Patients with fibrotic disease have a significantly higher risk of developing cancer. My lab focuses on understanding the pathomechanisms of fibrosis and its contribution to cancer. We showed that in scar tissue cells called fibroblasts are, like cancer cells, able to proliferate abnormally and escape immune surveillance, and that a cure may lie in treatments that reactivate and enhance immune function. We demonstrated that these fibroblasts also evade the immune system using the same immune-dampening proteins as do cancer cells and that a gene activator called JUN is a master regulator of fibrotic processes in mice. Turning on the activity of this gene resulted in fibrosis of the lung, liver, skin, bone marrow, and the kidney in a mouse model. We recently showed that in tissue samples from end-stage lung fibrosis patients, JUN directly activates the genes coding for CD47 and PD-L1, leading to increased production of these proteins in fibrotic scar-forming lung cells. We also found a critical role of another inflammatory molecule called Interleukin 6 in fibrotic disease, driving mechanisms that increase the fibroblasts’ resistance to immune-cell regulation. As a practicing pathologist and hematopathologist, I am particularly interested in the interphase of inflammation, fibrosis and cancer, with the ultimate goal of developing effective treatments.