Cancer is not just a mass of rapidly dividing cells—it’s a master of disguise. One of the reasons it remains so difficult to treat is because it learns to evade, suppress, or manipulate the immune system, which is supposed to identify and destroy abnormal cells. Understanding how cancer does this is key to developing new, more effective therapies.
Normally, the immune system patrols the body for threats. Cells that mutate or behave abnormally are flagged and removed by T-cells and other immune defenses. But cancer cells often develop mechanisms to avoid this surveillance. One of the most well-known strategies is disguising themselves as normal by downregulating surface markers that immune cells look for. If the immune system can’t detect a threat, it won’t respond.
Some cancer cells also express molecules like PD-L1, which bind to receptors on T-cells (such as PD-1) and send a signal telling them to stand down. This interaction essentially turns off the immune response. This is the basis of immune checkpoint evasion, one of the most powerful tools in the cancer cell’s arsenal.
In addition to evasion, cancer cells actively suppress immune activity. They can release chemicals that attract regulatory T-cells and myeloid-derived suppressor cells—both of which work to calm the immune response. The tumor microenvironment becomes an immunosuppressive zone, where even nearby immune cells lose their ability to attack.
Some cancers take it further, hijacking immune system components for their own growth. For example, certain types of leukemia use growth signals that are meant for normal white blood cells, helping them multiply unchecked. Tumors can also promote the formation of abnormal blood vessels, ensuring they get nutrients while also limiting the access of immune cells.
Even if the immune system does mount an attack, cancer cells often mutate rapidly. This means that even if some are recognized and destroyed, others survive with slight genetic changes that help them escape future detection—a process known as immune editing.
To counter these tactics, scientists have developed immunotherapies that boost or redirect the immune system. One major breakthrough has been immune checkpoint inhibitors—drugs that block PD-1 or CTLA-4 pathways, reactivating T-cells and allowing them to attack the tumor. These therapies have shown dramatic results in cancers like melanoma and lung cancer, sometimes leading to complete remission.
Another powerful approach is CAR-T cell therapy. Here, a patient’s T-cells are removed, genetically engineered to better recognize cancer cells, and reintroduced into the body. These modified cells can then seek out and destroy cancer that had previously gone unnoticed.
Despite progress, not all patients respond to immunotherapy. Some tumors remain hidden or develop resistance. Research now focuses on identifying biomarkers that predict which patients will benefit and combining treatments to prevent resistance.
Cancer’s ability to trick the immune system is a central reason why it remains so challenging. But as we learn more about its deceptive strategies, the fight is turning in our favor—one immune cell at a time.
The Zuara Press 