GSE147929 Myocardial Infarction accelerates breast cancer progression via innate immune reprogramming (RNA-seq: sham vs LAD ligation)

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 : Expression profiling by high throughput sequencingOrganism : Mus musculusBreast cancer patients have increased risk of myocardial infarction (MI), but whether these events impact cancer pathogenesis is not known. In mouse models of breast cancer, MI increased circulating Ly6Chigh monocytes and their recruitment to tumors, accelerating cancer progression and metastasis. Analysis of the bone marrow reservoir revealed that MI epigenetically reprogrammed Ly6Chigh monocytes to an immunosuppressive phenotype that was maintained in monocytes in the circulation and tumor at the transcriptional level. Depletion of Ly6Chigh monocytes abrogated MI-induced cancer progression and increased activated cytotoxic T cells in the tumor. In early-stage breast cancer patients, post-diagnosis incident cardiovascular events, such as MI, increased the risk of recurrence and cancer-specific mortality, highlighting the clinical relevance of our findings. Collectively, our results indicate that MI induces cross-disease communication that accelerates breast cancer progression.
Source: GEO: Gene Expression Omnibus - Category: Genetics & Stem Cells Tags: Expression profiling by high throughput sequencing Mus musculus Source Type: research