Dexamethasone does not counteract the response of acute promyelocytic leukaemia cells to all-trans retinoic acid

Br J Haematol. 1999 Jul;106(1):107-10. doi: 10.1046/j.1365-2141.1999.01481.x.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents, Hormonal / therapeutic use*
  • Blotting, Northern
  • CD18 Antigens / metabolism
  • Cell Division / drug effects
  • Cell Transformation, Neoplastic / drug effects
  • Dexamethasone / therapeutic use*
  • Humans
  • Leukemia, Promyelocytic, Acute / drug therapy*
  • Leukemia, Promyelocytic, Acute / metabolism
  • Leukemia, Promyelocytic, Acute / pathology
  • Thrombomodulin / metabolism
  • Tretinoin / therapeutic use*
  • Tumor Cells, Cultured

Substances

  • Antineoplastic Agents, Hormonal
  • CD18 Antigens
  • Thrombomodulin
  • Tretinoin
  • Dexamethasone