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Using a murine model, CI was induced by inflicting a large anterior myocardial infarction in APCmin mice, prone to developing precancerous intestinal tumors, and tumor growth was measured. Furthermore, to rule out hemodynamic impairment, a heterotopic heart transplantation model was used in which an infarcted or sham-operated heart was transplanted into a recipient mouse while the native heart was left in situ. After 6 weeks, tumor number, volume, and proliferation were quantified. Candidate secreted proteins were selected because they were previously associated with both tumor colon growth and myocardial output in post-MI proteomic studies.