For a long time, researchers thought that chronic liver inflammation was the driving force of cancer, because the inflammation allows the cancer cells to divide, preventing them from dying. But a recent study by the University of California San Diego School of Medicine that used a model based on nonalcoholic steatohepatitis (NASH), showed that perhaps the real driving force of liver cancer involves a process with the intriguing name of immunosurveillance. Immunosurveillance—am I the only one who envisions cells wearing trench coats and wearing black-framed sunglasses? —is one of our immune system’s ways of stopping cancer from forming, according to a recent Newswise article.
In this study, researchers engineered genetic mutations of nonalcoholic steatohepatitis in mice, causing liver cancer cells to form from inflammation. NASH is essentially the build-up of fat in the liver, which causes inflammation, cirrhosis, and cancer. The inflammation led to the buildup of immunosuppressive lymphocytes. These lymphocytes use a molecule called PD-L1 to disturb cytotoxic T-cells (white blood cells that kill cancer cells), which allow more tumors to form and grow. The researchers then used a drug and further genetic engineering to prevent PD-L1 from disturbing the cytotoxic T-cells, which meant that the lymphocytes were destroyed and the cytotoxic T-cells were regenerated, allowing them to eliminate the tumors in the mice.
The study’s demonstration of the immune system’s role in fighting cancer was understandable for the most part. However, the non-patient friendly way in which this particular article was written, was concerning to me. I understand that the study’s audience is meant to be scientific researchers and professors, but I began to think about the necessity for this type of medical information to also appeal to patients who are not all versed in the medical field.