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    Retinoid receptor signaling and autophagy in acute promyelocytic leukemia.

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    Authors
    Orfali, Nina
    McKenna, Sharon L
    Cahill, Mary R
    Gudas, Lorraine J
    Mongan, Nigel P
    Affiliation
    Cork Cancer Research Center, University College Cork, Cork, Ireland; Department of Pharmacology, Weill Cornell Medical College, New York, NY 10065, USA.
    Issue Date
    2014-05-15
    MeSH
    Animals
    Autophagy
    Cell Differentiation
    Hematopoiesis
    Humans
    Leukemia, Promyelocytic, Acute
    Receptors, Retinoic Acid
    Retinoids
    Signal Transduction
    
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    Citation
    Retinoid receptor signaling and autophagy in acute promyelocytic leukemia. 2014, 324 (1):1-12 Exp. Cell Res.
    Journal
    Experimental cell research
    URI
    http://hdl.handle.net/10147/322508
    DOI
    10.1016/j.yexcr.2014.03.018
    PubMed ID
    24694321
    Abstract
    Retinoids are a family of signaling molecules derived from vitamin A with well established roles in cellular differentiation. Physiologically active retinoids mediate transcriptional effects on cells through interactions with retinoic acid (RARs) and retinoid-X (RXR) receptors. Chromosomal translocations involving the RARα gene, which lead to impaired retinoid signaling, are implicated in acute promyelocytic leukemia (APL). All-trans-retinoic acid (ATRA), alone and in combination with arsenic trioxide (ATO), restores differentiation in APL cells and promotes degradation of the abnormal oncogenic fusion protein through several proteolytic mechanisms. RARα fusion-protein elimination is emerging as critical to obtaining sustained remission and long-term cure in APL. Autophagy is a degradative cellular pathway involved in protein turnover. Both ATRA and ATO also induce autophagy in APL cells. Enhancing autophagy may therefore be of therapeutic benefit in resistant APL and could broaden the application of differentiation therapy to other cancers. Here we discuss retinoid signaling in hematopoiesis, leukemogenesis, and APL treatment. We highlight autophagy as a potential important regulator in anti-leukemic strategies.
    Item Type
    Article
    Language
    en
    ISSN
    1090-2422
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.yexcr.2014.03.018
    Scopus Count
    Collections
    Cork University Hospital

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