Scientists have identified dementia-like protein clumping in pancreatic cells at risk of developing cancer, a discovery that could open new avenues for the treatment and prevention of one of the UK’s deadliest cancers. Pancreatic cancer claims approximately 6,900 lives annually in the UK and is often diagnosed at a late stage, limiting treatment options.
Published today (15 August) in Developmental Cell, the research was funded by Cancer Research UK, with additional support from Wellcome, the Medical Research Council, and the Biotechnology and Biological Sciences Research Council.
Researchers at the Cancer Research UK Scotland Centre investigated pancreatic cells in mice to understand why healthy cells turn cancerous. They discovered that pre-cancerous cells—those at risk of becoming cancerous—exhibited defects in autophagy, the cell’s natural recycling process.
The team observed abnormal clumping of “problem proteins” in these pre-cancer cells, a behavior commonly associated with neurological conditions such as dementia. Similar clumping was also found in human pancreatic tissue samples, indicating that this may be a key feature in pancreatic cancer development.
Professor Simon Wilkinson, Cancer Research UK Senior Fellow at the University of Edinburgh’s Institute of Genetics and Cancer, commented:
“Our research highlights the potential role of autophagy disruption in the earliest stages of pancreatic cancer. By learning from other diseases where protein clumping occurs, such as dementia, we may gain valuable insights into how this aggressive cancer develops and how it might be prevented.”
Unlike other cancers, survival rates for pancreatic cancer have not significantly improved over recent decades. Genetic mutations, particularly in the KRAS gene, are commonly associated with pancreatic cancer, but researchers are increasingly recognizing that genetic factors alone do not explain the disease’s development.
Autophagy helps cells maintain health by recycling excess molecules. In the pancreas, it regulates digestive proteins and hormones essential for food breakdown. While cancer cells can sometimes exploit autophagy to fuel growth, this study suggests that the combination of KRAS mutations and disrupted autophagy may trigger the onset of pancreatic cancer.
The researchers plan to explore these processes further to determine whether they could be used to predict, slow, or even reverse the earliest stages of pancreatic cancer. They will also investigate whether age, sex, diet, or other factors influence these cellular changes.
Dr. Iain Foulkes, Executive Director of Research and Innovation at Cancer Research UK, emphasized:
“Understanding how pancreatic cancer develops is a top priority. Research into its causes, early detection, and better treatments remains critical to reducing deaths and improving patient outcomes.”
The study, titled “ER-phagy and proteostasis defects prime pancreatic epithelial state changes in KRAS-mediated oncogenesis,” provides a promising step toward understanding the cellular mechanisms that drive pancreatic cancer, offering potential targets for future therapies.
YOU MAY ALSO LIKE
