ReviewFrontiers in oncology2016
Protein Phosphatase 2A as a Therapeutic Target in Acute Myeloid Leukemia.
Review in Frontiers in oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
38 citing papers in PubMed, 67 citations in OpenAlex.
- Greatwall kinase regulates acute myeloid leukaemia cell division through a non-canonical mechanism.EMBO reports · 2026Article
- Integrator 20th anniversary: a molecular machine indispensable in development and disease.Trends in molecular medicine · 2026Review
- Anticancer agent FTY720 upregulates cell cycle regulator BTG2 via the SET/TAF-Iβ -PP2A-SMAD3 signaling pathway and induces G2/M arrest in leukemia.Genes & genomics · 2026Article
- NUP214 in Acute Myeloid Leukemia.Cells · 2025Review
- Assessment of chromatin remodeling of acute myeloid leukemia cells treated with gilteritinib: a case report.Journal of medical case reports · 2025Article
- The Emerging Role of Ubiquitin-Specific Protease 36 (USP36) in Cancer and Beyond.Biomolecules · 2024Review
- Oxidative stress is two-sided in the treatment of acute myeloid leukemia.Cancer medicine · 2024Review
- Insights into the molecular response ofScience and technology of advanced materials · 2024Article
- Constitutively active CaMKII Drives B lineage acute lymphoblastic leukemia/lymphoma in tp53 mutant zebrafish.PLoS genetics · 2023Article
- Oncoprotein SET dynamically regulates cellular stress response through nucleocytoplasmic transport in breast cancer.Cell biology and toxicology · 2023Article
- Combination Therapies Targeting Apoptosis in Paediatric AML:International journal of molecular sciences · 2023Article
- YTHDF2 exerts tumor-suppressor roles in gastric cancer via up-regulating PPP2CA independently of mBiological procedures online · 2023Article
- Article
- Thirty years of SET/TAF1β/I2PP2A: from the identification of the biological functions to its implications in cancer and Alzheimer's disease.Bioscience reports · 2022Review
- Review
- Is Nucleoredoxin a Master Regulator of Cellular Redox Homeostasis? Its Implication in Different Pathologies.Antioxidants (Basel, Switzerland) · 2022Review
- PP2A promotes apoptosis and facilitates docetaxel sensitivity via the PP2A/p-eIF4B/XIAP signaling pathway in prostate cancer.Oncology letters · 2022Article
- Crosstalk between hnRNP K and SET in ATRA-induced differentiation in acute promyelocytic leukemia.FEBS open bio · 2021Article
- SET levels contribute to cohesion fatigue.Molecular biology of the cell · 2021Article
- FAM122A promotes acute myeloid leukemia cell growth through inhibiting PP2A activity and sustaining MYC expression.Haematologica · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) is a heterogeneous malignant disorder of hematopoietic progenitor cells in which several genetic and epigenetic aberrations have been described. Despite progressive advances in our understanding of the molecular biology of this disease, the outcome for most patients is poor. It is, therefore, necessary to develop more effective treatment strategies. Genetic aberrations affecting kinases have been widely studied in AML; however, the role of phosphatases remains underexplored. Inactivation of the tumor-suppressor protein phosphatase 2A (PP2A) is frequent in AML patients, making it a promising target for therapy. There are several PP2A inactivating mechanisms reported in this disease. Deregulation or specific post-translational modifications of PP2A subunits have been identified as a cause of PP2A malfunction, which lead to deregulation of proliferation or apoptosis pathways, depending on the subunit affected. Likewise, overexpression of either SET or cancerous inhibitor of protein phosphatase 2A, endogenous inhibitors of PP2A, is a recurrent event in AML that impairs PP2A activity, contributing to leukemogenesis progression. Interestingly, the anticancer activity of several PP2A-activating drugs (PADs) depends on interaction/sequestration of SET. Preclinical studies show that pharmacological restoration of PP2A activity by PADs effectively antagonizes leukemogenesis, and that these drugs have synergistic cytotoxic effects with conventional chemotherapy and kinase inhibitors, opening new possibilities for personalized treatment in AML patients, especially in cases with SET-dependent inactivation of PP2A. Here, we review the role of PP2A as a druggable tumor suppressor in AML.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.