Eyal Gottlieb
艾亚尔·戈特利布
PhD
Professor of Cancer Metabolism癌症代谢教授
👥Biography 个人简介
Eyal Gottlieb is a leader in mitochondrial cancer metabolism who has made key contributions to understanding how oncometabolites and TCA cycle enzyme mutations drive tumor development. His laboratory discovered that fumarate accumulation due to FH (fumarate hydratase) loss leads to pseudohypoxia and epigenetic reprogramming through histone and DNA demethylase inhibition, linking TCA cycle dysfunction to the cancer epigenome. Gottlieb has characterized how SDH (succinate dehydrogenase) mutations generate succinate-driven oncometabolic changes promoting paraganglioma and pheochromocytoma. His work has established mitochondrial metabolite accumulation as a cancer driver mechanism.
🧪Research Fields 研究领域
🎓Key Contributions 主要贡献
Fumarate as Oncometabolite
Discovered that fumarate accumulation due to FH loss inhibits histone and DNA demethylases, driving epigenetic reprogramming that promotes tumorigenesis in hereditary leiomyomatosis and renal cell carcinoma.
TCA Cycle Enzyme Mutations in Cancer
Characterized how mutations in SDH, FH, and IDH generate oncometabolites that rewire epigenetic landscapes and pseudo-hypoxic responses, connecting mitochondrial dysfunction to cancer initiation.
Representative Works 代表性著作
Accumulation of Krebs Cycle Intermediates and Over-Expression of HIF1 in Tumours which Result from Germline FH and SDH Mutations
Human Molecular Genetics (2005)
Early characterization of oncometabolite accumulation in FH/SDH-mutant tumors.
Fumarate Inhibits the TET Family of Dioxygenases and Is Implicated in Renal Cell Carcinoma
Nature Genetics (2016)
Mechanism linking fumarate to epigenetic reprogramming in renal cancer.
🏆Awards & Recognition 奖项与荣誉
📄Data Sources 数据来源
Last updated: 2026-01-15 | All information from publicly available academic sources
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