ReviewCancer science2016
Action mechanisms of histone deacetylase inhibitors in the treatment of hematological malignancies.
Review in Cancer science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 63 citations in OpenAlex.
- Ribitoborate Synergism with Histone Deacetylase Inhibitor Romidepsin as a Potential Treatment for Breast Cancer.International journal of molecular sciences · 2026Article
- Next-Generation HDAC Inhibitors: Advancing Zinc-Binding Group Design for Enhanced Cancer Therapy.Cells · 2025Review
- Identification and validation of genes associated with prognosis of cisplatin-resistant ovarian cancer.BMC cancer · 2024Article
- Monocytic Differentiation in Acute Myeloid Leukemia Cells: Diagnostic Criteria, Biological Heterogeneity, Mitochondrial Metabolism, Resistance to and Induction by Targeted Therapies.International journal of molecular sciences · 2024Review
- Histone deacetylase inhibitors: targeting epigenetic regulation in the treatment of acute leukemia.Therapeutic advances in hematology · 2024Review
- Review
- CAMTA1-PPP3CA-NFATc4 multi-protein complex mediates the resistance of colorectal cancer to oxaliplatin.Cell death discovery · 2022Article
- Epigenetic Regulation Towards Acquired Drug Resistance in Cancer.Sub-cellular biochemistry · 2022Article
- H3K23/H3K36 hypoacetylation and HDAC1 up-regulation are associated with adverse consequences in obstructive sleep apnea patients.Scientific reports · 2021Article
- A Set of 17 microRNAs Common for Brain and Cerebrospinal Fluid Differentiates Primary Central Nervous System Lymphoma from Non-Malignant Brain Tumors.Biomolecules · 2021Article
- Involvement of Alarmins in the Pathogenesis and Progression of Multiple Myeloma.International journal of molecular sciences · 2021Review
- Prospective evaluation of the lymph node proteome in dogs with multicentric lymphoma supplemented with sulforaphane.Journal of veterinary internal medicine · 2020Article
- Targeting ERK-Hippo Interplay in Cancer Therapy.International journal of molecular sciences · 2020Review
- HDAC8: A Promising Therapeutic Target for Acute Myeloid Leukemia.Frontiers in cell and developmental biology · 2020Article
- HDAC-selective Inhibitor Cay10603 Has Single Anti-tumour Effect in Burkitt's Lymphoma Cells by Impeding the Cell Cycle.Current medical science · 2019Article
- Review
- Autoimmune Cytopenias in Chronic Lymphocytic Leukemia: Focus on Molecular Aspects.Frontiers in oncology · 2019Review
- HDAC and HMT Inhibitors in Combination with Conventional Therapy: A Novel Treatment Option for Acute Promyelocytic Leukemia.Journal of oncology · 2019Article
- pH driven precipitation of quisinostat onto PLA-PEG nanoparticles enables treatment of intracranial glioblastoma.Colloids and surfaces. B, Biointerfaces · 2018Article
- The impact of Mir-9 regulation in normal and malignant hematopoiesis.Oncology reviews · 2018Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone deacetylases (HDACs) critically regulate gene expression by determining the acetylation status of histones. Studies have increasingly focused on the activities of HDACs, especially involving non-histone proteins, and their various biological effects. Aberrant HDAC expression observed in several kinds of human tumors makes HDACs potential targets for cancer treatment. Several preclinical studies have suggested that HDAC inhibitors show some efficacy in the treatment of acute myelogenous leukemia with AML1-ETO, which mediates transcriptional repression through its interaction with a complex including HDAC1. Recurrent mutations in epigenetic regulators are found in T-cell lymphomas (TCLs), and HDAC inhibitors and hypomethylating agents were shown to act cooperatively in the treatment of TCLs. Preclinical modeling has suggested that persistent activation of the signal transducer and activator of transcription signaling pathway could serve as a useful biomarker of resistance to HDAC inhibitor in patients with cutaneous TCL. Panobinostat, a pan-HDAC inhibitor, in combination with bortezomib and dexamethasone, has achieved longer progression-free survival in patients with relapsed/refractory multiple myeloma (MM) than the placebo in combination with bortezomib and dexamethasone. Panobinostat inhibited MM cell growth by degrading protein phosphatase 3 catalytic subunit α (PPP3CA), a catalytic subunit of calcineurin. This degradation was suggested to be mediated by the blockade of the chaperone function of heat shock protein 90 due to HDAC6 inhibition. Aberrant PPP3CA expression in advanced MM indicated a possible correlation between high PPP3CA expression and the pathogenesis of MM. Furthermore, PPP3CA was suggested as a common target of panobinostat and bortezomib.
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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.