Bcl-2 expression and glucocorticoid-induced apoptosis of leukemic and lymphoma cells

Leuk Lymphoma. 1996 Jan;20(3-4):199-205. doi: 10.3109/10428199609051608.


The lytic response of lymphoid cells to glucocorticoid hormones (GC) is prototypical of the induction of apoptosis: a special form of cellular demise for the removal of unwanted or redundant cells. Initiation and execution of a death programme are therefore major checkpoints in GC-sensitivity. Although Bcl-2 protein can prevent or delay apoptosis of lymphoma and leukemia cells, exposed to multiple cytotoxic agents, its antagonism of GC-induced apoptosis appears most critical in conferring resistance to corticosteroids. Moreover, Bcl-2 may modulate GC-signalling to apoptosis through its association with fundamental cellular processes such as energy state, Ca2+ homeostasis and transmembrane transport. However, this signalling pathway can also be interrupted by Bcl-2- independent mechanisms. This review discusses the various cellular and oncogenetic factors that control GC sensitivity of leukemia/lymphoma cells and proposes a hypothesis of how GC may induce a death programme, sensitive to blockade by Bcl-2.

MeSH terms

  • Adenosine Triphosphate / metabolism
  • Animals
  • Apoptosis / drug effects*
  • CD3 Complex / physiology
  • Cell Division / drug effects
  • Dexamethasone / pharmacology*
  • Gene Expression Regulation, Neoplastic / drug effects
  • Glucocorticoids / pharmacology*
  • Humans
  • Leukemia / metabolism
  • Leukemia / pathology*
  • Lymphocytes / cytology*
  • Lymphoma / metabolism
  • Lymphoma / pathology*
  • Mice
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins c-bcl-2
  • Rats
  • Tumor Cells, Cultured


  • CD3 Complex
  • Glucocorticoids
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Dexamethasone
  • Adenosine Triphosphate