The compound, 3-bromopyruvate (3-BP), has been shown to eradicate cancer in an animal model. Whether the apoptotic fragments resulting from 3-BP treatment result in immunogenic cell death is unknown. We demonstrate that 3-bromopyruvate-induced apoptosis of mouse 4T1 breast cancer cells stimulated immature dendritic cells (DCs) of the immortal JAWS II cell line to produce pro-inflammatory cytokine IL-12 and increase expression of co-stimulatory molecules CD80 and CD86. Increased uptake of fragments from dying tumor cells correlated with increased surface levels of calreticulin and the release of high group motility box 1 (HMGB1) from cancer cells. The anti-phagocytic signal CD47 was reduced by treatment with 3-bromopyruvate. 3-BP treated breast cancer cells were able to activate dendritic cells through TLR4 signaling. Killing by 3-BP was compared to that induced by mitoxantrone and doxorubicin, among the few chemotherapeutics that induce immunogenic cell death. 3-BP killing was likewise compared to camptothecin, a compound that fails to induce immunogenic cell death. Importantly, 3-BP did not markedly decrease the levels of the key peptide presenting molecule MHC I on DCs that were co-cultivated with dying tumor cells. 3-BP treatment of the aggressive triple negative BT-20 human breast cancer cell line also resulted in immunogenic cell death with activation of human dendritic cells in vitro.