The transition from healthy marrow to overt disease is not a sudden event, but tends to follow a long period of sub-clinical deterioration in the marrow with changes occurring both in the hematopoietic cells and in the stromal environment. It is therefore important to consider the bone marrow as a whole when characterizing the progression of events that can lead up to disease and looking for points at which early intervention may delay or block disease progression.
The Bone Marrow Failure Group focuses on changes at the genetic level, in cell signaling, inflammation and metabolism that are associated with the development of myelodysplasia (MDS) and the progression to leukemia. We are combining expertise in clinical research and stem cell biology to develop composite cell culture systems that model the bone marrow environment and are using these firstly to characterize the events underlying MDS in detail and secondly as a platform to test new candidate agents and strategies. Mouse models of MDS are also employed to validate results in a physiological setting before proceeding to the clinical trials that bring the benefits of our research to patient care.
| Group Leaders | Prof. Dr. med. Uwe Platzbecker
PD Dr. Michael Cross
|
| Group members | Marie Schneider (Post doc)
Amanpreet Kaur Bains (PhD Student)
Waseem Nasr (PhD Student)
Samuel Kinde Birru (PhD Student)
Nicole Noack (MTA)
Julia Schulz (MTA)
Mandy Richter (MTA) |
| Current research grants | José Carreras Leukämie Stiftung
Sander Stiftung
DFG
Horizon 2020 (Transscan) |
Selected Publications
Loss of lenalidomide-induced megakaryocytic differentiation leads to therapy resistance in del(5q) myelodysplastic syndrome.Martinez-Høyer S, Deng Y, Parker J, Jiang J, Mo A, Docking TR, Gharaee N, Li J, Umlandt P, Fuller M, Jädersten M, Kulasekararaj A, Malcovati L, List AF, Hellström-Lindberg E, Platzbecker U, Karsan A. Nat Cell Biol. 2020 Apr 6. doi: 10.1038/s41556-020-0497-9.
Integrating the "Immunome" in the Stratification of Myelodysplastic Syndromes and Future Clinical Trial Design.Winter S, Shoaie S, Kordasti S, Platzbecker U.J Clin Oncol. 2020 Feb 14:JCO1901823.
Setting Fire to ESA and EMA Resistance: New Targeted Treatment Options in Lower Risk Myelodysplastic Syndromes. Kubasch AS, Platzbecker U. Int J Mol Sci. 2019 Aug 7;20(16).
The wolf of hypomethylating agent failure: what comes next?
Kubasch AS, Platzbecker U. Haematologica. 2019 Aug;104(8):1505-1508.
Treatment of MDS. Platzbecker U. Blood. 2019 Jan 22. pii: blood-2018-10-844696.
Transferrin receptor 2 controls bone mass and pathological bone formation via BMP and Wnt signaling. Rauner M, Baschant U, Roetto A, Pellegrino RM, Rother S, Salbach-Hirsch J, Weidner H, Hintze V, Campbell G, Petzold A, Lemaitre R, Henry I, Bellido T, Theurl I, Altamura S, Colucci S, Muckenthaler MU, Schett G, Komla Ebri D, Bassett JHD, Williams GR, Platzbecker U, Hofbauer LC. Nat Metab. 2019 Jan;1(1):111-124.
Erythropoietin inhibits osteoblast function in myelodysplastic syndromes via the canonical Wnt pathway. Balaian E, Wobus M, Weidner H, Baschant U, Stiehler M, Ehninger G, Bornhäuser M, Hofbauer LC, Rauner M, Platzbecker U. Haematologica. 2018 Jan;103(1):61-68.
Phospholipase A2 products predict the hematopoietic support capacity of horse serum. Ditz T, Schnapka-Hille L, Noack N, Dorow J, Ceglarek U, Niederwieser D, Schiller J, Fuchs B, Cross M. Differentiation. 2018 Dec 6;105:27-32.
Features of lineage-specific hematopoietic metabolism revealed by mitochondrial proteomics.
Billing C, Walker M, Noack N, Böhme C, Ceglarek U, Niederwieser D, Whetton A, Cross M.
Proteomics. 2017 Aug;17(15-16).
Myelodysplastic syndromes and bone loss in mice and men.
Weidner H, Rauner M, Trautmann F, Schmitt J, Balaian E, Mies A, Helas S, Baschant U, Khandanpour C, Bornhäuser M, Hofbauer LC, Platzbecker U.
Leukemia. 2017 Apr;31(4):1003-1007.
Myelodysplasia is in the niche: novel concepts and emerging therapies.
Bulycheva E, Rauner M, Medyouf H, Theurl I, Bornhäuser M, Hofbauer LC, Platzbecker U.
Leukemia. 2015 Feb;29(2):259-68.
