AI Article Synopsis
- Germline pathogenic variants in certain genes indicate genetic susceptibility to hereditary breast and ovarian cancer syndrome, highlighting the role of tumor-immune interactions in breast cancer development.
- A study of 66 women revealed alterations in four immune cell subpopulations between healthy controls and those with a genetic predisposition; however, no significant differences were found between healthy carriers and controls.
- Three of these immune subpopulations were also found to be elevated in triple-negative breast cancer patients, suggesting an activated immune response in healthy gpath() carriers that could inform future risk-reducing strategies.
Article Abstract
Germline pathogenic variants in and (gpath(/)) represent genetic susceptibility for hereditary breast and ovarian cancer syndrome. Tumor-immune interactions are key contributors to breast cancer pathogenesis. Although earlier studies confirmed pro-tumorigenic immunological alterations in breast cancer patients, data are lacking in healthy carriers of gpath(/). Peripheral blood mononuclear cells of 66 women with or without germline predisposition or breast cancer were studied with a mass cytometry panel that identified 4 immune subpopulations of altered frequencies between healthy controls and healthy gpath() carriers, while no difference was observed in healthy gpath() carriers compared to controls. Moreover, 3 (one IgD-CD27CD95 B cell subpopulation and two CD45RA-CCR7+CD38 CD4 T cell subpopulations) out of these 4 subpopulations were also elevated in triple-negative breast cancer patients compared to controls. Our results reveal an activated peripheral immune phenotype in healthy carriers of gpath() that needs to be further elucidated to be leveraged in risk-reducing strategies.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11126817 | PMC |
| http://dx.doi.org/10.1016/j.isci.2024.109882 | DOI Listing |
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