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Available4.3
18 reviewsSUMMARYTumor-induced systemic accumulation and polarization of neutrophils to an immunosuppressive phenotypeis a potent driver of metastasis formation. Yet, how mammary tumors reprogram granulopoiesis at the molecular level and when tumor imprinting occurs during neutrophil development remains underexplored. Here,we combined single-cell, chromatin and functional analyses to unravel the tumor-driven reprogramming ofgranulopoiesis in the bone marrow, along with intervention studies aimed at reversing this process. Weobserve that mammary tumors accelerate commitment to the neutrophil lineage at the expense of lymphopoiesis and erythropoiesis without stimulating the development of a novel myeloid lineage. Moreover, tumordirected immunosuppressive imprinting of neutrophils starts early in hematopoiesis. Treatment with anti-IL1β normalizes tumor-induced granulopoiesis, reducing neutrophil immunosuppressive phenotype andmitigating metastatic spread. Together, these data provide molecular insights into the aberrant, tumor-drivenneutrophil differentiation pathway leading to metastasis-promoting chronic inflammation and how it can bereversed to reduce metastatic spread.
5.0
29 reviews