Dendritic cells (DCs) act at the interface of the innate and adaptive arms of the immune system. Their primary function is to orchestrate adaptive immune responses by presenting antigens and providing costimulatory signals to T cells. For CD8+ T cells, recognition of a cognate antigenic peptide bound to class I major histocompatibility complex (MHC-I) presented by a DC along with co-stimulation results in its activation—a proliferative burst and the acquisition of a potent cytotoxic effector program. In the context of a tumor, DCs are thought to activate CD8+ T cells primarily through antigen cross-presentation, in which DCs generate antigenic peptides derived from exogenous proteins through proteasomal or lysosomal degradation and subsequently load these peptides onto MHC-I molecules for display. Here, using two murine tumor models lacking the MHC-I molecule H-2Kb (Kb), we found that cancer cell-intrinsic MHC-I expression was required for optimal CD8+ T cell priming. Furthermore, using genetically modified mouse strains lacking MHC-I or otherwise deficient in cross-presentation,we observed that DCs were capable of acquiring and presenting intact peptide/(p)MHC-I from cancer cells, and that this was sufficient for their ability to activate tumor antigen-specific CD8+ T cells ex vivo. Finally, we confirmed that antigen presenting cells (APCs) were capable of presenting acquired, cancer cell-derived class I human leukocyte antigen (HLA-I; human MHCI) molecules from human lymphoma cells, both in vitro and in xenograft experiments. Together, these results suggest that MHC-dressing, the presentation of exogenous pMHC-I complexes by DCs, makes a significant contribution to overall tumor antigen presentation.