GRAND RAPIDS, Mich. (WOOD) — A research team from the Van Andel Institute in Grand Rapids believes it has found a connection between a common precursor to cancer and how cancer develops.

Dr. Gerd Pfeifer, a professor in the VAI’s Department of Epigenetics and the senior author of the study, believes the link is oxidative stress — a breakdown in the body’s immune system usually brought on by prolonged inflammation.

“Inflammation is linked to many cancer types but it’s not actually clear what the mechanism is, how inflammation may cause cancer,” Pfeifer told News 8.

The study, which was published last week in the medical journal “Science Advances,” walks through how researchers were able to trace inflammation directly to certain cancers.

Inflammation is a natural reaction from the immune system, bringing resources to the site of an injury or infection to fix the problem and start the healing process. Part of that process involves reactive oxygen species, an unstable molecule that easily reacts to other molecules in a cell.

The problems start when the body’s immune system doesn’t react properly. Sometimes after the injury or infection has subsided, the immune response doesn’t wind down and those reactive oxygen molecules continue to build up. That can trigger oxidative stress.

“Inflammation has always been linked to oxidative stress,” Pfeifer said. “This is coming from the immune cells during infection and inflammation. The immune cells produce these small molecules called hydrogen peroxide. And they are very reactive, so they can damage cells, damage proteins, damage DNA. And so this particular damage (could possibly cause genetic) mutations.”

By tracking oxidative stress, Pfeifer and his team were able to map two types of DNA damage. They were able to use their findings and compare them with mutation signatures published in the COSMIC Database, the world’s largest databank on cancer mutations. They found mutation signatures that are commonly found in stomach and esophageal cancers and adenocarcinoma.

“(Those cancers) have always been linked to inflammation. So we think that the inflammation in these tissues can promote DNA damage, which can then eventually be seen in the tumors. It’s like looking at the whole step from inflammation, going to DNA damage mutations and then cancer,” Pfeifer said. “Once we understand the mechanism of how the cancers arise, once we know what the condition or the exposure of a tissue to some kind of cancer-causing agents, then we can think about prevention.”

Pfeifer, who has been conducting cancer research for nearly 30 years, hopes the team’s findings lead to more educated guesses and eventually direct evidence on other carcinogens.

“One good example is lung cancers and cigarette smoking. That’s been well established for many years. Or skin tumors like melanoma and sun exposure,” Pfeifer said. “But then there are cancer types where we really have no good guesses at the moment.”

Inflammation isn’t the only common precursor for cancer and it’s not a precursor for every type of cancer, but Pfeifer believes the finding can provide more avenues toward prevention and early detection.

“(Inflammation is not found) in all cancers, but many types,” Pfeifer told News 8. “For example, the liver tumors linked to either the hepatitis virus or in some cases fatty liver disease, which also causes lots of inflammation. And then things like cervical cancer and the papilloma viruses. Inflammatory bowel disease often comes with an increasing risk of colorectal cancers.”

Pfeifer and the VAI team plan to test their findings against other forms of cancer to see if they can spot more common mutation signatures.