Grant: Project Grant

Cancer and aging are seemingly distinct events. However, similar changes in the ability of our cells to respond to environmental challenges are observed in both aging and cancer. For example, damage to DNA, our hereditary material, accumulates in both cancer cells and older cells. Normally, when DNA becomes damaged, pathways become activated to repair the damage. These repair pathways are known to become disrupted in cancer and now some pathway components are proving to be effective targets in particular types of cancer therapy. In older cells, DNA damage accumulates, however the underlying reason for this is not known. To date, most work in cancer research has been performed in young cells, young model organisms or in human cancer cell lines. Since most cancers occur in older individuals, we believe that it will be much more relevant to study DNA repair during aging, especially since there is very little known about how these processes might change or contribute to cancer development. Confounding issues certainly arise with age, but at the cellular level, where cancer and aging biologically converge, pathways that protect our DNA from mutations clearly need to be studied in cells that have aged. My lab uses the model organism budding yeast. Over the past 60 years, work in yeast has provided a foundation of knowledge critical for understanding the molecular events leading to cancer in humans. Since yeast cells are well characterized regarding DNA repair and they also age, they represent a powerful model for rapidly asking how age is related to DNA repair. Thus, characterizing DNA repair in old yeast cells will provide important clues for why DNA repair efficiency decreases and cancer increases exponentially with age in our population.