Specifically, Wu et al. noted that the “balance between DNA damage and capacity of DNA repair mechanisms determines the final therapeutic outcome” and “the capacity of cancer cells to complete DNA repair mechanisms is important for therapeutic resistance and has a negative impact upon therapeutic efficacy”, and thus theorized that “harmacological inhibition of recently detected targets of DNA repair with several small-molecule compounds . . . . has the potential to enhance the cytotoxicity of anticancer agents”.
Especificamente, Wu et al. sinalaron que o “balance entre os danos no ADN e a capacidade dos mecanismos de reparación do ADN determina o resultado terapéutico final” e “a capacidade das células cancerosas de completar os mecanismos de reparación do ADN é importante para a resistencia terapéutica e ten un impacto negativo sobre a eficacia terapéutica”, e así teorizaron que “a inhibición farmacolóxica de dianas recentemente detectadas da reparación do ADN con varios compostos de moléculas pequenas . . . ten o potencial de amplificar a citotoxicidade de axentes anticancro”.