ArticleOncotarget2016
PML/RARa inhibits PTEN expression in hematopoietic cells by competing with PU.1 transcriptional activity.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- PML::RARα+ myeloid cells display metabolic alterations that can be targeted to treat resistant/relapse acute promyelocytic leukemias.Leukemia · 2025Article
- Retinoid X Receptor agonists as selective modulators of the immune system for the treatment of cancer.Pharmacology & therapeutics · 2023Review
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- The treatment of acute promyelocytic leukemia in 2023: Paradigm, advances, and future directions.Frontiers in oncology · 2022Review
- Inflammation as a regulator of hematopoietic stem cell function in disease, aging, and clonal selection.The Journal of experimental medicine · 2021Review
- PU.1 enforces quiescence and limits hematopoietic stem cell expansion during inflammatory stress.The Journal of experimental medicine · 2021Article
- Article
- NPM1 Mutated, BCR-ABL1 Positive Myeloid Neoplasms: Review of the Literature.Mediterranean journal of hematology and infectious diseases · 2020Review
- Article
- Review
- Biomodulatory Treatment With Azacitidine, All-Frontiers in pharmacology · 2018Article
- The forkhead box C1 (FOXC1) transcription factor is downregulated in acute promyelocytic leukemia.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Acute promyelocitic leukemia (APL) is characterized by the pathognomonic presence in leukemic blasts of the hybrid protein PML/RARA, that acts as a transcriptional repressor impairing the expression of genes that are critical to myeloid differentiation. Here, we show that primary blasts from APL patients express lower levels of the oncosuppressor protein PTEN, as compared to blast cells from other AML subtypes or normal bone marrow, and demonstrate that PML-RARA directly inhibits PTEN expression. We show that All-Trans Retinoic Acid (ATRA) triggers in APL cells an active chromatin status at the core regulatory region of the PTEN promoter, that allows the binding of the myeloid-regulating transcription factor PU.1, and, in turn, the transcriptional induction of PTEN. ATRA, via PML/RARA degradation, also promotes PTEN nuclear re-localization and decreases expression of the PTEN target Aurora A kinase. In conclusion, our findings support the notion that PTEN is one of the primary targets of PML/RARA in APL.
Indexed as
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What OpenQuestion holds
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.