| Literature DB >> 22341437 |
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. Copyright ÂEntities:
Year: 2012 PMID: 22341437 PMCID: PMC3322332 DOI: 10.1016/j.cell.2012.01.043
Source DB: PubMed Journal: Cell ISSN: 0092-8674 Impact factor: 41.582