A recently described master regulator protein may explain the development of aberrant cell growth in the pancreas spurred by inflammation
A team from the Perelman School of Medicine at the University of Pennsylvania profiled gene expression of mouse pancreatic ductal and duct-like cells from different states - embryonic development, acute pancreatitis and K-ras mutation-driven carcinogenesis - to find the molecular regulation of these processes.
Broadly speaking, two cellular compartments are important in a normal pancreas, endocrine cells, which produce hormones including insulin, and exocrine cells – acinar and ductal -- which make and secrete digestive enzymes.
A cover article from the lab of Anil Rustgi, MD, Chief, Division of Gastroenterology, published early online in Genes and Development, details the molecular changes of exocrine cells during inflammation, so-called acinar-ductal metaplasia (ADM), a prelude to pancreatic ductal adenocarcinoma.
They used cell lineage tracing to follow what happens to the regulator protein called Prrx1 as cells change characteristics. Another protein, Sox9, which is downstream of Prrx1 in the cell signal pathway, is also important in understanding how pancreatic cancer forms, as the group has established the first link of Prrx1 to Sox9. The findings suggest that Prrx1 and Sox9 influence the emergence of an intermediate cell type that can give rise to cancer.
Inflammation is Key Culprit
Inflammation of the pancreas, or pancreatitis, is a leading reason for hospital admission, according to the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), and chronic pancreatitis is a risk factor for cancer of the pancreas. Each year, about 210,000 people in the United States are admitted to the hospital with acute pancreatitis.
Acute pancreatitis is caused by alcohol abuse, gallstones, and autoimmune disorders. When things go wrong, inflammatory pancreatitis happens, and the change from an acute state to a chronic state can lead to cancer.
When a patient recovers from pancreatitis, the change in cell fate reverts to the original cell type. But, if the pancreatitis is chronic, changed cells stay changed.
"We hope that studies like this one that identify key molecules and pathways that govern the cancerous fate of cells can be used as diagnostic predictors of treatment outcome and severity for cancer," says Rustgi.
University of Pennsylvania School of Medicine: http://www.uphs.upenn.edu/news/
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I read about a researcher in China named Rongxiang Xu who's working on stem cell treatments that can be administered so stem cell cultivation could be handled entirely in situ. It sounds like these could be complementary technologies. Has Labspaces covered Xu before?
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In the article on the discovery of dinosaurs (They’re back, Review, 6 June) you state: “In Sussex, a local doctor uncovered fragmentary remains of what appeared to be two more species of colossal extinct land reptiles.” You grossly underplay the contribution of Lewes-born Gideon Mantell, geologist and palaeontologist, author and diarist, friend to princes and international scholars as well as local doctor. Mantell not only discovered (aided by his wife) the first remains of the iguanodon in 1824 but named it – as it resembled the tooth of an iguana. This was the first known land dinosaur, Mary Anning having identified the first sea-living dinosaur.Mantell went on to put together more pieces of the jigsaw with extra fossil discoveries. In contrast to Richard Owen, whose models form the basis for the Crystal Palace dinosaurs, Mantell stated correctly that iguanodon would have walked on their back legs, using their forearms to fight or gather food. He did, however, attribute the thumb spike to a nose horn though later corrected this assumption. The Natural History Museum has a display on Gideon and his wife Mary’s contribution as well as the large “Mantell-piece” of Iguanodon fossils that he had on show in his museum in Brighton. He sold it, along with many more priceless items, to the British Museum in 1838. Gideon Mantell’s reputation deserves better than your throwaway remark. Debby MatthewsLewes, East Sussex Continue reading...
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