• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

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

作者信息

Romano M F, Lamberti A, Turco M C, Venuta S

机构信息

Department of Biochemistry, Institute Pascale, Naples, Italy.

出版信息

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

DOI:10.3109/10428190009148846
PMID:10674897
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.

摘要

相似文献

1
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.
2
Triggering of CD40 antigen inhibits fludarabine-induced apoptosis in B chronic lymphocytic leukemia cells.CD40抗原的激活可抑制氟达拉滨诱导的B细胞慢性淋巴细胞白血病细胞凋亡。
Blood. 1998 Aug 1;92(3):990-5.
3
DHMEQ, a new NF-kappaB inhibitor, induces apoptosis and enhances fludarabine effects on chronic lymphocytic leukemia cells.新型核因子-κB抑制剂DHMEQ可诱导慢性淋巴细胞白血病细胞凋亡并增强氟达拉滨的作用。
Leukemia. 2006 May;20(5):800-6. doi: 10.1038/sj.leu.2404167.
4
The novel nuclear factor-kappaB inhibitor LC-1 is equipotent in poor prognostic subsets of chronic lymphocytic leukemia and shows strong synergy with fludarabine.新型核因子-κB抑制剂LC-1在慢性淋巴细胞白血病的不良预后亚组中具有同等效力,并与氟达拉滨显示出强烈的协同作用。
Clin Cancer Res. 2008 Dec 15;14(24):8102-11. doi: 10.1158/1078-0432.CCR-08-1673.
5
CD40 triggering enhances fludarabine-induced apoptosis of chronic lymphocytic leukemia B-cells through autocrine release of tumor necrosis factor-alpha and interferon-gama and tumor necrosis factor receptor-I-II upregulation.CD40激活通过自分泌肿瘤坏死因子-α和干扰素-γ以及上调肿瘤坏死因子受体-I-II增强氟达拉滨诱导的慢性淋巴细胞白血病B细胞凋亡。
Haematologica. 2003 Feb;88(2):148-58.
6
Modulation of NF-kappa B activity and apoptosis in chronic lymphocytic leukemia B cells.慢性淋巴细胞白血病B细胞中NF-κB活性和细胞凋亡的调节
J Immunol. 2000 Feb 15;164(4):2200-6. doi: 10.4049/jimmunol.164.4.2200.
7
Leflunomide induces apoptosis in fludarabine-resistant and clinically refractory CLL cells.来氟米特诱导氟达拉滨耐药且临床难治性 CLL 细胞凋亡。
Clin Cancer Res. 2012 Jan 15;18(2):417-31. doi: 10.1158/1078-0432.CCR-11-1049. Epub 2011 Nov 9.
8
Tipping the Noxa/Mcl-1 balance overcomes ABT-737 resistance in chronic lymphocytic leukemia.使 Noxa/Mcl-1 平衡向有利于 Noxa 的方向倾斜可克服慢性淋巴细胞白血病中 ABT-737 的耐药性。
Clin Cancer Res. 2012 Jan 15;18(2):487-98. doi: 10.1158/1078-0432.CCR-11-1440. Epub 2011 Nov 29.
9
Fludarabine induces apoptosis of human T-cell leukemia virus type 1-infected T cells via inhibition of the nuclear factor-kappaB signal pathway.氟达拉滨通过抑制核因子-κB信号通路诱导人1型嗜T细胞白血病病毒感染的T细胞凋亡。
Leukemia. 2007 May;21(5):1044-9. doi: 10.1038/sj.leu.2404622. Epub 2007 Mar 8.
10
Tumor necrosis factor receptor-associated factor 1 gene overexpression in B-cell chronic lymphocytic leukemia: analysis of NF-kappa B/Rel-regulated inhibitors of apoptosis.肿瘤坏死因子受体相关因子1基因在B细胞慢性淋巴细胞白血病中的过表达:NF-κB/Rel调控的凋亡抑制因子分析
Blood. 2002 Nov 15;100(10):3749-56. doi: 10.1182/blood.V100.10.3749.