ArticlePloS one2009
Combined bezafibrate and medroxyprogesterone acetate: potential novel therapy for acute myeloid leukaemia.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 72 citations in OpenAlex.
- One size does not fit all: An in vitro evaluation of the effects of bezafibrate and medroxyprogesterone acetate on human SH-SY5Y and U-87 MG cancer cells.FEBS open bio · 2026Article
- The structural basis of aldo-keto reductase 1C3 inhibition by 17α-picolyl and 17(Journal of enzyme inhibition and medicinal chemistry · 2025Article
- Aldo-keto reductase (AKR) superfamily website and database: An update.Chemico-biological interactions · 2024Article
- High-density lipoprotein cholesterol and multiple myeloma: A systematic review and meta-analysis.Atherosclerosis plus · 2023Article
- Review
- X-ray structure of human aldo-keto reductase 1C3 in complex with a bile acid fused tetrazole inhibitor: experimental validation, molecular docking and structural analysis.RSC medicinal chemistry · 2023Article
- Polycystic ovary syndrome: pathophysiology and therapeutic opportunities.BMJ medicine · 2023Review
- AKR1C3 expression in T acute lymphoblastic leukemia/lymphoma for clinical use as a biomarker.Scientific reports · 2022Article
- Valproic acid disables the Nrf2 anti-oxidant response in acute myeloid leukaemia cells enhancing reactive oxygen species-mediated killing.British journal of cancer · 2022Article
- Crosstalk Between ROS and Autophagy in Tumorigenesis: Understanding the Multifaceted Paradox.Frontiers in oncology · 2022Review
- Oncogenic Mechanisms and Therapeutic Targeting of Metabolism in Leukemia and Lymphoma.Cold Spring Harbor perspectives in medicine · 2021Review
- Aldo-Keto Reductases and Cancer Drug Resistance.Pharmacological reviews · 2021Review
- Oxidative Stress in Cancer Cell Metabolism.Antioxidants (Basel, Switzerland) · 2021Review
- Combined bezafibrate, medroxyprogesterone acetate and valproic acid treatment inhibits osteosarcoma cell growth without adversely affecting normal mesenchymal stem cells.Bioscience reports · 2021Article
- Exploiting metabolic vulnerabilities for personalized therapy in acute myeloid leukemia.BMC biology · 2019Review
- AKR1C3 (type 5 17β-hydroxysteroid dehydrogenase/prostaglandin F synthase): Roles in malignancy and endocrine disorders.Molecular and cellular endocrinology · 2019Review
- Single arm phase II trial assessing the safety, compliance with and activity of Bezafibrate and medroxyProgesterone acetate (BaP) therapy against myeloid and lymphoid cancers.Contemporary clinical trials communications · 2019Article
- Bioisosteres of Indomethacin as Inhibitors of Aldo-Keto Reductase 1C3.ACS medicinal chemistry letters · 2019Article
- Potent and Highly Selective Aldo-Keto Reductase 1C3 (AKR1C3) Inhibitors Act as Chemotherapeutic Potentiators in Acute Myeloid Leukemia and T-Cell Acute Lymphoblastic Leukemia.Journal of medicinal chemistry · 2019Article
- AKR1C enzymes sustain therapy resistance in paediatric T-ALL.British journal of cancer · 2018Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe majority of acute myeloid leukaemia (AML) patients are over sixty years of age. With current treatment regimens, survival rates amongst these, and also those younger patients who relapse, remain dismal and novel therapies are urgently required. In particular, therapies that have anti-leukaemic activity but that, unlike conventional chemotherapy, do not impair normal haemopoiesis. PRINCIPAL
findingsHere we demonstrate the potent anti-leukaemic activity of the combination of the lipid-regulating drug bezafibrate (BEZ) and the sex hormone medroxyprogesterone acetate (MPA) against AML cell lines and primary AML cells. The combined activity of BEZ and MPA (B/M) converged upon the increased synthesis and reduced metabolism of prostaglandin D(2) (PGD(2)) resulting in elevated levels of the downstream highly bioactive, anti-neoplastic prostaglandin 15-deoxy Delta(12,14) PGJ(2) (15d-PGJ(2)). BEZ increased PGD(2) synthesis via the generation of reactive oxygen species (ROS) and activation of the lipid peroxidation pathway. MPA directed prostaglandin synthesis towards 15d-PGJ(2) by inhibiting the PGD(2) 11beta -ketoreductase activity of the aldo-keto reductase AKR1C3, which metabolises PGD(2) to 9alpha11beta-PGF(2alpha). B/M treatment resulted in growth arrest, apoptosis and cell differentiation in both AML cell lines and primary AML cells and these actions were recapitulated by treatment with 15d-PGJ(2). Importantly, the actions of B/M had little effect on the survival of normal adult myeloid progenitors. SIGNIFICANCE: Collectively our data demonstrate that B/M treatment of AML cells elevated ROS and delivered the anti-neoplastic actions of 15d-PGJ(2). These observations provide the mechanistic rationale for the redeployment of B/M in elderly and relapsed AML.
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