DNA methylation memory of pancreatic acinar-ductal metaplasia transition state altering Kras-downstream PI3K and Rho GTPase signaling in the absence of Kras mutation.

Abstract excerpt

BACKGROUND: A critical area of recent cancer research is the emergence of transition states between normal and cancer that exhibit increased cell plasticity which underlies tumor cell heterogeneity. Pancreatic ductal adenocarcinoma (PDAC) can arise from the combination of a transition state termed acinar-to-ductal metaplasia (ADM) and a gain-of-function mutation in the proto-oncogene KRAS. During ADM, digestive...

Topics

Join the communities discussing this publication.

• Acinar Cells
• Carcinoma, Pancreatic Ductal
• Kruppel-Like Factor 4
• Kruppel-Like Transcription Factors
• Metaplasia