FLT3LG as an inflammatory hub bridging tumor immune surveillance to therapy response in breast cancer.
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ABSTRACT: Breast cancer remains one of the most deadly cancers, highlighting the urgent need for better prognostic markers and treatment targets. Emerging evidence suggests that inflammation-driven immune dysregulation plays a pivotal role in breast cancer progression and therapy resistance. Single-cell RNA sequencing and comprehensive gene network analysis based on inflammation identified FLT3LG as a crucial protective factor in breast cancer. Tumors with lower FLT3LG expression showed poorer survival outcomes across multiple patient cohorts. Functional analysis revealed its role in immune regulation, particularly in the activation of B cells and T cells, as well as in chemokine signaling. Genetic profiling revealed distinct mutation patterns: PIK3CA mutations were enriched in tumors with high FLT3
SUBMITTER: Lu Y
PROVIDER: S-EPMC12568875 | biostudies-literature | 2025 Oct
REPOSITORIES: biostudies-literature
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