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

被引：11

作者：

Romano, MF ^{[1
]}

Lamberti, A ^{[1
]}

Turco, MC ^{[1
]}

Venuta, S ^{[1
]}

机构：

[1] Dept Biochem, Naples, Italy

来源：

LEUKEMIA & LYMPHOMA | 2000年 / 36卷 / 3-4期

关键词：

apoptosis; CD40; NF-kappa B/Rel;

D O I：

10.3109/10428190009148846

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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-kappa B/Rel transcription factors. The anti- apoptotic effect of CD40 was abolished using a phosphorothioate kappa B 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-kappa B/Rel activity on leukemic cell response to apoptogenic agents.

引用

页码：255 / 262

页数：8

共 53 条

[1] Prolonged phenotypic, functional, and molecular change in group I Burkitt lymphoma cells on short-term exposure to CD40 ligand [J].