In medical school, we are taught to focus on the visible. The objective findings: a mass, a lesion, a cluster of poorly differentiated cells under a microscope. Yet diagnosis marks not the beginning of cancer, rather the moment where hidden biological transformation finally declares itself. Up to 40% of all cancers are avoidable (1) – a sobering statistic, and a command for prevention to be prioritised.
Meaningful prevention should, however, address the origins. All malignancies share the signature trait of a loss of boundaries – in genetics, immune surveillance and the tissue characteristics that typically maintain cellular function. A single mutated cell does not itself mark oncological disease, but the shift in ecological restrictions is what allows cancer to dominate. Chronic inflammation serves as one of the most striking examples of this, and is an escalating concern in today’s world. Reducing its effect may therefore hold the key to restoring these ‘inflamed’ cellular boundaries, averting cancer before it even develops.
This idea stems from the 1800s, with Virchow’s identification of tumour-embedded leukocytes indicating an inflammation-cancer link (2). Now, substantial evidence supports this, with chronic inflammation considered an additional hallmark of cancer, contributing to around 25% of malignancies (3). Fascinatingly, the same immune response that is paramount against acute stress becomes detrimental upon chronic activation. Reactive oxygen species (ROS) generation governs DNA damage, inducing oncogenic mutations and genomic instability. Moreover, excessive cytokines including tumour necrosis factor-alpha (TNF-α) and interleukin-1 (IL-1) stimulate cellular proliferation, while vascular endothelial growth factor (VEGF) governs angiogenesis to support tumour growth (4).
Importantly, this is not inevitable. Emerging pharmacological interventions inhibiting the inflammatory pathway show promise. For example, the CANTOS trial, initially aiming to improve cardiovascular disease using the IL-1β-targeting antibody canakinumab, demonstrated effective prevention of lung cancer incidence in participants (5). Furthermore, vaccination against oncogenic viruses (like human papilloma virus) and treatment of bacterial infection (H. pylori) demonstrate how interruption of chronic inflammatory activation greatly diminishes cervical and gastric cancer risk respectively; the universal application of this offers transformative potential in cancer control (6).
Such examples indicate a clear 2050 prevention model, where inflammation is precisely determined and maintained. Indeed, metabolic optimisation could be implemented. Exercise prevents cancer incidence in numerous ways, including lowering inflammation and shifting IL-6’s action into its anti-cancer form (7). Likewise, fibre-rich diets and decreased alcohol intake diminish systemic inflammation, limiting cancer occurrence (8). Vitally, identifying individuals at greatest susceptibility through profiling of circulating markers like IL-6 and C-reactive protein (CRP) can guide targeted, timely interventions before malignancy prevails. This is also being explored through novel biomarkers, including inflammation-induced DNA methylation patterns (9). However, inflammatory burden occurs unevenly, reflecting socioeconomic inequities including pollution, stress, and food insecurity. A truly effective model thus demands systemic change: nutritious food availability, cleaner air, and public education.
By the time cancer is detected, biological equilibrium has already been lost, with chronic inflammation being a key driver. Thus, by 2050, progress should focus not solely on treatment strategies, but by intervening and restoring balance before neoplasia emerges.
References:
- Fink H, Langselius O, Vignat J, Rumgay H, Rehm J, Martinez RX, et al. Global and regional cancer burden attributable to modifiable risk factors to inform prevention. Nature Medicine. 2026 Feb 3;
- Korniluk A, Koper O, Kemona H, Dymicka-Piekarska V. From inflammation to cancer. Irish Journal of Medical Science (1971 -). 2016 May 7;186(1):57–62.
- Liu X, Yin L, Shen S, Hou Y. Inflammation and cancer: paradoxical roles in tumorigenesis and implications in immunotherapies. Genes & Diseases. 2021 Oct;10(1).
- Singh N, Baby D, Rajguru JP, Patil PB, Thakkannavar SS, Pujari VB. Inflammation and Cancer. Annals of African Medicine. 2019;18(3):121–6.
- Ridker PM, MacFadyen JG, Thuren T, Everett BM, Libby P, Glynn RJ, et al. Effect of interleukin-1β inhibition with canakinumab on incident lung cancer in patients with atherosclerosis: exploratory results from a randomised, double-blind, placebo-controlled trial. Lancet (London, England) [Internet]. 2017 Oct 21 [cited 2026 Feb 26];390(10105):1833–42. Available from: https://pubmed.ncbi.nlm.nih.gov/28855077/
- Greten FR, Grivennikov SI. Inflammation and Cancer: Triggers, Mechanisms, and Consequences. Immunity. 2019 Jul;51(1):27–41.
- Orange ST, Leslie J, Ross M, Mann DA, Henning Wackerhage. The exercise IL-6 enigma in cancer. Trends in Endocrinology and Metabolism. 2023 Nov 1;34(11):749–63.
- Han E, Lee E, Sukhu B, Garcia J, López Castillo H. The relationship between dietary inflammatory potential and cancer outcomes among cancer survivors: A systematic review and meta-analysis of cohort studies. Translational Oncology [Internet]. 2023 Oct 10 [cited 2026 Feb 27];38:101798. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10582578/
- Murata M. Inflammation and cancer. Environmental Health and Preventive Medicine. 2018 Oct 20;23(1).
I am a medical student at the University of Oxford with a strong interest in cancer research and translational oncology. I am currently undertaking an intercalated degree project focused on cancer screening, particularly multi-cancer early detection (MCED) approaches and their potential to enable earlier diagnosis. More broadly, I am interested in how advances in tumour biology can be translated into clinically meaningful diagnostic tools.
Image note: The header image accompanying this article was generated by the FEBS Communications team using artificial intelligence for illustrative purposes only. It does not depict real experimental data, clinical material or microscopy, and should not be interpreted as a scientific image.