In this issue, Hattori and colleagues capitalized on targeted small-molecule covalent inhibitors of one KRAS mutant with a G12C substitution and of other oncoproteins to create drug–peptide conjugates that serve as cancer neoantigens that prompt an immune response to oncogene-mutant cancer cells. This immunotherapy strategy can serve as an effective approach to overcome the treatment-induced resistance that limits the effectiveness of essentially all small molecule–based targeted anticancer drugs.

See related article by Hattori et al., p. 132 (9).

You do not currently have access to this content.