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Bladder cancer, inflammageing and microbiomes
Ageing is correlated with elevated bladder cancer incidence, morbidity and mortality. Advanced age is also associated with elevated markers of chronic inflammation and perturbations in gut and urinary tract microbiota. One reason for the increased incidence and mortality of bladder cancer in the eld...
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Published in: | Nature reviews. Urology 2022-08, Vol.19 (8), p.495-509 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Ageing is correlated with elevated bladder cancer incidence, morbidity and mortality. Advanced age is also associated with elevated markers of chronic inflammation and perturbations in gut and urinary tract microbiota. One reason for the increased incidence and mortality of bladder cancer in the elderly might be that age-associated changes in multiple microbiomes induce systemic metabolic changes that contribute to immune dysregulation with potentially tumorigenic effects. The gut and urinary microbiomes could be dysregulated in bladder cancer, although the effect of these changes is poorly understood. Each of these domains — the immune system, gut microbiome and urinary microbiome — might also influence the response of patients with bladder cancer to treatment. Improved understanding of age-related alterations to the immune system and gut and urinary microbiomes could provide possible insight into the risk of bladder cancer development and progression in the elderly. In patients with bladder cancer, improved understanding of microbiota might also provide potential targets for therapeutic intervention.
In this Perspective, the authors discuss the complex links among inflammation, dysbiosis, ageing and cancer, examining data that suggest that ageing and inflammation can promote bladder cancer development, how ageing might lead to or promote dysbiosis, and how dysbiosis could influence treatment response. |
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ISSN: | 1759-4812 1759-4820 |
DOI: | 10.1038/s41585-022-00611-3 |