The Metimmox trial, which has been running at Norwegian hospitals (Akershus University Hospital, St. Olav’s University Hospital, Haukeland University Hospital, Hospital of Southern Norway, and Oslo University Hospital) for the past 2 years, has experienced some exciting results and has been featured on several news portals. Both “Dagensmedisin” and “HealthTalk” (both in Norwegian) have featured Acredit’s Professor Anne Hansen Ree in articles featuring the successful results of the study.
In the Metimmox study, it was found that about 18% of patients with colorectal cancer (CRC) treated with the cancer immune therapy drug nivolumab were able to experience complete response, meaning their bodies were able to learn to recognise and destroy their cancerous cells. A further 32% of patients were able to slow or stop the progression of their cancer. In the control arm (without immune therapy), these two results were not seen.
The Metimmox trial was looking into the potential for the use of an immune checkpoint inhibitor as a “booster” for the regular Nordic FLOX treatment received by all patients as a standard treatment for microsatellite-stable (MSS) CRC. By using an immune checkpoint inhibitor, researchers hypothesised that the body would be able to better recognise and eliminate the cancer they were experiencing.
Cancer is a difficult disease to treat because it is essentially a disease of “self” – it is made up of improperly growing cells from within our own bodies. Drugs such as oxaliplatin, 5-fluorouracil and other chemotherapies are regularly administered to Norwegian CRC patients to destroy these cancerous cells, but they are not always effective for many reasons. These drugs attack the tumours through biochemical processes. When the drugs destroy the cancer cells, antigens are released by those cells, which are then picked up by certain immune cells, dendritic cells. These dendritic cells take the antigens and show them to the immune system’s invader controllers, killer T-cells, which are responsible for going out to the body to kill the invading cells. Cancerous cells have a protein on their outer surface called PD-L1. This protein tells the T-cells that they’re normal and not to attack them. Nivolumab blocks the T-cells’ binding to PD-L1 proteins, which signals the T-cells to destroy the cancer cells. Essentially, nivolumab helps remove the cloaking device from cancerous cells, giving patients a better chance of recovery.