ArticleBMC cancer2026
Metabolome-microbiome convergence under circadian disruption accelerates mammary tumorigenesis: multi-omics integration insights.
Article in BMC cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Circadian rhythm disruption (CRD), common in shift work and jet lag, promotes mammary tumorigenesis through coordinated reprogramming of tumor metabolism and the local microbiome. CRD increased immunosuppressive metabolites - kynurenic acid, spermidine, and argininosuccinic acid - that suppressed effector T-cell activity and drove macrophage polarization toward anti-inflammatory phenotypes. 16S rRNA sequencing revealed enrichment of immune-modulatory Firmicutes and Bacilli within CRD tumors. Experimental and multi-omics integrative analyses strongly support metabolome-microbiome crosstalk driving immune suppression under CRD. Inhibition of arginase-1 (ARG1) with nor-NOHA restored cytotoxic T-cell responses and reduced lung metastases. These findings establish metabolome-microbiome interactions as a central mechanism of CRD-induced immunosuppression and metastasis, revealing potential therapeutic targets for circadian disruption-associated breast cancer.
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