ReviewFrontiers in oncology2015
Therapeutic Re-Activation of Protein Phosphatase 2A in Acute Myeloid Leukemia.
Review in Frontiers in oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Germline mutations in PPP2R1B in patients with a personal and family history of cancer.JCI insight · 2025Article
- Emerging Roles of B56 Phosphorylation and Binding Motif in PP2A-B56 Holoenzyme Biological Function.International journal of molecular sciences · 2024Review
- 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
- Atypical Chronic Myeloid Leukemia: New Developments from Molecular Diagnosis to Treatment.Medicina (Kaunas, Lithuania) · 2021Review
- Atypical Chronic Myeloid Leukemia: Where Are We Now?International journal of molecular sciences · 2020Review
- Review
- Protein phosphatase 2A activation as a therapeutic strategy for managing MYC-driven cancers.The Journal of biological chemistry · 2020Article
- Redox inhibition of protein phosphatase PP2A: Potential implications in oncogenesis and its progression.Redox biology · 2019Review
- A Cancer-Associated Missense Mutation in PP2A-Aα Increases Centrosome Clustering during Mitosis.iScience · 2019Article
- Protein phosphatase 2A as a therapeutic target in inflammation and neurodegeneration.Pharmacology & therapeutics · 2019Review
- Benzene-induced mouse hematotoxicity is regulated by a protein phosphatase 2A complex that stimulates transcription ofThe Journal of biological chemistry · 2019Article
- The impact of phosphatases on proliferative and survival signaling in cancer.Cellular and molecular life sciences : CMLS · 2018Review
- Forskolin increases the effect of everolimus on aromatase inhibitor-resistant breast cancer cells.Oncotarget · 2018Article
- Therapeutic targeting of PP2A.The international journal of biochemistry & cell biology · 2018Review
- Sex chromosome loss and the pseudoautosomal region genes in hematological malignancies.Oncotarget · 2016Review
- All roads lead to PP2A: exploiting the therapeutic potential of this phosphatase.The FEBS journal · 2016Review
- Protein Phosphatase 2A as a Therapeutic Target in Acute Myeloid Leukemia.Frontiers in oncology · 2016Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Protein phosphatase 2A (PP2A) is a serine/threonine phosphatase that is required for normal cell growth and development. PP2A is a potent tumor suppressor, which is inactivated in cancer cells as a result of genetic deletions and mutations. In myeloid leukemias, genes encoding PP2A subunits are generally intact. Instead, PP2A is functionally inhibited by post-translational modifications of its catalytic C subunit, and interactions with negative regulators by its regulatory B and scaffold A subunits. Here, we review the molecular mechanisms of genetic and functional inactivation of PP2A in human cancers, with a particular focus on human acute myeloid leukemias (AML). By analyzing expression of genes encoding PP2A subunits using transcriptome sequencing, we find that PP2A dysregulation in AML is characterized by silencing and overexpression of distinct A scaffold and B regulatory subunits, respectively. We review the mechanisms of functional PP2A activation by drugs such as fingolimod, forskolin, OP449, and perphenazine. This analysis yields two non-mutually exclusive mechanisms for therapeutic PP2A re-activation: (i) allosteric activation of the phosphatase activity, and (ii) stabilization of active holo-enzyme assembly and displacement of negative regulatory factors from A and B subunits. Future studies should allow the development of specific and potent pharmacologic activators of PP2A, and definition of susceptible disease subsets based on specific mechanisms of PP2A dysregulation.
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Registered trials
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.