Randomized trial demonstrates KMT2D's role in PDAC, indicating its potential as a tumor suppressor.
Key Points
This research investigates the role of KMT2D in pancreatic ductal adenocarcinoma (PDAC) development associated with KRAS mutations and its relationship with TP53.
Utilized genetically engineered mouse models driven by mutant Kras with and without Tp53
Conducted exome sequencing and RNA-Seq analysis to assess gene expression and mutation status
Evaluated tumor incidence and survival rates in mouse models and human PDAC samples
Loss of Kmt2d increased tumor incidence and decreased survival in KRAS-driven models, independent of Tp53
KMT2D low expression in human PDAC correlated with lower survival
RNA-Seq revealed enrichment in pathways involved in cell growth following Kmt2d depletion