CD40 and B chronic lymphocytic leukemia cell response to fludarabine: the influence of NF-kappaB/Rel transcription factors on chemotherapy-induced apoptosis

Leuk Lymphoma. 2000 Jan;36(3-4):255-62. doi: 10.3109/10428190009148846.

Abstract

The levels of tumour necrosis factor receptor (TNF-R) superfamily members can be altered in lymphoid leukemias, indicating a possible role of such molecules in the biology of these neoplasias. In B chronic lymphocytic leukemia cells, the CD40/CD40L system has been shown to be effective in inhibiting the apoptotic response to fludarabine. The modulation of apoptosis relied on the CD40-induced activity of NF-kappaB/Rel transcription factors. The anti-apoptotic effect of CD40 was abolished using a phosphorothioate kappaB decoy oligodeoxynucleotide. These findings illustrate an example of the biological activity of TNF-R-like molecules in leukemias. They also show the influence of NF-kappaB/Rel activity on leukemic cell response to apoptogenic agents.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Apoptosis* / immunology
  • Apoptosis* / physiology
  • CD40 Antigens / physiology*
  • Humans
  • Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy*
  • Leukemia, Lymphocytic, Chronic, B-Cell / immunology*
  • Leukemia, Lymphocytic, Chronic, B-Cell / pathology
  • NF-kappa B / antagonists & inhibitors
  • NF-kappa B / physiology*
  • Oncogene Proteins v-rel / antagonists & inhibitors
  • Oncogene Proteins v-rel / physiology
  • Tumor Cells, Cultured
  • Vidarabine / analogs & derivatives*
  • Vidarabine / pharmacology

Substances

  • Antineoplastic Agents
  • CD40 Antigens
  • NF-kappa B
  • Oncogene Proteins v-rel
  • Vidarabine
  • fludarabine