A recent study conducted on mice has successfully pinpointed a gene that is responsible for that can put an end to the development of pancreatic cancer.
The study was aimed at finding the genetic components that were somehow involved in the development of pancreatic cancer and included simulating deadly cancer in mice.
Pancreatic cancer is particularly deadly as compared to other cancers. During the phase where a tumor can be treated, it shows no symptoms. Symptoms only tend to appear when the disease is in its advanced stage and is largely incurable. Due to this and its resistance to treatment, it has a meager 5% survival rate.
The National Cancer Institute (NCI) issued a report that predicts that by the year 2020 pancreatic cancer would be the second principal mortality cause in the USA. Currently, it stands at fourth place.
Using historic values and patterns the NCI has forecasted that in the current year there will be around 57000 new cases and around 46000 patients will breathe their last due to it.
Previously it was thought that the KRAS oncogene in the cells is the primary suspect. But the recent research has pointed towards another gene that plays a pivotal role in the development and spread of cancer.
An oncogene is a gene inside a cell that has gone ‘bad’. Normally it allows cells to grow properly but a malfunction of it can cause the cell to exhibit unusual growth and develop into cancer.
The new research was conducted and authored by a team at New York University Langone Health’s Perlmutter Cancer Center. The main correspondent was Dr. Diane Simeone who serves as a director of the Pancreatic Cancer Center at the same University.
Simeone’s team began the study to investigate the role played by a specific gene, namely, the “ataxia-telangiectasia group D complementing” (ATDC) in pancreatic tumor formation. The samples for the study were sourced from mice and human patients. The detailed findings from the study are to be published in the Genes & Development Journal.
The research was aimed at investigating the hypothesis that a tumor is actually a result of cells turning on their repair mechanism and never turning it off.
Adult cells are understood to return to a stage of development to repair any injury or damage to them. This phase supplies new cells to replace the ones that got damaged. This is a fairly short process and the replacement and repair are stopped once the necessary measures have been taken.
It was hypothesized that some genetic disorders may cause the healing process to become erratic and out of control. This goes on to develop into cancer.
Dr. Simeone’s team singled out the acinar cells found in the pancreas as the epicenter for investigation. These cells are primarily responsible for the manufacture of digestive enzymes.
The enzymes produced by the acinar cells tend to damage the inner lining of the small intestine and to make up for the damage the acinar cells enter a stem-cell-like high growth phase to take up the repairs.
The researchers deduced that if the Acinar cells happen to contract DNA mutations, they can become cancerous. When mutated they will still enter the stem-cell phase but won’t exit it.
To elaborate the process acinar cells can, under certain conditions, transform into “acinar-to-ductal metaplasia” (ADM). ADM is an intermediary stage that leads up to high-growth cell types. These cells then transform into a second stage called “pancreatic intraepithelial neoplasia” (PanIN). During the PanIN the cell multiplication goes haywire and multiplication is excessive.
The team simulated pancreatitis in mice, a condition in which inflammation causes the acinar cells to transform into the ADM phase, i.e. they become high-growth ductal cells.
“Adult ductal cells share some similarities with embryonic primitive ducts and may retain the ability to generate endocrine cells in the adult.”, said Dr. Simeone.
The researchers found that the ATDC gene expression was elevated after pancreatitis caused tissue damage, and it got heightened to levels that caused the acinar cells to transform into ductal cells.
The co-existence of both the ATDC and the KRAS oncogene proved to be a deadly combination as all of the subject mice with it developed aggressive pancreatic cancer.
This is where the team struck gold. The researchers went on to remove the ATDC from the combination and not even a single test subject developed cancer. Further, the acinar cells didn’t progress to the ADM stage.
Diane and his team were really surprised with the outcome. He said, “We thought the deletion would slow cancer growth, not completely prevent it.”
He added, “We found that deleting the ATDC gene in pancreatic cells 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.”
Detailed experimentation on the study led to the discovery of chain reactions, signaling proteins and further genes that shed light on how ATDC can be pivotal in triggering cancer.
The genes and signaling proteins identified are pinpointed for further analysis and can be the subject of new therapeutic and prevention strategies against pancreatic cancer.