Journal
MOLECULAR CANCER RESEARCH
Volume 4, Issue 3, Pages 197-207Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/1541-7786.MCR-05-0154
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Funding
- Intramural NIH HHS Funding Source: Medline
- NCI NIH HHS [CA81343] Funding Source: Medline
- NIEHS NIH HHS [ES011391] Funding Source: Medline
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The heritable disorder ataxia telangiectasia (AT) is caused by mutations in the AT-mutated (ATM) gene with manifestations that include predisposition to lymphoproliferative cancers and hypersensitivity to ionizing radiation (IR). We investigated gene expression changes in response to IR in human lymphoblasts and fibroblasts from seven normal and seven AT-affected individuals. Both cell types displayed ATM-dependent gene expression changes after IR, with some responses shared and some responses varying with cell type and dose. Interestingly, after 5 Gy IR, lymphoblasts displayed ATM-independent responses not seen in the fibroblasts at this dose, which likely reflect signaling through ATM-related kinases, e.g., ATR, in the absence of ATM function.
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