Cancer and aging are two interconnected phenomena that have puzzled scientists and researchers for years. A recent study conducted by researchers at the Icahn School of Medicine at Mount Sinai sheds light on this complex relationship and offers new hope in the fight against cancer, especially in older adults.
Published in the prestigious journal Science, the study delves into the mechanisms through which an aging immune system can fuel tumor growth. This groundbreaking research reveals how age-related inflammation can promote the development of cancer by suppressing the body’s natural defenses against tumor cells.
The lead author of the study, Matthew D. Park, PhD, explains, “As the immune system ages, it triggers harmful inflammation that can drive cancer growth. This process involves the accumulation of pro-tumor macrophages, which inhibit the immune cells responsible for destroying tumor cells, weakening the body’s ability to fight cancer.”
However, the researchers discovered a potential solution to this problem. By blocking specific inflammatory pathways, particularly those involving molecules called interleukin-1⍺ (IL-1⍺) and IL-1β, they were able to reverse the damaging effects of age-related inflammation in mouse models. This breakthrough offers a promising new approach to cancer prevention and treatment in humans.
The study highlights the crucial role of communication between early lung cancer lesions and immune stem cells in the bone marrow through IL-1⍺/β signaling. This communication pathway underscores how an aging immune system can contribute to the progression of cancer.
While cancer risk increases with age, the reasons behind this phenomenon have remained largely elusive. The research team used mouse models to investigate how aging influences cancer progression and found that tumor growth was accelerated in older mice compared to younger ones. Importantly, rejuvenating the immune system significantly reduced cancer growth in older mice, indicating that targeting the aging immune system could be a key strategy in cancer prevention.
Through detailed analysis of murine and human cancer tissues, the researchers identified specific cells and immune-related factors that contribute to cancer growth in elderly individuals. By blocking these factors, specifically IL-1⍺/β, they were able to mitigate cancer growth in aged mice, providing further evidence of the link between age-related inflammation and cancer progression.
Co-senior author Thomas Marron, MD, PhD, Director of the Early Phase Trial Unit at Mount Sinai’s Tisch Cancer Institute, emphasizes the potential of targeting the aging immune system to reduce cancer risk in older adults. He suggests that enhancing the immune response through immunotherapy may be more effective than directly targeting tumors. The discovery that anakinra, a drug already used for inflammatory conditions, can counteract the effects of immune aging on cancer opens up new possibilities for repurposing existing medications for cancer prevention.
Ongoing clinical trials are now underway to investigate whether targeting the immune system can prevent cancer progression, with a focus on developing preventive measures that reduce harmful inflammation in older adults. The ultimate goal of the researchers is to significantly reduce the incidence of cancer by addressing the underlying factors that contribute to age-related cancer risk.
This groundbreaking study not only sheds light on the relationship between aging and cancer but also paves the way for innovative approaches to cancer prevention and treatment. By targeting the aging immune system and its inflammatory pathways, researchers are hopeful that they can make significant strides in combating cancer, particularly in older populations.
