Alveolar Macrophage abundance and pro-metastatic phenotype are modulated by myeloid intrinsic canonical Wnt/β-catenin signaling
I have worked to demonstrate that activating β-catenin signaling in macrophages, especially alveolar macrophages, drives a pro-inflammatory phenotype. There are several putative effector pathways that underlie this effect which can be delineated through further analysis of the activated β-catenin vs. control alveolar macrophage transcriptomic landscapes. I am eager to connect these alterations in alveolar macrophage inflammatory programs with their effects on tumor progression and metastasis to the lung in vivo. Furthermore, I hope these findings can be translated to improve our identification of potential biomarkers in solid cancer biology.