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dc.contributor.authorOrfali, Nina
dc.contributor.authorMcKenna, Sharon L
dc.contributor.authorCahill, Mary R
dc.contributor.authorGudas, Lorraine J
dc.contributor.authorMongan, Nigel P
dc.date.accessioned2014-07-07T09:18:43Z
dc.date.available2014-07-07T09:18:43Z
dc.date.issued2014-05-15
dc.identifier.citationRetinoid receptor signaling and autophagy in acute promyelocytic leukemia. 2014, 324 (1):1-12 Exp. Cell Res.en_GB
dc.identifier.issn1090-2422
dc.identifier.pmid24694321
dc.identifier.doi10.1016/j.yexcr.2014.03.018
dc.identifier.urihttp://hdl.handle.net/10147/322508
dc.description.abstractRetinoids 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.
dc.language.isoenen
dc.rightsArchived with thanks to Experimental cell researchen_GB
dc.subject.meshAnimals
dc.subject.meshAutophagy
dc.subject.meshCell Differentiation
dc.subject.meshHematopoiesis
dc.subject.meshHumans
dc.subject.meshLeukemia, Promyelocytic, Acute
dc.subject.meshReceptors, Retinoic Acid
dc.subject.meshRetinoids
dc.subject.meshSignal Transduction
dc.titleRetinoid receptor signaling and autophagy in acute promyelocytic leukemia.en_GB
dc.typeArticleen
dc.contributor.departmentCork Cancer Research Center, University College Cork, Cork, Ireland; Department of Pharmacology, Weill Cornell Medical College, New York, NY 10065, USA.en_GB
dc.identifier.journalExperimental cell researchen_GB
dc.description.fundingNo fundingen
dc.description.provinceMunsteren
dc.description.peer-reviewpeer-reviewen
refterms.dateFOA2018-08-24T07:43:03Z
html.description.abstractRetinoids 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.


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