G. Jeffrey Aaron

Open figure viewer Oncology practices have been strongly influenced by the genetic sequencing of tumors, with actionable biomarkers guiding patient treatments, a practice that is largely referred to as precision oncology (1). Activating mutations in the KRAS oncogene occur in 90% to 95% of pancreatic ductal adenocarcinoma (PDAC) cases, with the most common alterations being KRASG12D (40%), KRASG12V (30%), and KRASG12R (20%; ref. 2).

Open figure viewer Pancreatic ductal adenocarcinoma (PDAC) is a deadly disease with a 5-year survival rate of approximately 12.5% (1). KRAS mutation is considered to be the initiating event and oncogenic driver of PDAC (2). The central dogma of mutant KRAS signaling states that KRAS utilizes multiple effectors, including RAF, PIK3CA, RAL, and others, to promote proliferation and tumorigenesis (3–5).

Open figure viewer Pancreatic cancer has the lowest 5-year survival rate among major organ cancers (13%) and ranks as the third leading cause of cancer mortality in the United States (1). Pancreatic ductal adenocarcinoma (PDAC) comprises 90% of all pancreatic cancer cases (2).