“The research we have done is striking in that we showed pre-existing inflammation may be one of the factors that accelerates metastasis to the inflamed site” said Vijaya L. Iragavarapu-Charyulu, Ph.D., the principle investigator of the study from the Charles E. Schmidt College of Medicine at Florida Atlantic University. “We hope that this study is a fundamental building block for future studies on how other inflammatory diseases may predispose patients for increased metastasis.”
To make their discovery, Iragavarapu’s group used two groups of mice, one of which was genetically modified so it could not produce the CHI3L1 glycoprotein. Then they induced the two groups of mice to become asthmatic, after which the mice were challenged with breast cancer cells. After four weeks researchers observed that there was less inflammation in the mice lacking CHI3L1 expression, and that the tumors in these mice did not grow as fast. These mice also had less metastasis to the lungs. This proved that CHI3L1was an important inflammatory protein that promoted tumor growth and metastasis.
“There is increasing evidence of a link between inflammation and cancer,” said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology. “While normally inflammation helps us fight of infections, chronic inflammation has been linked to increased risk of tumor development. These new studies begin to shed light on an important way this link between inflammation and malignancy may work, providing a potential starting point for developing inflammation-based therapeutics to treat cancer.”