|Awarded On||August 20, 2014|
|Title||Role of DNA2 Nuclease in Cellular Tolerance of Replication Stress and Telomere Maintenance - Implications for Cancer Biology and Anticancer Therapy|
|Award Mechanism||Individual Investigator|
|Institution/Organization||Baylor College of Medicine|
|Principal Investigator/Program Director||Grzegorz Ira|
|Cancer Sites||All Sites|
The key to successful targeted cancer therapy is to identify intrinsic features that distinguish cancer cells from normal cells. Cancer specific unlimited proliferation signals, due to the activation of the oncogenes or loss of tumor suppressors, result in immortalization. The consequences of unlimited proliferation include loss of chromosome ends, called telomeres, and largely increased spontaneous DNA damage associated with uncontrolled chromosomes duplication. To counteract these processes, cancer cells increase the usage of a specific DNA repair pathway called Break-Induced Replication, which helps cells to repair frequent chromosome breaks and, in some cancers types such as sarcomas, he...