PhD candidate at Johns Hopkins School of Medicine studying Fibrolamellar Hepatocellular Carcinoma (FLC). FLC is a rare liver tumor that affects adolescents and young adults and shows little to no sensitivity to traditional chemotherapies. It is driven by a ~400kb deletion on chromosome 19 that forms a fusion protein between exon 1 of DNAJB1 (Hsp40) and exons 2-10 of PRKACA leading to aberrant PKA activity. This fusion has been shown to be sufficient to induce tumors and transcriptional knockdown results in tumor regression in-vivo. However, due to on target toxicities, global PKA inhibition is not a viable treatment option.This fusion protein (DNAJB1-PRKACA) has abnormal sub-cellular localization compared to wild-type PRKACA. I’m using isogenic in-vitro and in-vivo models to understand the consequences of mis localized PRKACA and how this may alter the epigenome to identify new therapies.