Diversity in Life Sciences

Genome-wide sequencing initiatives have generated extensive amounts of genotypic and molecular phenotypic data, identifying genetic predispositions (mutations) for developing disease. However, the genetic background is different for every patient. The challenge, therefore, is to understand how to interpret this information to determine how select encoded proteomic variants can not only promote human disease but also influence its response to treatment, and then design effective therapies that are specific for each patient. This aspect of personalized medicine is critically important in the pursuit to eliminate health disparities. As such, major unanswered questions in the field are: how does breast cancer develop and why are certain patients resistant to established therapies?

Despite the significant advances in medicine, increasing evidence suggests a more personalized approach is needed toward treating the individual patient and not the general disease. To accomplish this, integrative approaches are being developed to better understand the molecular mechanisms of disease initiation, progression, as well as drug response. Since these mechanisms are largely studied on the genomic level, we do not yet have a clear integration of how mutations that cause changes in protein structure and can lead to such varied phenotypes, particularly in cancer. My background in enzymology, protein chemistry, structural and cellular biology uniquely positions me to pursue these questions from using a lens of structural biology. My laboratory investigates structural mechanisms of genome maintenance in chemo-resistant cancers, with the goal of defining novel targets for anti-cancer therapies against aggressive tumors.