ArticleThe Journal of experimental medicine2006
In vivo analysis of the role of aberrant histone deacetylase recruitment and RAR alpha blockade in the pathogenesis of acute promyelocytic leukemia.
Article in The Journal of experimental medicine, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- Targeted Cancer Stem Cell Therapeutics: An Update.Current topics in medicinal chemistry · 2025Review
- Metabolic reprogramming and epigenetic modifications in cancer: from the impacts and mechanisms to the treatment potential.Experimental & molecular medicine · 2023Review
- Pharmaceutical/Clinical Strategies in the Treatment of Acute Promyelocytic Leukemia: All-Trans Retinoic Acid Encapsulation by Spray-Drying Technology as an Innovative Approach-Comprehensive Overview.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Co-targeting leukemia-initiating cells and leukemia bulk leads to disease eradication.Leukemia · 2022Article
- Selective Inhibition of HDAC Class I Sensitizes Leukemia and Neuroblastoma Cells to Anticancer Drugs.Biomedicines · 2021Article
- Recent Advances in Targeting of Breast Cancer Stem Cells Based on Biological Concepts and Drug Delivery System Modification.Advanced pharmaceutical bulletin · 2020Review
- Therapeutic Strategies Targeting Cancer Stem Cells and Their Microenvironment.Frontiers in oncology · 2019Review
- Therapies targeting cancer stem cells: Current trends and future challenges.World journal of stem cells · 2015Review
- Article
- How animal models of leukaemias have already benefited patients.Molecular oncology · 2013Review
- The cell biology of disease: Acute promyelocytic leukemia, arsenic, and PML bodies.The Journal of cell biology · 2012Review
- Valproic acid induces differentiation and transient tumor regression, but spares leukemia-initiating activity in mouse models of APL.Leukemia · 2012Article
- The SUMO E3-ligase PIAS1 regulates the tumor suppressor PML and its oncogenic counterpart PML-RARA.Cancer research · 2012Article
- Treatment with 5-azacytidine accelerates acute promyelocytic leukemia leukemogenesis in a transgenic mouse model.Genes & cancer · 2011Article
- All-trans retinoic acid is capable of inducing folate receptor β expression in KG-1 cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2010Article
- Acute promyelocytic leukaemia: novel insights into the mechanisms of cure.Nature reviews. Cancer · 2010Review
- Retinoid signaling regulates breast cancer stem cell differentiation.Cell cycle (Georgetown, Tex.) · 2009Article
- CK2 mediates phosphorylation and ubiquitin-mediated degradation of the PML tumor suppressor.Molecular and cellular biochemistry · 2008Article
- Diagnosis and treatment of acute promyelocytic leukemia.Current oncology reports · 2007Review
- PML-retinoic acid receptor alpha inhibits PML IV enhancement of PU.1-induced C/EBPepsilon expression in myeloid differentiation.Molecular and cellular biology · 2007Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
The promyelocytic leukemia-retinoic acid receptor alpha (PML-RARalpha) protein of acute promyelocytic leukemia (APL) is oncogenic in vivo. It has been hypothesized that the ability of PML-RARalpha to inhibit RARalpha function through PML-dependent aberrant recruitment of histone deacetylases (HDACs) and chromatin remodeling is the key initiating event for leukemogenesis. To elucidate the role of HDAC in this process, we have generated HDAC1-RARalpha fusion proteins and tested their activity and oncogenicity in vitro and in vivo in transgenic mice (TM). In parallel, we studied the in vivo leukemogenic potential of dominant negative (DN) and truncated RARalpha mutants, as well as that of PML-RARalpha mutants that are insensitive to retinoic acid. Surprisingly, although HDAC1-RARalpha did act as a bona fide DN RARalpha mutant in cellular in vitro and in cell culture, this fusion protein, as well as other DN RARalpha mutants, did not cause a block in myeloid differentiation in vivo in TM and were not leukemogenic. Comparative analysis of these TM and of TM/PML(-/-) and p53(-/-) compound mutants lends support to a model by which the RARalpha and PML blockade is necessary, but not sufficient, for leukemogenesis and the PML domain of the fusion protein provides unique functions that are required for leukemia initiation.
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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.