Overview
We deploy genetic and small-molecule screens to systematically interrogate pancreatic ductal adenocarcinoma (PDAC) biology at scale. The goal is to move beyond single-gene hypotheses and let unbiased functional data nominate the targets, combinations, and resistance mechanisms that matter clinically.
Approach
CRISPR-based functional genomics screens identify genetic dependencies and synthetic lethal interactions across PDAC models.
Small-molecule and combination screens map which therapeutic pairings overcome adaptive resistance, informing rational trial design.
Computational pipelines integrate screen hits with clinical genomics so candidate targets are prioritised by translational relevance.
Why it matters
PDAC is notoriously resistant to monotherapy. Screening lets us pre-empt resistance and assemble combinations before they reach patients, feeding directly into our KRAS and DNA-damage-repair programs.