patients are expected to be diagnosed with the disease in 2012, and 37,390 patients are expected to die from it. The vast majority of these cases are pancreatic ductal adenocarcinomas, which develop in the ducts of the pancreas. These highly invasive tumors consist of an abundant desmoplastic stroma, in which are embedded malignant cancer cells expressing markers of pancreatic ductal cells. For patients with pancreatic ductal adenocarcinoma, the only curative option is surgery. The standard procedure is a pancreaticoduodenectomy, a surgical operation that removes the head of the pancreas but spares the remaining tissue. Unfortunately, most pancreatic cancer patients present with unresectable metastatic or locally advanced disease. In fact, only 20% of patients have resectable tumors at the time of diagnosis. But even for those patients who undergo surgery, the overall 5-year survival rate is of just 20%, as most of these patients will relapse within a year of their surgery. Hence, there is a critical need for novel drugs that can more efficaciously target these tumor cells and/or reduce the incidence of recurrence. Telomerase inhibitors have been proposed to be especially well-suited to block the regrowth of residual cancer cells after conventional cancer therapy. Not only do they selectively target the telomerasepositive cancer cells, but their growth inhibitory effects increase as the targeted cells perform an increasing number of cell divisions. In the present study, we have characterized the effects of a telomerase inhibitor, GRN163L, on the cellular lifespan and survival of a panel of pancreatic cancer cell lines. Telomerase is the enzyme responsible for the maintenance of telomeres, essential structures that cap and protect the ends of linear chromosomes. Human telomeres are made of tandem copies of n DNA repeats and of associated proteins, which together form a protective capping complex. This cap protects chromosomal ends from degradation, interchromosomal fusions and from being MCE Company Glesatinib (hydrochloride) recognized as double-stranded DNA breaks, a form of DNA K 01-162 damage. Because of problems associated with the replication of the ends of linear DNA molecules, the so-called end-replication problems, telomeres shorten each time human somatic cells divide and this attrition l