ArticleActa neuropathologica communications2015
Targeting class I histone deacetylase 2 in MYC amplified group 3 medulloblastoma.
Article in Acta neuropathologica communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 92 citations in OpenAlex.
- Trial
- Phase I/II intra-patient dose escalation study of vorinostat in children with relapsed solid tumor, lymphoma, or leukemia.Clinical epigenetics · 2019Trial
- The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026Review
- Targeting TET3 suppresses group 3 medulloblastoma stemness and progression via impairing hypomethylation of Otx2 super-enhancer.Cell reports. Medicine · 2025Article
- Small-Molecule Drugs in Pediatric Neuro-Oncology.Current oncology (Toronto, Ont.) · 2025Review
- CoREST in pieces: Dismantling the CoREST complex for cancer therapy and beyond.Science advances · 2025Review
- Recent Advancements in the Development of HDAC/Tubulin Dual-Targeting Inhibitors.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Aberrant histone modifications in pediatric brain tumors.Frontiers in oncology · 2025Review
- Potential role of short-chain fatty acids in the pathogenesis and management of acute lymphocytic leukemia.Annals of translational medicine · 2024Review
- Mechanistic insights into medulloblastoma relapse.Pharmacology & therapeutics · 2024Review
- Suberanilohydroxamic acid (SAHA), a HDAC inhibitor, suppresses the effect of Treg cells by targeting the c-Myc/CCL1 pathway in glioma stem cells and improves PD-L1 blockade therapy.Journal of neuro-oncology · 2024Article
- Combination drug screen identifies synergistic drug interaction of BCL-XL and class I histone deacetylase inhibitors in MYC-amplified medulloblastoma cells.Journal of neuro-oncology · 2024Article
- MYC overexpression and SMARCA4 loss cooperate to drive medulloblastoma formation in mice.Acta neuropathologica communications · 2023Article
- Class I HDAC inhibition reduces DNA damage repair capacity of MYC-amplified medulloblastoma cells.Journal of neuro-oncology · 2023Article
- Class I HDAC inhibitor entinostat synergizes with PLK1 inhibitors in MYC-amplified medulloblastoma cells.Journal of neuro-oncology · 2023Article
- Tacedinaline (CI-994), a class I HDAC inhibitor, targets intrinsic tumor growth and leptomeningeal dissemination in MYC-driven medulloblastoma while making them susceptible to anti-CD47-induced macrophage phagocytosis via NF-kB-TGM2 driven tumor inflammation.Journal for immunotherapy of cancer · 2023Article
- A novel dual epigenetic approach targeting BET proteins and HDACs in Group 3 (MYC-driven) Medulloblastoma.Journal of experimental & clinical cancer research : CR · 2022Article
- Medulloblastoma in the Modern Era: Review of Contemporary Trials, Molecular Advances, and Updates in Management.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Review
- Review
- Molecular profile reveals immune-associated markers of medulloblastoma for different subtypes.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
Abstract
introductionMedulloblastoma (MB) is the most frequent malignant brain tumor in children. Four subgroups with distinct genetic, epigenetic and clinical characteristics have been identified. Survival remains particularly poor in patients with Group 3 tumors harbouring a MYC amplification. We herein explore the molecular mechanisms and translational implications of class I histone deacetylase (HDAC) inhibition in MYC driven MBs. MATERIAL AND
methodsExpression of HDACs in primary MB subgroups was compared to normal brain tissue. A panel of MB cell lines, including Group 3 MYC amplified cell lines, were used as model systems. Cells were treated with HDAC inhibitors (HDACi) selectively targeting class I or IIa HDACs. Depletion of HDAC2 was performed. Intracellular HDAC activity, cellular viability, metabolic activity, caspase activity, cell cycle progression, RNA and protein expression were analyzed.
resultsHDAC2 was found to be overexpressed in MB subgroups with poor prognosis (SHH, Group 3 and Group 4) compared to normal brain and the WNT subgroup. Inhibition of the enzymatic activity of the class I HDACs reduced metabolic activity, cell number, and viability in contrast to inhibition of class IIa HDACs. Increased sensitivity to HDACi was specifically observed in MYC amplified cells. Depletion of HDAC2 increased H4 acetylation and induced cell death. Simulation of clinical pharmacokinetics showed time-dependent on target activity that correlated with binding kinetics of HDACi compounds.
conclusionsWe conclude that HDAC2 is a valid drug target in patients with MYC amplified MB. HDACi should cover HDAC2 in their inhibitory profile and timing and dosing regimen in clinical trials should take binding kinetics of compounds into consideration.
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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.