Inflammation triggers colon cancer cells to spread to other organs, according to Arizona State University research led by Raymond DuBois. The findings will help create more targeted drugs in order to prevent and treat colon cancer.
DuBois said, “We’ve long known that simple things like taking aspirin or other anti-inflammatory drugs (called nonsteroidal anti-inflammatory drugs, or NSAIDs), have beneficial effects on reducing the risk of colorectal cancer. But non-aspirin NSAIDs can cause serious cardiovascular side effects when taken over a long period of time, so we’ve needed to discover better drug targets. This study points us in the right direction.”
Current survival rates among colon cancer patients are up to five years with treatment. This may be due to colon cancer becoming resistant to chemotherapy, or the role that inflammation plays.
The researchers found that colon cancer tumor could outwit its host using inflammatory mediator to expand its cancer stem cells in order to seek out other organs. There was an apparent link between the pro-inflammatory mediator prostaglandin E2 and increased colorectal cancer stem cells.
DuBois added, “The normal role of PGE2 is to come to the rescue when you do something, like cut your finger. It attracts the body’s immune cells and stimulates pathways that heal the wound site. The level of PGE2 goes up and then goes down within a few days of healing the wound. But in cancer, the cells keep making PGE2 chronically, so it’s like this wounding process that never heals. In doing so, it generates these cancer stem cells that promote cancer progression and metastatic spread.”
When PGE2 binds to its receptors on the surface of the cancer cell, it signals a cascade of cancer cells to renew, differentiate, and eventually become resistant to chemotherapy.
DuBois explained his mouse model, “We use a combination of approaches that utilize human tissues and mouse models to complete our studies. We take samples from human colon cancers and then purify the cancer stem cell population. When we treat these stem cells with PGE2, we found that they are 1,000 times more metastatic than the cells we don’t treat with PGE2.”
DuBois concluded, “Now, if we can just target and eliminate the stem cells from people with colon cancer, we can develop a new therapeutic approach to treat colorectal cancer and improve outcomes.”
Screening guidelines for colon cancer
Screening for colon cancer occurs when a person does not have any symptoms of colon cancer. Screening looks to uncover polyps along the colon and remove them before they can become cancerous.
Regular colon cancer screening begins at the age of 50 as a preventative measure. Screening involves high-sensitivity fecal occult blood testing, sigmoidoscopy, or colonoscopy, which begins at the age of 50 and goes until the age of 75.
Screening may occur prior to the age of 50, if you have or had a close relative with colon cancer or polyps, if you have an inflammatory bowel disease like Crohn’s disease, or if you have a genetic syndrome that increases your risk of colon cancer.
Your doctor will determine when screening is best for you. And remember, early detection is your best defense against colon cancer.