Summary
This study reveals that respiratory viral infections (influenza and SARS-CoV-2) disrupt the dormancy of disseminated breast cancer cells in the lung through interleukin-6-dependent mechanisms, triggering rapid proliferation and metastatic expansion within weeks. The mechanism involves impaired lung T cell activation, with CD4+ T cells paradoxically sustaining metastatic burden by inhibiting CD8+ T cell cytotoxicity. These experimental findings are supported by large human observational databases showing that SARS-CoV-2 infection substantially increases cancer-related mortality and lung metastasis risk in breast cancer survivors.
UK applicability
The findings have direct relevance to UK cancer care and survivorship, particularly given the widespread SARS-CoV-2 exposure in the UK population. UK Biobank data were explicitly analysed in this study, making the results directly applicable to UK cancer survivors and informing clinical guidance on infection monitoring and management in this vulnerable population.
Key measures
Dormant disseminated cancer cell (DCC) phenotype transition; interleukin-6 levels; carcinoma cell expansion kinetics; CD4+ and CD8+ T cell activation and cytotoxicity; cancer-related mortality risk; lung metastasis incidence in infected versus uninfected cancer survivors
Outcomes reported
The study demonstrated that influenza and SARS-CoV-2 infections cause dormant breast cancer cells in the lung to lose their quiescent phenotype and proliferate, expanding into metastatic lesions within two weeks in a mouse model. Human observational data from UK Biobank and Flatiron Health databases showed that SARS-CoV-2 infection substantially increased cancer-related mortality and lung metastasis risk in cancer survivors.
Topic tags
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