ArticleOncogene2008
Selective anti-leukaemic activity of low-dose histone deacetylase inhibitor ITF2357 on AML1/ETO-positive cells.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 45 citations in OpenAlex.
- ITF2357 exerts anti‑tumor activity in colorectal cancer via the miR‑1938/ADAM12 axis.Molecular biology reports · 2026Article
- Epigenetic Activation of Plasmacytoid DCs Drives IFNAR-Dependent Therapeutic Differentiation of AML.Cancer discovery · 2022Article
- HDAC Inhibitors in Acute Myeloid Leukemia.Cancers · 2019Review
- New insights into transcriptional and leukemogenic mechanisms of AML1-ETO and E2A fusion proteins.Frontiers in biology · 2016Article
- New Therapeutic Approaches in Polycythemia Vera.Clinical lymphoma, myeloma & leukemia · 2015Review
- Novel and emerging therapies for the treatment of polycythemia vera.Expert review of hematology · 2015Review
- Histone deacetylase inhibition synergistically enhances pemetrexed cytotoxicity through induction of apoptosis and autophagy in non-small cell lung cancer.Molecular cancer · 2014Article
- Chromatin-associated CSF-1R binds to the promoter of proliferation-related genes in breast cancer cells.Oncogene · 2014Article
- Redistribution of H3K27me3 and acetylated histone H4 upon exposure to azacitidine and decitabine results in de-repression of the AML1/ETO target gene IL3.Epigenetics · 2014Article
- CD72 regulates the growth of KIT-mutated leukemia cell line Kasumi-1.Scientific reports · 2013Article
- SIAH proteins: critical roles in leukemogenesis.Leukemia · 2013Review
- AML1/ETO sensitizes via TRAIL acute myeloid leukemia cells to the pro-apoptotic effects of hypoxia.Cell death & disease · 2013Article
- Time- and residue-specific differences in histone acetylation induced by VPA and SAHA in AML1/ETO-positive leukemia cells.Epigenetics · 2013Article
- Histone deacetylase inhibitors (HDACIs): multitargeted anticancer agents.Biologics : targets & therapy · 2013Article
- Article
- The role of HDACs inhibitors in childhood and adolescence acute leukemias.Journal of biomedicine & biotechnology · 2011Review
- The DAC system and associations with acute leukemias and myelodysplastic syndromes.Investigational new drugs · 2010Article
- Novel histone deacetylase inhibitors in clinical trials as anti-cancer agents.Journal of hematology & oncology · 2010Review
- Histone deacetylase inhibitor ITF2357 is neuroprotective, improves functional recovery, and induces glial apoptosis following experimental traumatic brain injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009Article
- Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We analysed the in vitro effects of a new hydroxamate derivative, ITF2357, on AML cells. ITF2357 potently induced histone acetylation. ITF2357 0.1 microM blocked proliferation and induced apoptosis in AML1/ETO-positive Kasumi-1 cells, while AML1/ETO-negative HL60, THP1 and NB4 cell lines were sensitive only to 1 microM ITF2357. Apoptosis was induced by 0.1 microM ITF2357 in AML1/ETO-positive primary blasts and U937-A/E cells induced to express AML1/ETO, but not in U937-A/E cells non-expressing AML1/ETO. In Kasumi-1 cells 0.1 microM ITF2357 induced AML1/ETO degradation through a caspase-dependent mechanism. ITF2357 0.1 microM also determined DNMT1 efflux from, and p300 influx to, the nucleus. Moreover, 0.1 microM ITF2357 determined local H4 acetylation and release of DNMT1, HDAC1 and AML1/ETO, paralleled by recruitment of p300 to the IL-3 gene promoter. ITF2357 treatment, however, did not induce re-expression of IL-3 gene. Accordingly, the methylation level of IL-3 promoter, as well as of several other genes, was unmodified. In conclusion, ITF2357 emerged as an anti-leukaemic agent very potent on AML cells, and on AML1/ETO-positive cells in particular. More relevantly, clearly emerged from our results that ITF2357 could be an ideal agent to treat AML subtypes presenting AML1/ETO fusion protein which determine HDAC involvement in leukaemogenesis.
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