For many patients, initial cancer treatments are not sufficient, and the residual cancer cells that survive these treatments can cause relapses. However, new research is seeking to utilize the immune system to target residual disease, thereby helping patients avoid relapses and live longer.
“Using a new mechanism of action that directly targets cancer cells, we hope to enhance the ability of NK cells – that is, natural killer cells – to eliminate residual disease,” says RJ Tesi, MD, CEO of INmune Bio Inc., (NASDAQ: INMB), a clinical-stage oncology immunotherapy company. “NK cells are part of our innate immune system and are essential for survival. In addition to directly killing infected and cancerous cells, NK cells facilitate communication between the innate and adaptive immune systems.”
As Dr. Tesi continues to explain, NK cells play a critical role in eliminating cancer cells that remain after treatments such as surgery, radiation, and chemotherapy. Although modern cancer therapies can effectively eliminate most of the cancer in a patient, to eliminate all cancer cells, the patient’s immune system needs to do its part and kill the residual disease. When cancer cells evade NK cells by effectively becoming invisible, the immune system cannot identify them and therefore cannot kill them. This immune system failure to eliminate residual disease is the cause of cancer relapse.
INKmune, the flagship product of INmune Bio Inc., activates resting NK cells to an activated state in order to kill cancer. Currently in clinical trials, this therapy is already showing promising results. NK cells activated by INKmune have demonstrated the ability to kill various types of cancer cells. To learn more, visit inmunebio.com.
“Chemotherapy and radiation reduce tumor burden, but they are not always curative on their own,” says Dr. Tesi. “To eradicate disease and turn cancer relapsers into survivors, we also need an effective immune response to control the residual cancer cells left behind after primary treatment.”
Source: StatePoint



