Pancreatic cancer is an extremely aggressive form of cancer that's difficult to diagnose in its early onset since it often does not cause any signs or symptoms. By the time that symptoms show, it is quite late and often resists treatment.
In fact, according to the National Cancer Institute (NCI), pancreatic cancer is the fourth leading cause of cancer death in the United States and some in fact predicted that it will be the the second leading cause of death by next year, 2020.
Previous studies show that the so-called KRAS oncogene seems to be the main driver behind pancreatic cancer, but recent research published in the journal Genes & Development, shows another gene called "ataxia-telangiectasia group D complementing" (ATDC) to be another major contributing factor.
Dr. Diane Simeone, who is the director of the Pancreatic Cancer Center at the New York University Langone Health's Perlmutter Cancer Center and the corresponding author of this new research, focused on acinar cells, which secretes digestive enzymes that causes damage to tissues in the small intestines. Acinar cells can become cancerous when they're stressed which in turn mutate and transform into what is called "acinar-to-ductal metaplasia" (ADM).
Dr Simeone's team initially used mice to create a model of pancreatitis ( an inflammatory condition that can cause acinar cells to turn into high-growth ductal cells), and they found out that the ATDC gene expression went up a few days after pancreatitis caused tissue damage, and it increased to the levels required for acinar cells to transform into ductal cells.
They further discovered in the study that all mice developed aggressive pancreatic cancer when the ATDC gene was present in combination with the KRA oncogene.
However, when the researchers removed the ATDC gene, none of the cancer-prone mice developed cancer nor did any acinar cells progressed further.
Dr. Simeone comments on how surprising the findings were, saying, "We thought the deletion [of the ATDC gene] would slow cancer growth, not completely prevent it. We found that this resulted in one of the most profound blocks of tumor formation ever observed in a well-known mice model engineered to develop pancreatic ductal adenocarcinoma, [...] which faithfully mimics the human disease."
They were able to further do several experiments that revealed more details which further explains how ATDC ends up triggering pancreatic cancer.
All these new information can lead to potential targets for new therapeutic and prevention strategies against pancreatic cancer.
