The　molecular　mechanism　of　platinum-based　drugs　in　concomitant　chemoradiation　therapy　relies　on　enhancement　of　DNA　damage　in　cancer　cells,　particularly　that　of　detrimental　clustered　lesions　and　cross-links　induced　by　the　abundant　low-energy　electrons　(LEEs)　generated　by　ionizing　radiation.　We　provide　the　complete　1-20　eV　electron-energy　dependence　of　the　yields　of　all　conformational　LEE-induced　lesions　to　biological　DNA,　when　it　binds　to　five　molecules　of　the　chemotherapeutic　drug　cisplatin.　Recording　at　1　eV　intervals　clearly　show　that　the　enhancement　of　all　lesions　is　particularly　intense　at　the　energies　of　coreexcited　transient　molecular　anions　(i.e.,　TMAs　at　5,　6,　and　10　eV).　New　TMAs　are　observed　at　14　and　18　eV,　only　in　yield　functions　of　cisplatin-DNA　complexes.　Enhancements　of　all　lesions　by　cisplatin　are　quantified　over　the　1-20　eV　range,　where　maxima　appear　at　14　and　18　eV.　The　most　detrimental　lesions　to　cell　survival　exhibit　the　highest　enhancements　by　factors　of　2-3.　Whereas　no　cluster　lesions　are　induced　by　electrons　of　energy　＜5　eV　in　DNA,　LEEs　of　any　energy　cause　clustered　damages　in　the　complex.　These　results　confirm　the　current　notion　that　LEEs　and　TMAs　play　a　dominant　role　in　the　molecular　mechanism　of　platinum-drug　chemoradiation　therapy.