Thomas G. P. Grünewald

ORCID: 0000-0003-0920-7377
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About
Contact & Profiles
Research Areas
  • Sarcoma Diagnosis and Treatment
  • RNA modifications and cancer
  • Cancer Genomics and Diagnostics
  • Cancer, Hypoxia, and Metabolism
  • CAR-T cell therapy research
  • Cancer, Lipids, and Metabolism
  • Lymphoma Diagnosis and Treatment
  • Protein Degradation and Inhibitors
  • RNA Research and Splicing
  • Virus-based gene therapy research
  • Cancer-related molecular mechanisms research
  • Cardiac tumors and thrombi
  • Neuroblastoma Research and Treatments
  • Cell Adhesion Molecules Research
  • Immune Cell Function and Interaction
  • Immunotherapy and Immune Responses
  • Congenital heart defects research
  • Colorectal Cancer Treatments and Studies
  • Genetic factors in colorectal cancer
  • Metabolism, Diabetes, and Cancer
  • Combustion and Detonation Processes
  • Risk and Safety Analysis
  • PI3K/AKT/mTOR signaling in cancer
  • Liver Disease Diagnosis and Treatment
  • Ubiquitin and proteasome pathways

German Cancer Research Center
2016-2025

Heidelberg University
2016-2025

Hopp Children's Cancer Center Heidelberg
2020-2025

University Hospital Heidelberg
2020-2025

Deutschen Konsortium für Translationale Krebsforschung
2016-2025

National Center for Tumor Diseases
2022-2025

Children's Cancer Center
2022-2025

DKFZ-ZMBH Alliance
2025

LMU Klinikum
2017-2024

Ludwig-Maximilians-Universität München
2015-2024

Christian Koelsche Daniel Schrimpf Damian Stichel Martin Sill Felix Sahm and 95 more David Reuß Mirjam Blattner Barbara C. Worst Christoph E. Heilig Katja Beck Peter Horak Simon Kreutzfeldt Elke Paff Sebastian Stark Pascal D. Johann Florian Selt Jonas Ecker Dominik Sturm Kristian W. Pajtler Annekathrin Reinhardt Annika K. Wefers Philipp Sievers Azadeh Ebrahimi Abigail K. Suwala Francisco Fernández‐Klett Belén Casalini Andrey Korshunov Volker Hovestadt F. Kommoss Mark Kriegsmann Matthias Schick Melanie Bewerunge‐Hudler Till Milde Olaf Witt Andreas E. Kulozik Marcel Kool Laura Romero‐Pérez Thomas G. P. Grünewald Thomas Kirchner Wolfgang Wick Michael Platten Andreas Unterberg Matthias Uhl Amir Abdollahi Jürgen Debus Burkhard Lehner Christian Thomas Martin Hasselblatt Werner Paulus Christian Hartmann Ori Staszewski Marco Prinz Jürgen Hench Stephan Frank Yvonne M.H. Versleijen‐Jonkers Marije E. Weidema Thomas Mentzel Klaus Griewank Enrique de Álava Juan Díaz‐Martín Miguel Á. Idoate Kenneth Tou En Chang Sharon Y. Y. Low Adrián Cuevas-Bourdier Michel Mittelbronn Martin Mynarek Stefan Rutkowski Ulrich Schüller Viktor Mautner Jens Schittenhelm Jonathan Serrano Matija Snuderl Reinhard Büttner Thomas Klingebiel Rolf Buslei Manfred Gessler Pieter Wesseling Winand N.M. Dinjens Sebastian Brandner Zane Jaunmuktane Iben Lyskjær Peter Schirmacher Albrecht Stenzinger Benedikt Brors Hanno Glimm Christoph Heining Òscar M. Tirado Miguel Sáinz‐Jaspeado Jaume Mora Javier Alonso Xavier García del Muro Sebastián Morán Manel Esteller Jamal Benhamida Marc Ladanyi Eva Wardelmann Cristina R. Antonescu Adrienne M. Flanagan Uta Dirksen Peter Hohenberger

Abstract Sarcomas are malignant soft tissue and bone tumours affecting adults, adolescents children. They represent a morphologically heterogeneous class of some entities lack defining histopathological features. Therefore, the diagnosis sarcomas is burdened with high inter-observer variability misclassification rate. Here, we demonstrate classification using machine learning classifier algorithm based on array-generated DNA methylation data. This sarcoma trained dataset 1077 profiles from...

10.1038/s41467-020-20603-4 article EN cc-by Nature Communications 2021-01-21

Abstract Metastases are the leading cause of mortality in patients with cancer. Metastasis formation requires cancer cells to adapt their cellular phenotype. However, how metabolism supports this adaptation is poorly defined. We use 2D versus 3D cultivation induce a shift phenotype breast cells. discover that proline catabolism via dehydrogenase (Prodh) growth culture. Subsequently, we link vivo metastasis formation. In particular, find PRODH expression and increased metastases compared...

10.1038/ncomms15267 article EN cc-by Nature Communications 2017-05-11

Under cell stress, global protein synthesis is inhibited to preserve energy. One mechanism sequester and silence mRNAs in ribonucleoprotein complexes known as stress granules (SGs), which contain translationally silent mRNAs, preinitiation factors, RNA-binding proteins. Y-box binding 1 (YB-1) localizes SGs, but its role SG biology unknown. We now report that YB-1 directly binds activates the 5′ untranslated region (UTR) of G3BP1 thereby controlling availability nucleator for assembly....

10.1083/jcb.201411047 article EN cc-by-nc-sa The Journal of Cell Biology 2015-03-23

Abstract Establishing and maintaining tolerance to self-antigens or innocuous foreign antigens is vital for the preservation of organismal health. Within thymus, medullary thymic epithelial cells (mTECs) expressing autoimmune regulator (AIRE) have a critical role in self-tolerance through deletion autoreactive T promotion regulatory (T reg ) cell development 1–4 . weeks birth, separate wave differentiation occurs periphery upon exposure derived from diet commensal microbiota 5–8 , yet types...

10.1038/s41586-022-05309-5 article EN cc-by Nature 2022-09-07

EWSR1-FLI1, the chimeric oncogene specific for Ewing sarcoma (EwS), induces a cascade of signaling events leading to cell transformation. However, it remains elusive how genetically homogeneous EwS cells can drive heterogeneity transcriptional programs. Here, we combine independent component analysis single-cell RNA sequencing data from diverse types and model systems with time-resolved mapping EWSR1-FLI1 binding sites open chromatin regions characterize dynamic cellular processes associated...

10.1016/j.celrep.2020.01.049 article EN cc-by Cell Reports 2020-02-01

Ewing tumors comprise the second most common type of bone-associated cancer in children and are characterized by oncogenic EWS/FLI1 fusion proteins early metastasis. Compelling evidence suggests that elevated levels intracellular oxidative stress contribute to enhanced aggressiveness numerous cancers, possibly including tumors. Using comprehensive microarray analyses RNA interference, we identified six-transmembrane epithelial antigen prostate 1 (STEAP1)-a membrane-bound mesenchymal stem...

10.1158/1541-7786.mcr-11-0524 article EN Molecular Cancer Research 2011-11-12
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