HNF1A, KRT81, and CYP3A5: three more straws on the back of pancreatic cancer?

Andrew J. Scott, John C. Wilkinson


In this post-genomic era of cancer research, our ability to molecularly define various subtypes of cancer raises tremendous promise for the concepts of patient targeted therapies and precision medicine. A particular bright spot in the utility of cancer subtyping is the example of breast cancer, which has been well defined at the molecular level: tumor subtypes are currently classified based upon the expression of estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2, and current targeted treatment strategies based on subtype assessment have increased clinical responses in the last decade (1). In stark contrast to the subtype success achieved in breast cancer analysis is the present state of pancreatic ductal adenocarcinoma (PDAC). PDAC is one of the most lethal malignancies and the fourth leading cause of cancer deaths, associated with a dismal 5-year survival rate of only ~5%. This poor outlook results from late-stage diagnosis of disease, as non-invasive early detection methods remain elusive in the clinic, and current treatment modalities extend patient lifespan by only several weeks to months (2).