Our laboratory in focused on understanding how telomeres contribute to human health and disease. Telomeres are DNA/protein caps at the ends of chromosomes that are essential to genome stability. Due to the "end replication problem", telomeres shorten each time a cell divides and when they become too short, they trigger apoptosis or permanent cell cycle arrest. Telomeres are maintained by telomerase, composed of a reverse transcriptase (TERT) that synthesizes new telomeres from an endogenously encoded RNA template (TR). Telomerase expression is tightly controlled such that only a few cell types have telomerase activity. When telomeres become too short, they cause a spectrum of diseases including bone marrow failure, liver fibrosis, and, most commonly, lung fibrosis. Our lab is primarily focused on understanding how telomere dysfunction causes lung disease. We approach this question using cell biology, animal modelling, and clinical samples that are available here at Pitt.

In addition, All cancers must overcome the end replication problem to maintain tumor growth and telomerase inhibitor are currently undergoing clinical trial. My laboratory is interested in understanding the mechanisms by which cancer cells escape the tumor suppressive effects of telomeres. Recent research has shown that mutations in the promoter of TERT are some of the most common mutations found in all of cancer. However, not all cancers maintain their telomeres by reactivating telomerase and diverse mechanism exist by which cancers overcome the end replication problem. My laboratory is interested in exploring all the mechanism by which telomeres are maintained in cancer cells in the hopes of identifying potential targets for limiting cancer growth.