ArticleTranslational cancer research2019
Fumarate hydratase deficiency induces chronic myeloid leukemia progression.
Article in Translational cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Tricarboxylic Acid Cycle Relationships with Non-Metabolic Processes: A Short Story with DNA Repair and Its Consequences on Cancer Therapy Resistance.International journal of molecular sciences · 2024Review
- Regulation of Hypoxia Dependent Reprogramming of Cancer Metabolism: Role of HIF-1 and Its Potential Therapeutic Implications in Leukemia.Asian Pacific journal of cancer prevention : APJCP · 2024Review
- HIF-1α signaling: Essential roles in tumorigenesis and implications in targeted therapies.Genes & diseases · 2024Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough tyrosine kinase inhibitors (TKIs) have profoundly improved the prognosis of chronic myeloid leukemia (CML), the mechanism of the progression to blast phase (BP) is currently unclear. Our previous study indicated that CML-BP cells utilize glycolysis to proliferate and that the fumarate level is elevated in CML-BP cells. Fumarate hydratase (FH) catalyzes fumarate to malate. A functional deficiency in FH could result in fumarate accumulation. Therefore, we wanted to determine whether an FH deficiency facilitates CML progression.
methodsFH expression in CML chronic phase (CP) and CML-BP was analyzed.
resultsOur findings showed that CML-BP patients had lower FH expression than CML-CP patients (P=0.025). Knocking down FH expression enhanced the invasiveness of K562 cells through HIF-1α-induced glycolysis. DNA damage repair was impaired after FH expression knockdown.
conclusionsOur findings suggested that reduced FH function may facilitate disease progression in CML through the combined effects of an elevated glycolysis level and a decreased DNA repair ability.
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