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Palabras clave – provistas por la editorial

poly (ADP-ribose) polymerase inhibitor; non-small cell lung cancer; DNA damage; radiotherapy; chemotherapy; combination therapy; coumarin; neoflavone; DNA repair enzymes; Tdp1 inhibitor; cancer; tumor; topotecan; topoisomerase 1 inhibitors; molecular modeling; chemical space; morpholino nucleosides; NAD+ analogs; DNA repair; PARP; 7-methylguanine; poly(ADP-ribose) polymerase 1; inhibitor; nucleosome; trapping; docking; molecular dynamics; fluorescence anisotropy; spFRET microscopy; DNA glycosylases; drug targets; APE1; protein–protein interactions; base excision repair; multifunctional disordered protein; fluorescence techniques; cell cycle checkpoint; cancer therapy; DNA repair inhibitors; synthetic lethality; fused in sarcoma; poly(ADP-ribose) polymerase; poly(ADP-ribose); protein phase separation; berberine; tetrahydroberberine; DNA repair enzyme; SAR; poly(ADP-ribosylation); PARP-1; Olaparib; KU55933; KU-0060648; SCR7 pyrazine; VERO cells; synergism; resistance; CDKN2A; soft tissue sarcomas (STS); gastrointestinal stromal tumors (GIST); AKT signaling; Rad51 recombinase; homology-mediated DNA repair; apoptosis; sensitization; XPA; ERCC1-XPF; CSB; UVB radiation; UVB mutagenesis; nucleotide excision repair (NER); cyclobutane–pyrimidine dimer (CPD) photolesion; veliparib; resveratrol; arsenic trioxide; spironolactone; usnic acid; thioether; tyrosyl-DNA phosphodiesterase 1; TDP1 inhibitor; inhibiting activity; TDP2; PARP1; synergy; HEK293 knockout cell line; polyphenols; PARP-1 inhibitors; n/a