September 2025
How ‘Inflammaging’ Drives Cancer, and
Points Researchers to Treatments
Inflammation fuels the high rate in people over 50, leading scientists to test anti-inflammatories to fight the disease.
People are more likely to get cancer as they age. Doctors now have an unconventional idea of how that might be reversed: using allergy drugs and other seemingly unlikely medications to damp a condition known as ‘inflammaging.’ Immunology and oncology researchers have spent years examining malignant tumors to learn why people over 50 account for nine in 10 cancer diagnoses in the U.S. They may have honed in on an answer: the aging immune system. Their studies of individual immune cells in human lung tumors as well as in old mice have revealed how chronic, pathogenic inflammation in older people, dubbed inflammaging, interferes with the immune system and fuels cancer growth. Researchers are testing whether existing anti-inflammatory medications usually used to fight rheumatoid arthritis or allergy conditions like asthma or eczema can slow cancer in older patients. They are also searching for new drugs. They believe aging is something we can transform.
Inflammation is the immune system’s reaction to a threat. Immune cells circulate in the body, attacking invaders such as viruses and cancer and calling for backup (more immune cells) when necessary. Working correctly, they can beat back covid or heal a cut on the finger. But the immune system can overreact, fueling inflammation that gets in the way of healing or leads to disease. It misfires like this more as people age. A big focus in the field right now is to separate beneficial inflammation, the type that protects us from microbes and from tumors, from the pathogenic inflammation that is enhancing cancer progression and promoting damage in the older brain. The idea of using drugs on cancer patients that damp inflammation is counterintuitive. Immunotherapies, which rev up the immune system to attack tumors, have transformed cancer care over the past several years. The common wisdom is that we want to ramp up inflammation as much as possible so that inflammation can be harnessed by the immune system to kill the cancer. The blind spot is that there are different types of inflammation. Often the assumption is that older people get sick more easily because their immune systems weaken. This does happen, but at the same time there is also a sort of hyperactivation. The body is just basically like a flower bed primed to grow cancer as you get older.
As a person ages, the immune system must work harder to kill infections or mutations, like cancer. But the immune system itself is aging and produces fewer of the type of immune cells that target and kill cancer. At the same time, it makes more of a type of immune cell that initially responds to infections. Known as myeloid cells, with aging they become more inclined to overreact and create inflammaging. These inflammatory cells may provide a “hit” necessary for older cells with mutations to turn cancerous. How can an aging immune system drive cancer? Myeloid cells in lung tumors churn out interleukin-1, or IL-1, a protein long-linked to inflammaging. The IL-1 summoned more myeloid cells to the lungs, leading to more inflammation and tumor growth. When given early, using a rheumatoid arthritis called anakinra in mice that blocks IL-1, slowed tumor growth. This may suggest that anti-inflammatory treatment would work best for older people at high risk for cancer, or with early-stage disease. While research findings in mice can’t always be generalized to humans, medicine may be able to potentially prevent lung cancer. Other drugs, known as JAK inhibitors, used to treat inflammatory diseases like eczema or ulcerative colitis, have similar potential for treating cancer in older patients.
In the future treatment will involve using technology to learn when to fire up the immune system or quiet it. That said, it’s not as simple as you either turn on the gas or hit the brake. The hope is to calm inflammation that flares up when ancient viruses that are integrated into the human genome reactivate, which can happen during aging. For more information or links to the research see research with Miriam Merad, MD, Andy Minn, MD, Thomas Marron, MD and Andrew Park, medical student.
Betsy McKay