Cancer Therapy Reduces Lung Scarring

Scientists at the Stanford Institute for Stem Cell Biology and Regenerative Medicine have discovered a striking parallel between scar tissue formation and tumor growth: they both evade immune surveillance. As a result of this similarity, therapies to reactivate the immune system to target cancer cells have been shown to also work for treating scar tissue in the lung. The work was published recently in Nature Communications.

Idiopathic lung fibrosis is caused by overactive scar tissue cells called fibroblasts. Though the precise triggers and accelerants of fibrosis progression are still not fully understood, what is known is that in general, lung scarring is bad news. Progression of the conditions greatly limits the patients’ ability to breathe normally, with devastating effects on their overall quality of life. The only clinical intervention for advanced-stage lung fibrosis is a lung transplant.

The study, led by pathology expert Gerlinde Wernig, MD, aimed to identify how the normal molecular pathways involved in preventing overactive fibroblasts are disrupted in the case of fibrosis. Why don’t circulating immune cells such as macrophages detect a problem?

“In idiopathic lung disease, these fibroblasts behave almost like cancer cells,” said Wernig.