%0 Case Reports
%T Exceptional response to lurbinectedin and irinotecan in BRCA-mutated platinum-resistant ovarian cancer patient: a case report.
%A Cortesi L
%A Venturelli M
%A Barbieri E
%A Baldessari C
%A Bardasi C
%A Coccia E
%A Baglio F
%A Rimini M
%A Greco S
%A Napolitano M
%A Pipitone S
%A Dominici M
%A Cortesi L
%A Venturelli M
%A Barbieri E
%A Baldessari C
%A Bardasi C
%A Coccia E
%A Baglio F
%A Rimini M
%A Greco S
%A Napolitano M
%A Pipitone S
%A Dominici M
%J Ther Adv Chronic Dis
%V 13
%N 0
%D 2022
%M 35070248
%F 4.97
%R 10.1177/20406223211063023
%X Lurbinectedin is responsible for DNA recognition and binding, producing double-strand DNA (dsDNA) breaks thus resulting in apoptosis. Sensitivity to lurbinectedin is linked to the nucleotide excision repair (NER) system. Furthermore, irinotecan, a topoisomerase I inhibitor, provokes dsDNA breaks that could be reinforced abrogating the NER system using lurbinectedin. BRCA-mutated patients, already treated with platinum-derived drugs, who suffered DNA damage, cannot repair the breaks due to lurbinectedin interaction, whereas irinotecan provokes a dsDNA break that promotes synthetic lethality. This article describes an exceptional response to lurbinectedin alone followed by the association with irinotecan in a BRCA-mutated platinum-resistant ovarian cancer patient. A 44-year-old BRCA1-mutated ovarian cancer patient was treated in sixth line with lurbinectedin and irinotecan with a time to further progression (TTFP) equal to 8 months. In our case, the association with irinotecan overcame the resistance to lurbinectedin alone. In conclusion, lurbinectedin and irinotecan demonstrated a promising response in platinum-resistant patients. However, further studies should be conducted to validate our findings and future trials will be important to further define the clinical utility of lurbinectedin.