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.
Cell, Volume 148, Issue 4, 633-635, 17 February 2012
After 22 years and over 11 years since major patents awarded plus a nobel prizee I am really tired of hearing about mice!
Been long and abused by management for a decade. Out of empathy. Help people or close up and I'll take my loss!