Summary
Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive malignancies with a very dismal prognosis. While genetic changes play a central role in pancreatic cancer development, these changes ultimately elicit their long-term effects via changes in cell identity due to altered gene expression. Notably, pancreatic cancer displays a very high degree of plasticity whereby cellular identity can rapidly change in a non-genetic manner in response to environmental signals or selective pressure. Our group investigates the molecular epigenetic mechanisms controlling gene transcription and therapy response in pancreatic cancer.
- Identify and characterize novel regulators of pancreatic cancer cell plasticity
- Exploit targetable transcriptional and epigenetic mechanisms controlling pancreatic cancer subtype identity and therapy response for patient treatment
- Develop and utilize relevant patient-centered experimental models for pancreatic cancer
- Test novel mechanism-based therapeutic approaches as a basis for future clinical studies