ArticleCancer research2017
Alox5 Blockade Eradicates JAK2V617F-Induced Polycythemia Vera in Mice.
Article in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- A blockade of leukotriene-mediated Alox5 function provides a new strategy for the treatment of <i>JAK2</I>V617F-induced polycythemia vera.Haematologica · 2025Article
- Normal Hematopoietic Stem Cells in Leukemic Bone Marrow Environment Undergo Morphological Changes Identifiable by Artificial Intelligence.International journal of molecular sciences · 2025Article
- The ETS domain-containing hematopoietic transcription factor PU.1 mediates the induction of arachidonate 5-lipoxygenase by multi-walled carbon nanotubes in macrophages in vitro.Archives of toxicology · 2025Article
- Systematic analysis based on bioinformatics and experimental validation identifiesAnnals of medicine · 2024Article
- Leukotrienes in Innate Immunity: Still Underappreciated after All These Years?Journal of immunology (Baltimore, Md. : 1950) · 2023Review
- Construction of a predictive model for immunotherapy efficacy in lung squamous cell carcinoma based on the degree of tumor-infiltrating immune cells and molecular typing.Journal of translational medicine · 2022Article
- Modeling of cancer-related body-wide effects identifies LTB4 as a diagnostic biomarker for pancreatic cancer.EBioMedicine · 2022Article
- A drug targeting 5-lipoxygenase enhances the activity of a JAK2 inhibitor in CD34Oncology letters · 2021Article
- Single-cell RNA-seq reveals the immune escape and drug resistance mechanisms of mantle cell lymphoma.Cancer biology & medicine · 2020Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Myeloproliferative neoplasms such as polycythemia vera (PV), which are associated with the JAK mutation V617F, remain incurable despite progress in the use of JAK2 inhibitors for treatment of some of these diseases. In this study, we employed mice that undergo JAK2V617F-induced PV as a tool to explore new candidate targets for therapy. Our investigations focused on the lipid metabolic enzyme arachidonate 5-lipoxygenase (Alox5), which we found to be strongly upregulated by JAK2V617F in hematopoietic cells in vitro and in vivo Notably, genetic deletion of Alox5 or its inhibition in mice with a bioactive small-molecule inhibitor was sufficient to attenuate PV development. This therapeutic effect was associated with induction of a blockade in cell-cycle progression and also with apoptosis in PV cells. Genetic loss exerted an inhibitory effect on PV-initiating cells. Similarly, Alox5 inhibition was sufficient to suppress colony formation in human JAK2V617F-expressing CD34
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