A new study sheds light on why pancreatic cancer is so aggressive. Researchers found that pancreatic ductal adenocarcinoma (PDAC) reactivates genes normally only active during fetal development. This “onco-fetal” behavior may help explain the cancer’s rapid growth and resistance to treatment.
The team examined stem cell markers in fetal, adult, and cancerous pancreatic tissues. They discovered that CD44 and c-Myc—genes active in fetal development—are mostly silent in healthy adults but strongly re-expressed in PDAC. This reactivation supports cancer cell growth, migration, and survival. Other markers, like CD117, show the tumor microenvironment also plays a role, while some, like OCT3/4, appear less important in this cancer type.
Clinically, these findings suggest new strategies for diagnosis and treatment. CD44 and c-Myc could serve as biomarkers for detecting PDAC and tracking its aggressiveness. Targeting these molecules, or the supportive tumor stroma, may improve therapy effectiveness and reduce recurrence. The study highlights that pancreatic cancer essentially hijacks embryonic growth programs to fuel its deadly behavior.