Göttingen Graduate Center for Neurosciences, Biophysics, and Molecular Biosciences

Dr. Ramona Schulz-Heddergott


  • 2003–2008: PhD student, Department of Neuroanatomy, University Medical Center Göttingen, Germany
  • 2008 – 2009: Postdoc, Sir William Dunn School of Pathology, University of Oxford, United Kingdom
  • 2009 – 2012: Postdoc, Molecular Oncology, University Medical Center Göttingen, Germany
  • 2013–2018: Research Fellow, Molecular Oncology, University Medical Center Göttingen, Germany
  • since 2018: Group leader, Molecular Oncology, University Medical Center Göttingen, Germany
  • since 2023: Granted by the Heisenberg Program, DFG




Major Research Interests

My research focuses on the stress-associated protein chaperone system and its suitability as actionable therapeutic target in gastrointestinal cancers. The chaperone system and its core heat-shock protein 90 (HSP90) stabilize hundreds of oncoproteins, enabling or enhancing their tumorigenic functions. Major clients of HSP90 consist in mutant versions of the tumor suppressor p53, a driver of nearly 50% of all human cancers. We are exploring the functions and therapeutic consequences of HSP90 and mutant p53 in the context of gastrointestinal tumors and their microenvironment. One topic is e.g., the identification of distinct pathway regulations by specific p53 mutants in colorectal (CRC) and pancreatic cancer (PDAC) and thus, whether specific p53 mutants might serve as predicators and/or target in cancer therapies. We use genetically engineered and chemically induced murine cancer models as well as patient-derived and murine organoid cultures to decipher mechanisms of tumor dynamics.


Homepage Department/Research Group
https://molonc.umg.eu/
https://gccc.umg.eu/kfo5002


Selected Recent Publications


  • Piqué-Borràs MR, Jevtic Z, Otzen Bagger F, Seguin J, Sivalingam R, Bezerra MF, Louwaige A, Juge S, Nellas I, Ivanek R, Tzankov A, Moll U, Cantillo OV, Schulz-Heddergott R, Fagnan A, Mercher T, Schwaller. The NFIA-ETO2 fusion blocks erythroid maturation and induces pure erythroid leukemia in cooperation with mutant TP53. Blood. 2023. Feb 3;.2022017273. PMID: 36735909

  • Isermann T, Sener ÖC, Stender A, Klemke L, Winkler N, Neesse A, Li J, Wegwitz F, Moll UM and Schulz-Heddergott R. Suppression of HSF1 activity by wildtype p53 creates a driving force for p53 loss-of-heterozygosity. Nature Comm. 2021 Jun 29;12(1):4019. PMID: 3418804

  • Klemke L, Fehlau CF, Winkler N, Toboll F, Singh SK, Moll UM and Schulz-Heddergott R. The gain-of-function p53 R248W allele promotes migration by STAT3 deregulation in human pancreatic cancer cells. Frontiers Oncol. 2021 Jun 11;11:642603. PMID: 34178628

  • Klemke L, De Oliveira T, Witt D, Stark N, Bohnenberger H, Bucala R, Conradi L-C, Schulz-Heddergott R. Hsp90-stabilized MIF supports tumor progression via macrophage recruitment and angiogenesis in colorectal cancer. Cell Death Dis. 2021. Feb 4;12(2):155. PMID: 33542244

  • Schulz-Heddergott R, Stark N, Edmunds SJ, Li J, Conradi L-C, Bohnenberger H, Ceteci F, Greten FR, Dobbelstein M, and Moll UM. Therapeutic ablation of gain-of-function mutant p53 in colorectal cancer inhibits Stat3-mediated tumor growth and invasion. Cancer Cell. 2018. 34(2):298- 314. PMID: 30107178