ArticleClinical cancer research : an official journal of the American Association for Cancer Research2015
Selective Inhibition of HDAC1 and HDAC2 as a Potential Therapeutic Option for B-ALL.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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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
46 citing papers in PubMed, 81 citations in OpenAlex.
- Trial
- Therapeutic Advances in Adult B-cell Acute Lymphoblastic Leukemia with KMT2A Rearrangements.Annals of hematology · 2026Review
- CircHIPK3 promotes the progression of B-cell acute lymphoblastic leukemia in children by binding to STAT3.Frontiers in pharmacology · 2026Article
- S-adenosylmethionine addiction confers sensitivity to methionine restriction inHaematologica · 2025Article
- Chromatin Regulatory Targets for Anticancer Therapeutics.Chemical reviews · 2025Review
- The deacetylases HDAC1/HDAC2 control JAK2Signal transduction and targeted therapy · 2025Article
- The NLRP1 Emerges as a Promising Therapeutic Target and Prognostic Biomarker Across Multiple Cancer Types: A Comprehensive Pan-Cancer Analysis.Cancer medicine · 2025Article
- Article
- HDAC inhibitor MS275 reprograms metabolism to induce differentiation and suppress proliferation in hepatocellular carcinoma.Frontiers in immunology · 2025Article
- Selective inhibition of HDAC class IIA as therapeutic intervention for KMT2A-rearranged acute lymphoblastic leukemia.Communications biology · 2024Article
- Article
- MDM2 Antagonist Idasanutlin Reduces HDAC1/2 Abundance and Corepressor Partners but Not HDAC3.ACS medicinal chemistry letters · 2024Article
- Histone deacetylase inhibitors: targeting epigenetic regulation in the treatment of acute leukemia.Therapeutic advances in hematology · 2024Review
- PROTAC chemical probes for histone deacetylase enzymes.RSC chemical biology · 2023Review
- Collateral lethality between HDAC1 and HDAC2 exploits cancer-specific NuRD complex vulnerabilities.Nature structural & molecular biology · 2023Article
- ANP32B suppresses B-cell acute lymphoblastic leukemia through activation of PU.1 in mice.Cancer science · 2023Article
- Targeting histone deacetylases for cancer therapy: Trends and challenges.Acta pharmaceutica Sinica. B · 2023Review
- Analyzing Lymphoma Development and Progression Using HDACi in Mouse Models.Methods in molecular biology (Clifton, N.J.) · 2023Article
- A 'click' chemistry approach to novel entinostat (MS-275) based class I histone deacetylase proteolysis targeting chimeras.RSC medicinal chemistry · 2022Article
- Impact of Histone Modifications and Their Therapeutic Targeting in Hematological Malignancies.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
purposeHistone deacetylase inhibitors (HDACi) have recently emerged as efficacious therapies that target epigenetic mechanisms in hematologic malignancies. One such hematologic malignancy, B-cell acute lymphoblastic leukemia (B-ALL), may be highly dependent on epigenetic regulation for leukemia development and maintenance, and thus sensitive to small-molecule inhibitors that target epigenetic mechanisms. EXPERIMENTAL
designA panel of B-ALL cell lines was tested for sensitivity to HDACi with varying isoform sensitivity. Isoform-specific shRNAs were used as further validation of HDACs as relevant therapeutic targets in B-ALL. Mouse xenografts of B-cell malignancy-derived cell lines and a pediatric B-ALL were used to demonstrate pharmacologic efficacy.
resultsNonselective HDAC inhibitors were cytotoxic to a panel of B-ALL cell lines as well as to xenografted human leukemia patient samples. Assessment of isoform-specific HDACi indicated that targeting HDAC1-3 with class I HDAC-specific inhibitors was sufficient to inhibit growth of B-ALL cell lines. Furthermore, shRNA-mediated knockdown of HDAC1 or HDAC2 resulted in growth inhibition in these cells. We then assessed a compound that specifically inhibits only HDAC1 and HDAC2. This compound suppressed growth and induced apoptosis in B-ALL cell lines in vitro and in vivo, whereas it was far less effective against other B-cell-derived malignancies.
conclusionsHere, we show that HDAC inhibitors are a potential therapeutic option for B-ALL, and that a more specific inhibitor of HDAC1 and HDAC2 could be therapeutically useful for patients with B-ALL.
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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.