Pancreatic cancer risk in hereditary pancreatitis

Abstract

Inflammation is part of the body's immune response in order to remove harmful stimuli—like pathogens, irritants or damaged cells—and start the healing process. Recurrent or chronic inflammation on the other side seems a predisposing factor for carcinogenesis and has been found associated with cancer development. In chronic pancreatitis mutations of the cationic trypsinogen (PRSS1) gene have been identified as risk factors of the disease. Hereditary pancreatitis (HP) is a rare cause of chronic pancreatic inflammation with an early onset, mostly during childhood. HP often starts with recurrent episodes of acute pancreatitis and the clinical phenotype is not very much different from other etiologies of the disease. The long-lasting inflammation however generates a tumor promoting environment and represents a major risk factor for tumor development This review will reflect our knowledge concerning the specific risk of HP patients to develop pancreatic cancer.

Pancreatic cancer biology and genetics from an evolutionary perspective

“…For example, patients with chronic pancreatitis owing to protease, serine 1 ( PRSS1 ) or serine peptidase inhibitor, Kazal type 1 ( SPINK1 ) mutations have a well-documented increased risk of developing pancreatic cancer, perhaps as a result of the increased epithelial cell divisions that occur during injury and repair processes, or from reactive oxygen species that cause DNA damage 26 . Both the ongoing cycles of injury and repair and reactive oxygen species would be expected to increase the net number of mutations that occur per division.…”

SPINK1 (Serine Peptidase Inhibitor, Kazal Type 1)

“…Prognosis The life expectancy of the pancreatitis patients is close to normal. However, patients have an increased risk of developing pancreatic cancer (Weiss, 2014).…”

Pancreatic Cancer Chemoprevention Translational Workshop

“…This vicious cycle of epithelial proliferation, inflammation, more epithelial proliferation, and more inflammation, etc . could be a reasonable target for chemoprevention 31–35 .…”