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Tumor-intrinsic LKB1-LIF signaling axis establishes a myeloid niche to promote immune evasion and tumor growth. | LitMetric

AI Article Synopsis

Article Abstract

Tumor mutations can influence the surrounding microenvironment leading to suppression of anti-tumor immune responses and thereby contributing to tumor progression and failure of cancer therapies. Here we use genetically engineered lung cancer mouse models and patient samples to dissect how mutations accelerate tumor growth by reshaping the immune microenvironment. Comprehensive immune profiling of -mutant vs wildtype tumors revealed dramatic changes in myeloid cells, specifically enrichment of Arg1 interstitial macrophages and SiglecF neutrophils. We discovered a novel mechanism whereby autocrine LIF signaling in -mutant tumors drives tumorigenesis by reprogramming myeloid cells in the immune microenvironment. Inhibiting LIF signaling in -mutant tumors, via gene targeting or with a neutralizing antibody, resulted in a striking reduction in Arg1 interstitial macrophages and SiglecF neutrophils, expansion of antigen specific T cells, and inhibition of tumor progression. Thus, targeting LIF signaling provides a new therapeutic approach to reverse the immunosuppressive microenvironment of -mutant tumors.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10370066PMC
http://dx.doi.org/10.1101/2023.07.15.549147DOI Listing

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