dc.contributor.author | Schenk, T | |
dc.contributor.author | Stengel, S | |
dc.contributor.author | Zelent, A | |
dc.date.accessioned | 2018-08-03T10:11:27Z | |
dc.date.issued | 2014-11-25 | |
dc.identifier | 11 | |
dc.identifier.citation | BRITISH JOURNAL OF CANCER, 2014, 111 pp. 2039 - 2045 | |
dc.identifier.issn | 0007-0920 | |
dc.identifier.uri | https://repository.icr.ac.uk/handle/internal/2253 | |
dc.identifier.eissn | 1532-1827 | |
dc.identifier.doi | 10.1038/bjc.2014.412 | |
dc.description.abstract | All-trans-retinoic acid (ATRA) is a physiologically active metabolite of vitamin A. Its antitumour activities have been extensively studied in a variety of model systems and clinical trials; however, to date the only malignancy responsive to ATRA treatment is acute promyelocytic leukaemia (APL) where it induces complete remission in the majority of cases when administered in combination with light chemotherapy and/or arsenic trioxide. After decades of studies, the efficacy of ATRA to treat other acute myeloid leukaemia (AML) subtypes and solid tumours remains poor. Recent studies directed to improve ATRA responsiveness in non-APL AML seem to indicate that the lack of effective ATRA response in these tumours may be primarily due to aberrant epigenetics, which negatively affect ATRA-regulated gene expression and its antileukaemic activity. Epigenetic reprogramming could potentially restore therapeutic effects of ATRA in all AML subtypes. This review discusses the current progresses in the understanding how ATRA can be utilised in the therapy of non-APL AML and other cancers. | |
dc.format.extent | 2039 - 2045 | |
dc.language | eng | |
dc.language.iso | eng | |
dc.publisher | NATURE PUBLISHING GROUP | |
dc.title | Unlocking the potential of retinoic acid in anticancer therapy | |
dc.type | Journal Article | |
rioxxterms.versionofrecord | 10.1038/bjc.2014.412 | |
rioxxterms.licenseref.startdate | 2014-11-25 | |
rioxxterms.type | Journal Article/Review | |
dc.relation.isPartOf | BRITISH JOURNAL OF CANCER | |
pubs.notes | affiliation: Zelent, A (Reprint Author), Miller Sch Med, Sylvester Comprehens Canc Ctr, Dept Med, Div Hemato Oncol, Miami, FL 33136 USA. Schenk, T.; Stengel, S., Inst Canc Res, Div Mol Pathol, Haemato Oncol Res Unit, London SW7 3RP, England. Zelent, A., Miller Sch Med, Sylvester Comprehens Canc Ctr, Dept Med, Div Hemato Oncol, Miami, FL 33136 USA. keywords: retinoic acid receptor; RAR; combination therapy; epi-drugs; LSD1; KDM1A keywords-plus: ACUTE MYELOID-LEUKEMIA; ACUTE PROMYELOCYTIC LEUKEMIA; DOSE CYTOSINE-ARABINOSIDE; RANDOMIZED-TRIAL; ELDERLY-PATIENTS; GROWTH-FACTORS; DIFFERENTIATION; CANCER; EPIGENETICS; INHIBITION research-areas: Oncology web-of-science-categories: Oncology author-email: [email protected] number-of-cited-references: 36 times-cited: 42 usage-count-last-180-days: 0 usage-count-since-2013: 20 journal-iso: Br. J. Cancer doc-delivery-number: AU4QW unique-id: ISI:000345597700002 oa: gold_or_bronze da: 2018-08-03 | |
pubs.notes | Not known | |
pubs.organisational-group | /ICR | |
pubs.organisational-group | /ICR | |
pubs.volume | 111 | |
pubs.embargo.terms | Not known | |
dc.contributor.icrauthor | Schenk, T | |
dc.contributor.icrauthor | Stengel, S | |