ArticlePloS one2013
Vorinostat induces apoptosis and differentiation in myeloid malignancies: genetic and molecular mechanisms.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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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
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Who cites it
38 citing papers in PubMed, 59 citations in OpenAlex.
- A clinical trial for patients with acute myeloid leukemia or myelodysplastic syndromes not eligible for standard clinical trials.Leukemia · 2017Trial
- New potent N-hydroxycinnamamide-based histone deacetylase inhibitors suppress proliferation and trigger apoptosis in THP-1 leukaemia cells.Archiv der Pharmazie · 2025Article
- HDAC inhibitor Vorinostat and BET inhibitor Plx51107 epigenetic agents' combined treatments exert a therapeutic approach upon acute myeloid leukemia cell model.Medical oncology (Northwood, London, England) · 2022Article
- Article
- The Roles of IRF-8 in Regulating IL-9-Mediated Immunologic Mechanisms in the Development of DLBCL: A State-of-the-Art Literature Review.Frontiers in oncology · 2022Review
- Atypical Teratoid Rhabdoid Tumours Are Susceptible to Panobinostat-Mediated Differentiation Therapy.Cancers · 2021Article
- Development of Dl1.72, a Novel Anti-DLL1 Antibody with Anti-Tumor Efficacy against Estrogen Receptor-Positive Breast Cancer.Cancers · 2021Article
- Preclinical and clinical progress for HDAC as a putative target for epigenetic remodeling and functionality of immune cells.International journal of biological sciences · 2021Review
- Identification of drug combinations on the basis of machine learning to maximize anti-aging effects.PloS one · 2021Article
- K562 erythroleukemia line as a possible reticulocyte source to culture Plasmodium vivax and its surrogates.Experimental hematology · 2020Article
- Article
- HDAC Inhibitors in Acute Myeloid Leukemia.Cancers · 2019Review
- HDAC3 Activity is Essential for Human Leukemic Cell Growth and the Expression of β-catenin, MYC, and WT1.Cancers · 2019Article
- Epigenetic Modifiers in Myeloid Malignancies: The Role of Histone Deacetylase Inhibitors.International journal of molecular sciences · 2018Review
- Novel tropolones induce the unfolded protein response pathway and apoptosis in multiple myeloma cells.Oncotarget · 2017Article
- Naturally occurring benzoic acid derivatives retard cancer cell growth by inhibiting histone deacetylases (HDAC).Cancer biology & therapy · 2017Article
- Key Roles of AXL and MER Receptor Tyrosine Kinases in Resistance to Multiple Anticancer Therapies.Current oncology reports · 2017Review
- Selective Inhibitors of Histone Deacetylases 1 and 2 Synergize with Azacitidine in Acute Myeloid Leukemia.PloS one · 2017Article
- Epimutational profile of hematologic malignancies as attractive target for new epigenetic therapies.Oncotarget · 2016Review
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAberrant epigenetic patterns are central in the pathogenesis of haematopoietic diseases such as myelodysplastic syndromes (MDS) and acute myeloid leukaemia (AML). Vorinostat is a HDACi which has produced responses in these disorders. The purpose of this study was to address the functional effects of vorinostat in leukemic cell lines and primary AML and MDS myeloid cells and to dissect the genetic and molecular mechanisms by which it exerts its action. METHODOLOGY/PRINCIPAL
findingsFunctional assays showed vorinostat promoted cell cycle arrest, inhibited growth, and induced apoptosis and differentiation of K562, HL60 and THP-1 and of CD33(+) cells from AML and MDS patients. To explore the genetic mechanism for these effects, we quantified gene expression modulation by vorinostat in these cells. Vorinostat increased expression of genes down-regulated in MDS and/or AML (cFOS, COX2, IER3, p15, RAI3) and suppressed expression of genes over-expressed in these malignancies (AXL, c-MYC, Cyclin D1) and modulated cell cycle and apoptosis genes in a manner which would favor cell cycle arrest, differentiation, and apoptosis of neoplastic cells, consistent with the functional assays. Reporter assays showed transcriptional effect of vorinostat on some of these genes was mediated by proximal promoter elements in GC-rich regions. Vorinostat-modulated expression of some genes was potentiated by mithramycin A, a compound that interferes with SP1 binding to GC-rich DNA sequences, and siRNA-mediated SP1 reduction. ChIP assays revealed vorinostat inhibited DNA binding of SP1 to the proximal promoter regions of these genes. These results suggest vorinostat transcriptional action in some genes is regulated by proximal promoter GC-rich DNA sequences and by SP1.
conclusionThis study sheds light on the effects of vorinostat in AML and MDS and supports the implementation of clinical trials to explore the use of vorinostat in the treatment of these diseases.
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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.