Aykut Demir
Leukaemia researcher at Heidelberg University and first author of the 2026 study showing that the enzyme IDH3 keeps acute myeloid leukaemia stem cells metabolically fit and resistant to venetoclax
Heidelberg University, Heidelberg (Simon Raffel group, at the time of the study, 2026)
Aykut Demir was first author of a 2026 paper in Blood (DEM2026) about acute myeloid leukaemia (AML), a fast-growing blood cancer. AML returns after treatment because a small group of leukaemic stem cells survives. These cells depend on the TCA cycle, the chain of reactions in mitochondria that burns fuel for energy, more than healthy blood stem cells do. The team found that the enzyme IDH3, one step of that cycle, is more abundant in leukaemic stem cells.
When they lowered IDH3A, the working part of the enzyme, citrate piled up inside the cells and both main energy pathways slowed. The resulting energy shortage switched on AMPK, the cell's fuel gauge, which shut down mTORC1, the growth-control complex, and so cut protein production. The cells then became more sensitive to venetoclax, a drug that blocks the survival protein BCL2. Healthy blood formation was spared. The work used patient cells, bone marrow organoids (miniature lab-grown tissue) and mice, and in a patient group, stem cells from people whose leukaemia resisted venetoclax plus azacitidine showed gene programmes of an active TCA cycle.
The paper lists Demir at Heidelberg University, in a team led by Simon Raffel at Heidelberg University Hospital with Andreas Trumpp of the German Cancer Research Center and Carsten Müller-Tidow among the co-authors. Other PubMed records under the same initials belong to different people, and a fuller career history could not be confirmed.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2026 | M | IDH3 regulates citrate homeostasis to control metabolic fitness and venetoclax resistance of AML stem cells DEM2026 First author: showed that loss of IDH3A in AML stem cells raises citrate, activates AMPK and shuts down mTORC1, making the cells more sensitive to venetoclax. |
Co-authors in the Atlas 2
People with a profile here who share at least one study with Aykut Demir.
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- Nicola Zamboni Group leader at ETH Zurich's Institute of Molecular Systems Biology who develops mass spectrometry methods to measure hundreds of metabolites at once, used in many collaborations on cell metabolism
- Simon Raffel Studies metabolic vulnerabilities of leukemia stem cells; senior author on a 2026 Blood paper on IDH3, citrate and mTORC1 in AML stem cell drug resistance
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