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- W4316369136 abstract "Immune checkpoint inhibitors (ICIs) have revolutionized the field of oncology since the last decade. However, heterogeneous treatment responses among patients and immune-related adverse effects (irAEs) are critical challenges and limitations in current clinical practice. Emerging studies have now indicated that microbiota may influence the clinical responses and toxicity of cancer therapy across multiple cancer types. Early evidence has demonstrated promising results by manipulating the gut microbial composition via faecal microbiota transplantation (FMT) to improve immunotherapeutic efficacy. This chapter will start from the basics by exploring the mechanisms of pharmacomicrobiomics interactions in the context of ICIs, which can be summarised by the “TIME” mechanistic framework—T cell modulation, innate immunity, metabolites & molecular mimicry, and epithelial injury. The chapter will further discuss the translational potential of these laboratory findings in clinical settings for truly benefiting cancer patients. Gut microbial features can potentially be predictive biomarkers for therapeutic responses, guiding treatment selection for patients. Importantly, unlike host genetics, the gut microbial composition can be easily modified by prebiotics, probiotics, antibiotics, dietary modulations, and FMT, which serves as a potential strategy to augment cancer therapeutic responses and toxicity. Pharmacomicrobiomics may play an essential role in future cancer therapeutic interventions opening a new avenue for precision medicine in oncology." @default.
- W4316369136 created "2023-01-16" @default.
- W4316369136 creator A5033829154 @default.
- W4316369136 creator A5063969589 @default.
- W4316369136 date "2023-01-01" @default.
- W4316369136 modified "2023-10-01" @default.
- W4316369136 title "Microbiota in Cancer Immunotherapy: The Next Milestone of Immuno-oncology?" @default.
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- W4316369136 doi "https://doi.org/10.1007/978-981-19-4492-5_17" @default.
- W4316369136 hasPublicationYear "2023" @default.
- W4316369136 type Work @default.