Ulla-Maja Bailey

TL;DR: Detailed genomic analysis of 456 pancreatic ductal adenocarcinomas identified 32 recurrently mutated genes that aggregate into 10 pathways: KRAS, TGF-β, WNT, NOTCH, ROBO/SLIT signalling, G1/S transition, SWI-SNF, chromatin modification, DNA repair and RNA processing.

TL;DR: Replication stress and DDR deficiency are independent of each other, creating opportunities for therapy in DDR-proficient PC and after platinum therapy.

TL;DR: It is demonstrated that distinct patterns of chromatin accessibility can be used to identify patient subgroups that are indistinguishable by gene expression profiles, highlighting the utility of Chromatin-based biomarkers for patient selection in the treatment of PDAC.

TL;DR: It is shown that patient-derived cell lines faithfully recapitulate the epithelial component of pancreatic tumors including previously described molecular subtypes and generates a novel signature of replication stress with potential clinical utility in predicting response to ATR and WEE1 inhibitor treatment.

TL;DR: This work shows OCS from 18 women to be monoclonal through analysis of DNA variants from isolated carcinoma and sarcoma components, and demonstrates that microtubule inhibitors, vinorelbine and eribulin, were more effective than standard-of-care platinum-based chemotherapy.