Statins may help prevent some forms of cancer, study finds

Statins are typically prescribed to help lower cholesterol levels in people whose “bad” cholesterol levels are too high.

Statins can be used in combination with lifestyle changes to help keep cholesterol in a healthy range. For example, people may minimize their saturated fat intake and increase their physical activity levels.

Non-study author Dr. Robert Salazar, a cardiologist with Memorial Hermann, explained the following to Medical News Today:

“Statins are typically used to manage high cholesterol in patients at elevated risk for atherosclerotic cardiovascular disease (ASCVD.) Generally speaking, a statin is started when a patient’s individual risk of heart attacks, strokes or peripheral arterial disease is high. Statin medications are also started when measured blood cholesterol levels are high or after a stroke or heart attack. The effectiveness of statin drugs is then checked using a follow up blood cholesterol level to ensure an adequate response.”

Alternative uses for statins for other health conditions are an ongoing area of research.

Researchers of the current study note that chronic inflammation contributes to cancer development.

Several inflammatory conditions contribute to an increased cancer risk. For example, chronic pancreatitis (an inflammation of the pancreas) raises the risk of pancreatic cancer.

The researchers of the current study note that interleukin 33 (IL-33) is one protein that helps initiate cancer-prone chronic inflammation. They wanted to understand more about the underlying mechanisms involved in this relationship and whether there was a way to alter it.

Researchers utilized mice, human tissue samples, and cell lines. They induced chronic inflammation in mice on the skin and in the pancreas. They found that IL-33 was highly expressed in the inflamed skin and pancreas.

Based on further analysis, they identified that inflammation induction activated a specific signaling pathway called TLR3/4, suggesting that this pathway may cause the IL-33 expression that occurs in chronic inflammation. They further identified another cellular mechanism, TBK1-IRF3, regulating IL-33 expression in chronic pancreatitis and dermatitis in mice.

Researchers then tested the use of pitavastatin to block IL-33 expression. Their work suggests that pitavastatin may successfully block IL-33 expression and, thus, the related chronic pancreatitis.

While looking at human tissue samples, they further confirmed that the IRF3-IL-33 signaling axis is active when the pancreas is inflamed and in cases of pancreatic cancer.

Finally, researchers looked at electronic health records from over 200 million people to look at the use of pitavastatin and the risk for pancreatic cancer. Researchers found that people taking pitavastatin were at a decreased risk for chronic pancreatitis and pancreatic cancer.

Study author Shadmehr Demehri, MD, PhD, explained the key findings of the research to MNT:

“15–20% cancer death worldwide relate to cancers that develop in the context of chronic inflammation. We set out to determine what factor initiates the development of chronic inflammation in various organs. Based on our discovery that an immune factor, called interleukin 33, is the driver of cancer-prone chronic inflammation, we investigated the cellular mechanism that regulates the expression of this immune factor. Our findings, reported in the current publication, reveal this mechanism and demonstrate how [a] statin drug can block this immune factor expression in experimental models and prevent chronic inflammation and cancer in them. Interestingly, we find statin use by patients (to treat high cholesterol) associates with reduced risk of pancreatitis (inflammation of pancreas) and reduced risk of pancreatic cancer.”

The study demonstrates another potential use for statins in the future. Salazar noted the following:

“This study and its findings are quite compelling in demonstrating additional benefits from statin drugs that are independent of cholesterol levels. In particular, lowering inflammation further protects patients from negative outcomes including heart attacks, strokes, dementia, autoimmune disease, premature aging and cancer.”

This preliminary research requires more research before these concepts can reach practical clinical application.

Since it relied on components like mouse models, it’s not perfectly clear how the data applies to humans. The research from patient health records was also from North America and Europe, so more diversity may be needed in this research area.

“It is critical to examine statin efficacy for cancer prevention in chronic inflammation directly in patients through clinical trials,” Demehri said.

“We also aim to extend our work to encompass the array of chronic inflammatory diseases that render patients prone to cancer (e.g., ulcerative colitis and hepatitis) to help prevent cancer in all patients affected by chronic inflammation.”

If future research continues to confirm the findings, it could benefit clinical practice. Non-study author Anton Bilchik, MD, PhD, surgical oncologist, chief of medicine, and director of the Gastrointestinal and Hepatobiliary Program at Providence Saint John’s Cancer Institute in Santa Monica, CA, noted the following to MNT:

“The findings are very provocative because pancreas cancer is a deadly cancer with limited treatment options. If the anti-inflammatory effect of statins can reduce the chance of developing pancreas cancer particularly in high risk patients this will be practice changing and play an important role not only in reducing the risk of heart attacks but also in cancer prevention.”