GSE137789 Myocardial Infarction accelerates breast cancer via innate immune reprogramming (ATAC-seq)

Contributors : Graeme J Koelwyn ; Emma M Corr ; Coen van Solingen ; Emily J Brown ; Kathleen B Albers ; Milessa S Afonso ; P M Schlegel ; Monika Sharma ; Lianne C Shanley ; Tessa J Barrett ; Karishma Rahman ; Valeria Mezzano ; Edward A Fisher ; Jonathan D Newman ; Daniela F Quail ; Erik R Nelson ; Bette J Caan ; Lee W Jones ; Kathryn J MooreSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusDisruptions of systemic homeostasis have emerged as critical regulators of cancer. Recent studies indicate that chronic or acute host stressors (e.g., obesity1, surgery2) alter cancer pathogenesis. Many cancer patients, particularly those with breast cancer, are at increased risk for cardiovascular disease due to treatment toxicity and resulting changes in lifestyle behaviors3-5. While elevated risk and incidence of cardiovascular events in breast cancer is well-established, whether such events impact cancer pathogenesis is not known. Herein, we show that an incident myocardial infarction (MI or heart attack) accelerates breast cancer outgrowth and cancer-specific mortality in mice and humans. In mouse models of breast cancer, MI epigenetically reprogrammed Ly6Chigh monocytes in the bone marrow reservoir to an immunosuppressive phenotype that was maintained at the transcriptional level in monocytes in the circulation and tumor. In parallel, MI increased circulating Ly6Chigh monocyte levels and recruitment to tumors, and depletion of th...
Source: GEO: Gene Expression Omnibus - Category: Genetics & Stem Cells Tags: Genome binding/occupancy profiling by high throughput sequencing Mus musculus Source Type: research