The briefly attached, covalently bonded TOP1-DNA structure at the 3' end of a cleaved DNA single strand is called a TOP1-DNA cleavage complex, or TOP1cc.

Irinotecan is an analogue of the cytotoxic natural alkaloid camptothecin, obtained from the Chinese tree Camptotheca acuminata.

[5] One irinotecan or SN-38 molecule stacks against the base pairs flanking the topoisomerase-induced cleavage site and poisons (inactivates) the TOP1 enzyme.

[9] Camptothecin analogues irinotecan and topotecan, which inhibit TOP1, are among the most effective FDA-approved anticancer chemotherapeutic agents used in clinical practice.

Irinotecan inactivation of TOP1 appears to be synthetically lethal in combination with deficiencies in expression of some specific DNA repair genes.

Irinotecan inactivation of TOP1 was synthetically lethal with deficient expression of the DNA repair WRN gene in patients with colon cancer.

[12] There are a number of pre-clinical studies indicating synthetic lethality of irinotecan with other genetic or epigenetic DNA repair deficiencies common in cancers.

[13] Another pre-clinical effort was a screening study to find a compound that would be synthetically lethal with a deficiency of N-myc downstream regulated gene 1 (NDRG1) expression.

[14] Exposure of human HeLA cells to UVB irradiation specifically stimulates the formation of covalent complexes between topoisomerase I and DNA.

[16] Topoisomerase I appears to have a direct role in nucleotide excision repair, a process that removes UVB-induced, and other, DNA damages.