Immune System's Role in Tumor Growth Explained
Researchers at the Salk Institute have identified a biological pathway where chronic exposure to interferon proteins causes mitochondrial dysfunction, leading to immunosuppression in cancer patients. This discovery explains why these proteins can transition from anti-cancer agents to pro-cancer factors, offering potential targets for improving immunotherapy.
Why it matters
Understanding this mechanism could lead to new therapies that prevent immunotherapy resistance, significantly improving long-term survival rates for cancer patients.
LA JOLLA (September 10, 2026) - Cancer biology and, in turn, cancer treatment have come a long way in the last few decades. Most people recognize this progress in breakthroughs like immunotherapy - a treatment strategy first deployed in 2011 that leverages the body's own immune cells to fight cancer and revolutionized the treatment landscape. However, progress doesn't mean all the questions have been answered.
One of those questions is why signaling proteins called interferons, which recruit the immune system to attack cancer cells, start helping the tumor grow rather than shrink when they linger too long. A Salk Institute team discovered a novel pathway that links chronic interferon II (a family of interferon proteins) exposure to mitochondrial dysfunction that ultimately causes immunosuppression. By explaining how interferon II turns from "good" to "bad," the foundational insights provide a path to future therapies that combat immunotherapy resistance.
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