kastritis P, Parca L, Andrés-Pons A, Singer S, Bork P, Beck M.
Genome Biol. 2016 Mar 14;17:47. doi: 10.1186/s13059-016-0912-5. PMID: 26975353
PI3K/AKT/mTOR-dependent stabilization of oncogenic far-upstream element binding proteins in hepatocellular carcinoma cells.
Samarin J, Laketa V, Malz M, Roessler S, Stein I, Horwitz E, Singer S, Dimou E, Cigliano A, Bissinger M, Falk CS, Chen X, Dooley S, Pikarsky E, Calvisi DF, Schultz C, Schirmacher P, Breuhahn K.
Hepatology. 2016 Mar;63(3):813-26. doi: 10.1002/hep.28357. Epub 2016 Jan 14. PMID: 26901106
Histone Deacetylase Inhibitors (HDACi) Cause the Selective Depletion of Bromodomain Containing Proteins (BCPs).
Mackmull MT, Iskar M, Parca L, Singer S, Bork P, Ori A, Beck M.
Mol Cell Proteomics. 2015 May;14(5):1350-60. doi: 10.1074/mcp.M114.042499. Epub 2015 Mar 9. PMID: 25755299
Overexpression of far upstream element (FUSE) binding protein (FBP)-interacting repressor (FIR) supports growth of hepatocellular carcinoma
Malz, M., Bovet, M., Samarin, J., Rabenhorst, U., Sticht, C., Bissinger, M., Roessler, S., Lorenzo Bermejo, J., Renner, M., Calvisi, D. F., Singer, S., Ganzinger, M., Weber, A., Gretz, N., Zornig, M., Schirmacher, P., and Breuhahn, K.
Hepatology 60,1241-50, 2014
Prosurvival function of the cellular apoptosis susceptibility/importin-α1 transport cycle is repressed by p53 in liver cancer.
Winkler J1, Ori A, Holzer K, Sticht C, Dauch D, Eiteneuer EM, Pinna F, Geffers R, Ehemann V, Andres-Pons A, Breuhahn K, Longerich T, Lorenzo Bermejo J, Gretz N, Zender L, Schirmacher P, Beck M, Singer S.
Hepatology. 2014 May 6. doi: 10.1002/hep.27207. [Epub ahead of print]
July 2014: Stephan Singer receives the Hella-Bühler-Award for his outstanding work in cancer research.