ArticleBreast cancer research : BCR2025
AXL promotes inflammatory breast cancer progression by regulating immunosuppressive macrophage polarization.
Article in Breast cancer research : BCR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Reprogramming the Immune Landscape of Inflammatory Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- IFI44 Orchestrates an IL-10-Driven M2 Macrophage Program in Breast Cancer: An Immune Prognostic Signature.Breast cancer (Dove Medical Press) · 2026Article
- From "metabolic storm" to "immune paralysis": the dynamic evolution of macrophages and metabolism reprogramming in ARDS.Frontiers in immunology · 2025Review
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Authors and funding
18 authors.
Funding
Abstract
backgroundTumor-associated macrophages (TAMs) are key promoters of inflammatory breast cancer (IBC), the most aggressive form of breast cancer. The receptor tyrosine kinase AXL is highly expressed in various cancer types, including IBC, but its role in TAMs remains unexplored.
methodsWe examined the effects of AXL inhibitor TP-0903 on tumor growth and tumor microenvironment (TME) component M2 macrophages (CD206
resultsWe found that inhibiting the AXL pathway significantly reduced IBC tumor growth and decreased CD206
conclusionsAXL signaling promotes IBC growth by inducing M2 macrophage polarization and driving the secretion of immunosuppressive molecules and cytokines via STAT6 signaling, thereby contributing to an immunosuppressive TME. Collectively, these findings highlight the potential of targeting AXL signaling as a novel therapeutic approach for IBC that warrants further investigation in clinical trials.
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