Accumulation of DNA damage, RNA decay and telomere dysfunction are well established events in the etiology of cancer, aging and disease. However, until recently, a lack of physiologically relevant model systems prevented our deep understanding of the pathways connecting genetic instability to tissue failure and malignant transformation.

At the Batista Lab, we utilize human stem cell differentiation and organoids to understand the etiology of disease and cancer after accumulation of DNA damage and exacerbated telomere shortening. We combine biochemical, molecular, and functional studies to determine the consequences of genetic instability in different cell populations, and decipher pathways that can be utilized to prevent or cure disease in patinets.