Abstract

Cancer remains a leading cause of morbidity and mortality worldwide, emphasizing the need for effective and accessible preventive strategies. Although genetic susceptibility contributes to carcinogenesis, modifiable environmental and lifestyle factors, particularly diet, physical inactivity, obesity, tobacco use, and alcohol consumption, account for a substantial proportion of cancer risk. Functional foods are natural or minimally processed foods that provide health benefits beyond basic nutrition because of their biologically active constituents. These compounds include polyphenols, flavonoids, carotenoids, glucosinolates, organosulfur compounds, omega-3 fatty acids, dietary fiber, and probiotics. Experimental, epidemiological, and emerging clinical evidence suggests that functional foods may contribute to cancer prevention by reducing oxidative stress and chronic inflammation, enhancing DNA repair, regulating cell proliferation and apoptosis, inhibiting angiogenesis, modifying epigenetic processes, and supporting a healthy gut microbiome. Dietary patterns rich in these foods, including the Mediterranean diet and predominantly plant-based diets, have been associated with a reduced risk of several malignancies, particularly colorectal, breast, gastric, and prostate cancers. This narrative review summarizes current evidence on the relationship between functional foods and cancer prevention, with emphasis on molecular mechanisms, epidemiological and clinical findings, the gut microbiome, precision nutrition, and practical implications for healthcare professionals. Functional foods should not be considered substitutes for established cancer-prevention measures, screening, or treatment. Rather, they should be incorporated into comprehensive prevention strategies that include tobacco avoidance, healthy weight maintenance, regular physical activity, vaccination against oncogenic viruses, and guideline-recommended cancer screening.

Keywords:Functional foods; Cancer prevention; Bioactive compounds; Inflammation; Gut microbiome; Precision nutrition; Carcinogenesis; Inflammation; Apoptosis; Autophagy; Molecular pathways; Diet

Abbreviations: AMPK: AMP-Activated Protein Kinase; AP-1: Activator Protein-1; ATG: Autophagy-Related Protein; BAK: BCL-2 Antagonist/Killer; BAX: BCL-2-Associated X Protein; BCL: 2-B-Cell Lymphoma-2; BCL-XL: B-Cell Lymphoma-Extra Large; COX-2: Cyclooxygenase-2; DHA: Docosahexaenoic Acid; EGCG: Epigallocatechin-3-Gallate; EPA: Eicosapentaenoic Acid; ER: Estrogen Receptor; GPX: Glutathione Peroxidase; GSH: Glutathione; HDAC: Histone Deacetylase; HIF-1α: Hypoxia-Inducible Factor-1 Alpha; HO-1: Heme Oxygenase-1; IGF: Insulin-like Growth Factor; IKK: IκB Kinase; IL-1β: Interleukin-1 Beta; IL-6: Interleukin-6; Inos: Inducible Nitric Oxide Synthase; IκB: Inhibitor of Nuclear Factor-Kappa B; Keap1: Kelch-like ECH-Associated Protein 1; LC3: Microtubule-Associated Protein 1 Light Chain 3; LPS: Lpopolysaccharide; MAPK: Mitogen-Activated Protein Kinase; mTOR: Mechanistic Target of Rapamycin; NF-κB: Nuclear Factor-Kappa B; Nrf2: Nuclear Factor Erythroid 2-Related Factor 2; PI3K: Phosphoinositide 3-Kinase; PKB/Akt: Protein Kinase B; RCT: Randomized Controlled Trial; RNS: Reactive Nitrogen Species; ROS: Reactive Oxygen Species; SCFAs: Short-Chain Fatty Acids; SIRT1: Sirtuin 1; SOD: Superoxide Dismutase; STAT3: Signal Transducer and Activator of Transcription 3; TNF-α: Tumor Necrosis Factor- Alpha; TRAIL: Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand; ULK1: Unc-51-Like Kinase 1; VEGF: Vascular Endothelial Growth Factor