ArticleJournal of cancer research and clinical oncology2019
Histone deacetylase inhibitor ITF2357 (givinostat) reverts transformed phenotype and counteracts stemness in in vitro and in vivo models of human glioblastoma.
Article in Journal of cancer research and clinical oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- ITF2357 exerts anti‑tumor activity in colorectal cancer via the miR‑1938/ADAM12 axis.Molecular biology reports · 2026Article
- The Role of HDAC6 in Glioblastoma Multiforme: A New Avenue to Therapeutic Interventions?Biomedicines · 2024Review
- Article
- Review
- Oncogenic BRAF and p53 Interplay in Melanoma Cells and the Effects of the HDAC Inhibitor ITF2357 (Givinostat).International journal of molecular sciences · 2023Article
- Inhibition of histone deacetylases attenuates tumor progression and improves immunotherapy in breast cancer.Frontiers in immunology · 2023Review
- The Histone Deacetylase Inhibitor ITF2357 (Givinostat) Targets Oncogenic BRAF in Melanoma Cells and Promotes a Switch from Pro-Survival Autophagy to Apoptosis.Biomedicines · 2022Article
- Differential molecular mechanistic behavior of HDACs in cancer progression.Medical oncology (Northwood, London, England) · 2022Review
- Givinostat-Liposomes: Anti-Tumor Effect on 2D and 3D Glioblastoma Models and Pharmacokinetics.Cancers · 2022Article
- Small Molecule Inhibitors in Adult High-Grade Glioma: From the Past to the Future.Frontiers in oncology · 2022Review
- The botanical drug PBI-05204, a supercritical COFrontiers in pharmacology · 2022Article
- Advances in Epigenetic Cancer Therapeutics.Cureus · 2020Review
- An immunochemistry-based screen for chemical inhibitors of DNA-protein interactions and its application to human CGGBP1.BMC cancer · 2020Article
- Discovery of a novel rhein-SAHA hybrid as a multi-targeted anti-glioblastoma drug.Investigational new drugs · 2020Article
- Givinostat: an emerging treatment for polycythemia vera.Expert opinion on investigational drugs · 2020Review
- Advances in the Knowledge of the Molecular Biology of Glioblastoma and Its Impact in Patient Diagnosis, Stratification, and Treatment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Review
- DNA damage response signaling pathways and targets for radiotherapy sensitization in cancer.Signal transduction and targeted therapy · 2020Review
- Epigenetic Control of Autophagy in Cancer Cells: A Key Process for Cancer-Related Phenotypes.Cells · 2019Review
- The Autophagy Status of Cancer Stem Cells in Gliobastoma Multiforme: From Cancer Promotion to Therapeutic Strategies.International journal of molecular sciences · 2019Review
- NRF2 orchestrates the redox regulation induced by radiation therapy, sustaining embryonal and alveolar rhabdomyosarcoma cells radioresistance.Journal of cancer research and clinical oncology · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
17 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeAberrant expression and activity of histone deacetylases (HDACs) sustain glioblastoma (GBM) onset and progression, and, therefore, HDAC inhibitors (HDACi) represent a promising class of anti-tumor agents. Here, we analyzed the effects of ITF2357 (givinostat), a pan-HDACi, in GBM models for its anti-neoplastic potential.
methodsA set of GBM- and patient-derived GBM stem-cell lines was used and the ITF2357 effects on GBM oncophenotype were investigated in in vitro and in vivo xenograft models.
resultsITF2357 inhibited HDAC activity and affected GBM cellular fate in a dose-dependent manner by inducing G
conclusionsThe present findings provide evidence of the key role played by HDACs in sustaining transformed and stem phenotype of GBM and strongly suggest that ITF2357 may have a clinical potential for the HDACi-based therapeutic strategies against GBM.
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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.