The ATDC gene has been identified by researchers from the NYU School of Medicine and University of Michigan as necessary for the development of pancreatic cancer.

Currently there is a theory that a number of cancers develop after adult cells return to more “primitive” cells with higher growth rates to better resupply cells lost through injury or inflammation. Should this change coincide with other genetic errors, the repair process stops working.

The scientists found that deleting the ATDC gene in pancreatic cells led to “one of the most profound blocks of tumour formation ever observed in a well-known mice model engineered to develop pancreatic ductal adenocarcinoma”.

The research looked specifically at acinar cells in the pancreas, which secrete digestive enzymes that potentially damage tissue. To counter this the acinar cells quickly return to stem cell types that resemble high-growth primitive cells, which allow regeneration but also are more likely to become cancerous.

Ultimately it was found that aggressive pancreatic cancer was caused by genetic mutations in every single one of the mice when the ATDC gene was present. No cancer was found in the same cancer-prone mice who lacked the gene, however.

The scientists also created pancreatitis in the mice by treating them with a signaling protein fragment that damages pancreatic tissues. The ATDC gene expression took a few days after the damage to increase, in keeping with the timeframe associated with acinar cells being reprogrammed into their ductal cell-type cells.

Also determined that the expression of ATDC triggered a cell-signaling protein that under some circumstances activates genes including SOX9, which has been linked to the development of ductal stem cells and to aggressive growth observed in pancreatic cancer.