ReviewExperimental hematology2016
Regain control of p53: Targeting leukemia stem cells by isoform-specific HDAC inhibition.
Review in Experimental hematology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
17 citing papers in PubMed, 29 citations in OpenAlex.
- Role of histone deacetylases in blood cancer: Exploring peptide‑based inhibitors as therapeutic strategies for leukemia treatment (Review).Oncology reports · 2026Review
- IHCH9033, a novel class I HDAC inhibitor, synergizes with FLT3 inhibitor and rescues quizartinib resistance in FLT3-ITD AML via enhancing DNA damage response.Experimental hematology & oncology · 2025Article
- Tyrosine Kinase Inhibitor Therapy Enhances Stem Cells Profile and May Contribute to Survival of Chronic Myeloid Leukemiastem Cells.Journal of clinical medicine · 2025Article
- Unveiling critical structural features for effective HDAC8 inhibition: a comprehensive study using quantitative read-across structure-activity relationship (q-RASAR) and pharmacophore modeling.Molecular diversity · 2024Article
- Exploring the role of histone deacetylase and histone deacetylase inhibitors in the context of multiple myeloma: mechanisms, therapeutic implications, and future perspectives.Experimental hematology & oncology · 2024Review
- Drug Resistance Mechanisms of Acute Myeloid Leukemia Stem Cells.Frontiers in oncology · 2022Review
- Characteristics of leukemic stem cells in acute leukemia and potential targeted therapies for their specific eradication.Cancer drug resistance (Alhambra, Calif.) · 2022Review
- Review
- Article
- Targeting of the Alox12-12-HETE in Blast Crisis Chronic Myeloid Leukemia Inhibits Leukemia Stem/Progenitor Cell Function.Cancer management and research · 2020Article
- Restoring T Cell Tolerance, Exploring the Potential of Histone Deacetylase Inhibitors for the Treatment of Juvenile Idiopathic Arthritis.Frontiers in immunology · 2019Review
- Concise Review: Chronic Myeloid Leukemia: Stem Cell Niche and Response to Pharmacologic Treatment.Stem cells translational medicine · 2018Review
- Irf8 regulates the progression of myeloproliferative neoplasm-like syndrome via Mertk signaling in zebrafish.Leukemia · 2018Article
- Predicting Chemotherapy Resistance in AML.Current hematologic malignancy reports · 2017Review
- The biomarkers of leukemia stem cells in acute myeloid leukemia.Stem cell investigation · 2017Review
- Pharmacological activation of wild-type p53 in the therapy of leukemia.Experimental hematology · 2016Review
- Histone deacetylase inhibitors as cancer therapeutics.Annals of translational medicine · 2016Article
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 2 institutions in 1 country.
Funding
Abstract
Leukemia stem cells (LSCs) are self-renewable, leukemia-initiating populations that are often resistant to traditional chemotherapy and tyrosine kinase inhibitors currently used for treatment of acute or chronic myeloid leukemia. The persistence and continued acquisition of mutations in resistant LSCs represent a major cause of refractory disease and/or relapse after remission. Understanding the mechanisms regulating LSC growth and survival is critical in devising effective therapies that will improve treatment response and outcome. Several recent studies indicate that the p53 tumor suppressor pathway is often inactivated in de novo myeloid leukemia through oncogenic-specific mechanisms, which converge on aberrant p53 protein deacetylation. Here, we summarize our current understanding of the various mechanisms underlying deregulation of histone deacetylases (HDACs), which could be exploited to restore p53 activity and enhance targeting of LSCs in molecularly defined patient subsets.
Indexed as
Identifiers
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.