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).
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| http://dx.doi.org/10.1158/2159-8290.CD-22-1199 | DOI Listing |
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