Abstract 2119: Bone Morphogenetic Protein Receptor 1a in myeloid cells regulates mouse prostate cancer growth

Abstract

Abstract The Bone Morphogenetic Protein (BMP) pathway is a member of the TGFβ signaling family and has mirrored the complex roles in diverse contexts during cancer development. BMP signaling is rarely mutated and can be frequently overexpressed in many human cancers. The dichotomous role of BMPs as both tumor promoters and suppressors appears to be largely context based in both the cancer cell and the surrounding microenvironment. Myeloid cells including macrophages and neutrophils have been shown to be tumor promoting when stimulated from BMP signaling. We discovered that conditional deletion of BMPR1a in myeloid cells (LysM-Cre) would affect tumor progression and found smaller tumors in a syngeneic FVBn prostate cancer model. Specific changes occurred in myeloid cells both in tumor-bearing mice and non-tumor naïve mice throughout multiple tissues. We profiled myeloid subsets both in the bone marrow, spleen and primary tumor. We found that BMPR1a loss in myeloid cells altered the differentiation and lineage capability of distinct populations by histologic, flow cytometry and high-dimensional mass cytometry analysis. These results indicate a distinct genetic requirement for BMP signaling in myeloid cells during tumor progression. Citation Format: Desiree M. Straign, Sergey V. Novitskiy, Philip Owens. Bone Morphogenetic Protein Receptor 1a in myeloid cells regulates mouse prostate cancer growth [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 2119.