Authors
This article focuses on the origin of pancreatic lesions associated with pancreatic cancer. Pancreatic ductal adenocarcinoma (PDAC) is currently the fourth leading cause of cancer death worldwide. Projections for 2030 indicate that it will become the second leading cause of cancer death. Unfortunately, ADK is often diagnosed at an advanced stage, resulting in a 5-year survival rate of less than 10%. Given that the most common precancerous lesions of ADK are currently not clinically detectable, it is crucial to understand the mechanisms underlying their formation and progression to enable early detection and more effective therapeutic intervention to combat ADK.
The acinar cells of the pancreas are responsible for the production of digestive enzymes. They have the capacity to regenerate under certain conditions, thanks to a process known as “acino-canal metaplasia” (ACM), which controls their survival, differentiation and proliferation. During this process, acinar cells undergo dedifferentiation and acquire progenitor cell characteristics, enabling them to adapt to their environment. This process is normally reversible, but in the event of inflammation, prolonged stress or activation of carcinogenic pathways, it can persist and lead to the formation of precancerous lesions in the pancreas. Our review examines this process, including the transcription factors and signalling pathways involved. It sheds light on the mechanisms behind the initiation and progression of pancreatic precancerous lesions.
