Franz Ketzer, PhD
Postdoctoral FellowAbout
Titles
Postdoctoral Fellow
Biography
Dr. Franz Ketzer received his BSc in Nutritional Sciences at Friedrich-Schiller-University Jena, Germany in 2016. He conducted his thesis on the effect of aluminum-nanoparticles on colon cancer cells supervised by Prof. Dr. Michael Glei, sparking his interest in cancer research. In 2018, he proceeded to complete the MSc curriculum in Molecular Medicine in Ulm, Germany, specializing in Molecular Oncology. During his MSc thesis, he studied the role of BLNK in the regulation of FOXO1 in B-cell acute lymphoblastic leukemia, supervised by Prof. Dr. Thomas Wirth and Dr. Alexey Ushmorov at the Institute of Physiological Chemistry. As part of the International Graduate School for Molecular Medicine Ulm (IGradU), he subsequently completed his PhD work in the same group but shifted his focus to the role of CCND3 in the maintenance of B-cell acute lymphoblastic leukemia. In 2022, he received his PhD (magna cum laude) in Molecular Medicine, after publishing his findings on the essential, anti-apoptotic role of CCND3 outside of its functions within the cell cycle in B- cell acute lymphoblastic leukemia. In June 2022, he joined the Müschen laboratory at Yale as a postdoctoral associate, with a focus on signaling molecules downstream of the B-cell-/T-cell receptor in the etiology of hematopoietic malignancies and autoimmune disease.
Appointments
Departments & Organizations
Education & Training
- PhD
- Ulm University, Molecular Medicine
Research
Publications
2022
CCND3 is indispensable for the maintenance of B-cell acute lymphoblastic leukemia
Ketzer F, Abdelrasoul H, Vogel M, Marienfeld R, Müschen M, Jumaa H, Wirth T, Ushmorov A. CCND3 is indispensable for the maintenance of B-cell acute lymphoblastic leukemia. Oncogenesis 2022, 11: 1. PMID: 35013097, PMCID: PMC8748974, DOI: 10.1038/s41389-021-00377-0.Peer-Reviewed Original ResearchCitationsAltmetricConceptsAnti-apoptotic effectsB-cell acute lymphoblastic leukemiaDriver mutationsCCND3 expressionAcute lymphoblastic leukemiaDifferent driver mutationsCDK4/6 kinase activityRole of FoxO1CDK4/6 inhibitionB-ALLDevelopment of resistanceLymphoblastic leukemiaCell cycle progressionMRNA levelsKinase activityPalbociclibCCND3Mutational backgroundD-type cyclinsFurther investigationCycle progressionGrowth arrestFOXO1CCND2Subsequent depletion
Academic Achievements & Community Involvement
honor Walter-Benjamin Postdoctoral Fellowship
International AwardGerman Research Foundation (DFG)Details03/01/2023Germany