期刊
CANCER BIOLOGY & THERAPY
卷 7, 期 11, 页码 1783-1786出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cbt.7.11.6779
关键词
Bloom syndrome; BLM; ATM; DNA damage; cancer therapy; ionizing radiation; xenografts; gene targeting
类别
资金
- National Institutes of Health [CA104253]
- Flight Attendant Medical Research Institute
Bloom syndrome is caused by homozygous mutations in BLM, which encodes a RecQ DNA helicase. Patient-derived cells deficient in BLM helicase activity exhibit genetic instability-apparent cytogenetically as sister chromatid exchanges-and activated DNA damage signaling. In this report, we show that BLM-knockout colorectal cancer cells exhibited endogenous, ATM-dependent double-strand DNA break responses similar to those recently observed in Bloom syndrome patient-derived cells. Xenograft tumors established from BLM-deficient cancer cells were not radiosensitive, but exhibited growth impairment that was comparable to that of wild type tumors treated with a single, high dose of ionizing radiation. These results suggest that pharmacological inhibitors of BLM would have a radiomimetic effect and that transient inhibition of BLM activity might be a viable strategy for anticancer therapy.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据