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Dexamethasone does not counteract the response of acute promyelocytic leukaemia cells to all‐ trans retinoic acid
Author(s) -
De Ridder Marleen C.,
Van Der Plas Arnout J.,
ErpelinckVerschueren Claudia A. J.,
Löwenberg Bob,
Jansen Joop H.
Publication year - 1999
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.1999.01481.x
Subject(s) - retinoic acid , dexamethasone , medicine , acute promyelocytic leukemia , endocrinology , tretinoin , corticosteroid , cancer research , chemistry , biochemistry , gene
Retinoic acid syndrome is a serious condition that may complicate the treatment of acute promyelocytic leukaemia patients. This syndrome may be treated effectively with high‐dose corticosteroid therapy and, as a result, many patients with acute promyelocytic leukaemia receive dexamethasone at some point during treatment. We investigated whether dexamethasone would also antagonize the beneficial effects of retinoic acid. In t(15;17)‐positive NB4 cells, dexamethasone did not affect the retinoic acid induced differentiation, normalization of PML‐nuclear bodies or the induction of thrombomodulin mRNA. Finally, dexamethasone did not inhibit the anti‐proliferative effect of retinoic acid but rather showed anti‐proliferative activity itself.