Telomeres and cancer: from crisis to stability to crisis to stability.
basic_science · Level V
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- Record sourced from PubMed, PMID 22341437.
- Also identified by DOI 10.1016/j.cell.2012.01.043 and PMC identifier 3322332.
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Abstract
Telomere attrition unleashes genomic instability, promoting cancer development. Once established, however, the malignant clone often re-establishes genomic stability through overexpression of telomerase. In two papers, one in this issue of Cell and one in the subsequent issue, DePinho and colleagues explore the consequences of telomerase re-expression and its validity as a therapeutic target in mouse models of cancer.