Our voice, our choice: a mixed-methods study exploring the nutritious food and beverage item preferences and perspectives of medically tailored grocery clients.

Cancer remains a leading cause of mortality worldwide, with approximately 20 million new cases and 9.7 million deaths reported in 2022, and projections reaching 35 million cases by 2050. Although significant advances have been made in early detection, targeted therapies, and immune checkpoint blockade, variability in treatment response and survival persists across tumor types. Such heterogeneity is not fully explained by tumor genomics alone and reflects the contribution of host-associated factors, including immune status, metabolic context, and microbial composition (, ). The human microbiome comprises bacteria, viruses, fungi, and archaea that colonize mucosal and epithelial surfaces and collectively encode a metabolic capacity comparable to that of the host genome. In this review, the term human microbiome is used to refer to host-associated microbial communities across anatomical sites, whereas the mechanistic discussion primarily refers to gut microbiome-derived signaling unless another body site is specified. Microbial communities regulate tumor biology through defined mechanisms. Dysbiosis promotes carcinogenesis via sustained activation of pattern recognition receptors, such as Toll-like receptors, leading to NF-κB–mediated inflammatory signaling, cytokine production, and immune dysregulation. Microbial genotoxins and metabolites further contribute to DNA damage, epigenetic modification, and oncogenic pathway activation, linking microbial composition to tumor initiation and progression (, ). Microbial metabolites constitute key intermediates linking microbial activity to host signaling networks. Short-chain fatty acids (SCFAs) regulate immune cell differentiation through histone deacetylase (HDAC) inhibition and G protein–coupled receptor (GPCR) signaling, influencing CD8 T-cell function and regulatory T-cell balance. Secondary bile acids interact with nuclear receptors such as FXR and membrane receptors such as TGR5, modulating metabolic pathways and immune responses within the tumor microenvironment (TME). Tryptophan-derived metabolites signal through aryl hydrocarbon receptor pathways, altering cytokine production and barrier integrity. Interactions between microbial metabolism and intracellular signaling cascades regulate tumor growth and immune surveillance (, ).