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ICAM1high Neutrophils Sculpt Tumor Evolution and Metastasis Through Symbiotic Adhesion and Reverse Migration
1Lester and Sue Smith Breast Center, Baylor College of Medicine, Houston, Texas.
Cancer Research
|May 28, 2026
Summary
Neutrophils influence tumor progression by promoting epithelial-like cancer cells and eliminating mesenchymal-like cells. This ICAM1high neutrophil subset drives tumor evolution and metastasis, with interactions varying by patient ancestry.
Area of Science:
- Immunology
- Oncology
- Cancer Biology
Background:
- Neutrophils are key immune cells in the tumor microenvironment.
- Their roles can be either pro-tumor or anti-tumorigenic.
- Understanding neutrophil heterogeneity is crucial for cancer therapy.
Purpose of the Study:
- To investigate the role of specific neutrophil subsets in triple-negative breast cancer (TNBC).
- To explore how neutrophils interact with tumor cells of different phenotypes.
- To analyze the impact of these interactions on tumor evolution and metastasis.
Main Methods:
- Analysis of neutrophils in human cancers and murine TNBC models.
- Assessment of ICAM1high neutrophil adhesion and cytotoxicity.
- Spatial transcriptomics and tissue microarray analyses in human TNBC.
Main Results:
- Identified an ICAM1high neutrophil subset enriched in the tumor microenvironment.
- ICAM1high neutrophils adhere to epithelial-like tumor cells, conferring mutual benefits.
- Mesenchymal-like tumor cells are susceptible to neutrophil-mediated cytotoxicity.
- These interactions drive tumor evolution into distinct ecosystems.
- Neutrophil adhesion and reverse migration facilitate metastatic intravasation.
- Tumor cell-neutrophil-endothelial cell interactions show variations based on patient ancestry.
Conclusions:
- Neutrophils significantly instruct TNBC phenotypes and metastatic potential.
- Tumor-immune co-evolution is driven by neutrophil interactions.
- Ancestry may influence the dynamics of these interactions in TNBC.
- Targeting ICAM1high neutrophils could offer therapeutic strategies.
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