David Weinkove, 4 February 2025 – World Cancer Day
Age is the biggest risk factor for cancer – higher even than smoking. So can we use findings from ageing research to prevent people getting cancer? This question was posed at a meeting of basic researchers, clinicians and industrialists organised by David Crosby and colleagues at Cancer Research UK on 28thJanuary 2025 and chaired by Lynne Cox and Walid Khaled. I attended as Chair of the British Society for Research on Ageing (BSRA).
Image: Sarah Blagden, University of Oxford, David Crosby, Cancer Research UK, Jon Beaman, MHRA, Liam Cassidy, Altos Labs
The answer is yes, in theory there are many possible routes whereby ageing research can be used for cancer prevention. However, there are lots of barriers to making this goal a reality, not all of them scientific. Firstly, we must define what we are trying to achieve. Interventions to prevent cancer would be very different from those required to treat late-stage cancer. Sarah Blagden described the precancerous state of epithelial dysplasia – when tissues lose structure and you see growths like polyps. This is not cancer but cancerous cells can arise from cells in these lesions. Preventing tissue dysplasia would be predicted to be an outcome of a pharmaceutical intervention that slowed ageing. However, developing such a drug would be challenging. Clinical trials would require a large number of participants to have enough to accurately measure the decrease in cancer incidence. And depending on the age of the subjects, it may need to run for several years. Of course, such a drug would need to be very safe to be given to large numbers of healthy people. The risk benefit equation is very different when considering a drug to treat some who already has cancer.
There are successful preventative drugs for cardiovascular disease. In this case, we treat people with high blood pressure or high cholesterol, which are both easy to measure, with known levels that are healthy, and we understand how they lead to disease, even though they are not in themselves a disease. By analogy, a similar approach should be possible for other age-related conditions including cancer if we have the right measures, called biomarkers, and understanding. Daniel Muñoz-Espin described how routine screening for lung cancer reveals many precancerous lesions in lungs. Unlike lesions in other organs, nothing can be done about them, because operating on the lung is not a sensible option unless the lesions become cancerous. However preventative treatments could be directed at those people with lesions. To prevent cancer requires not only great biomarkers, but also a clear understanding of how elevated biomarkers can lead to disease. Such a mechanism of action is critical to convince the clinicians that a marker is causative and worth addressing. One such route may be targeting the immune system. At the workshop, there was a lot of discussion of how the immune system malfunctions with age, and that could allow cancers to progress. An interesting example was the discovery of senescent macrophages associated with cancer (Scott Haston, UCL). For these viable cells to be targets for preventative treatments we need to better understand how they contribute to disease, how to detect them and how to target them safely.
I came away from the workshop with more focus of what ageing research needs to achieve if we are going to fulfil the promise that slowing biological ageing prevents disease. As a member of the Association of Medical Research Charities, the BSRA has had some great discussions with a number of other medical charities. More workshops like this one and stronger alliances with disease-focused charities will enable research on ageing to be better used in preventative medicine, allowing people to enjoy as many disease-free years as possible.
Cancer Research UK offer a Biology to Prevention Award that may be of interest to BSRA members.
Find out about BSRA funding opportunities