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Presentation Abstract:
Cardiovascular disease (CVD) events such as myocardial infarction (MI, or heart attack) disrupt systemic homeostasis. Such disruption has important implications for subsequent CVD risk. However, as many patients with MI present with other disease comorbidities, systemic responses to MI may also increase risk for non-CVD pathologies. For example, patients with cancer, particularly those with breast cancer, are at increased risk for CVD due to treatment toxicity and changes in lifestyle behaviors. While elevated risk and incidence of CVD events in breast cancer is well established, whether such events impact cancer pathogenesis is not known. We have identified that CVD events following a breast cancer diagnosis are an independent predictor of recurrence and cancer-specific mortality. In corollary mouse models of breast cancer, MI accelerates tumour growth and metastasis through reprogramming of innate immunity. Mechanistically, MI epigenetically reprograms monocytes in the bone marrow toward an immunosuppressive (pro-tumour) phenotype, which is maintained across the transcriptome in monocytes in the circulation and tumour. In parallel, MI increases circulating monocyte levels and recruitment to tumours, and depletion of these cells abrogates MI-induced tumour growth. Together, these findings demonstrate that MI-induced disruption of systemic homeostasis triggers cross-disease communication that accelerates breast cancer.

Bio:
Dr. Graeme Koelwyn is a postdoctoral fellow at Memorial Sloan Kettering Cancer Center in New York City. He received his B.Sc. (Exercise and Health Physiology) from the University of Calgary, his M.Sc. (Clinical Exercise Physiology) from the University of British Columbia, and his Ph.D. (Pathobiology and Translational Medicine) from New York University.
His research applies a systems biology and ‘omics-based approach to discern the causal pathways that link cardiovascular disease to other host pathologies, including cancer, and how interventions such as exercise can protect from such deleterious interactions. In particular, his research focusses on how cardiovascular disease and exercise can imprint systemic ‘learned’ responses in the innate immune system, altering concurrent and subsequent host responses to disease.

Please send your candidate feedback to the search committee Chair Jeremy Snyder and/or committee at fhs-crcomicssearch@sfu.ca

Committee Members:
Tania Bubela – Chair
Robert Hogg
Zabrina Brumme
Don Sin
Scott Tebbutt
Will Hsiao