Unmet Need
Pancreatic ductal adenocarcinomas (PDAs) are the most prevalent neoplastic disease of the pancreas. PDAs account for more than 90% of all pancreatic malignancies and are the fourth most frequent cause of cancer-related deaths worldwide. Almost all PDAs develop following the activation of the KRAS gene. This activation triggers epithelial transformation and recruitment of desmoplastic stroma through additional transcriptional and epigenetic regulation. Then there occurs sequential progression involving genetic hits in several tumor suppressor genes, resulting in the starting stages of PDA. Thus, there is a need for a way to de-activate the KRAS gene to decrease the possibility of the development of PDA.
Technology Overview
Johns Hopkins inventors have profiled dysregulated microRNAs (miRNAs). They started with the earliest premalignant pancreatic intraepithelial neoplasias (PanINs) in genetically engineered mutated KRAS and P53 (KPSC) mice. The mice were programmed to recapitulate human PDA tumorigenesis. The inventors identified cell-specific and compartment-specific regulators in PanINs and PDA. The regulators were then tested to see if they were useful for early PanIn detection or for interception of developing premalignant pancreatic lesions and other KRAS-driven premalignancies.
Stage of Development
The method and system has been tested and is being further developed.
