ArticleClinical and experimental medicine2025
FLT3LG as an inflammatory hub bridging tumor immune surveillance to therapy response in breast cancer.
Article in Clinical and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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 FLT3LG expression, whereas TP53 mutations predominated in tumors with low FLT3LG expression. Correlations with immune cell infiltration and checkpoint markers suggested that FLT3LG may predict enhanced responses to immune checkpoint inhibitors and certain targeted drugs. These findings support its potential as a multifunctional biomarker for prognosis and therapeutic decision making in breast cancer.
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