title: [CPT-11 (Irinotecan)].
abstract: CPT-11 is activated by hydrolysis to SN-38 that is primarily inactivated through biotrans-formation into SN-38 glucuronide ( SN-38 G) by UGT1As. Tailoring chemotherapy based on the genetic profile of patients and tumor would increase efficacy and decrease toxicity for patients. The toxicities of CPT-11 have been reported to correlate with the polymorphism of the number of TA repeats in UGT1A1 gene because of its gene transcriptional efficiency. UGT1A1*28 was chosen as the candidate gene to be investigated as a predictor of severe toxicity. Other studies determining predictive markers of CPT-11 efficacy have been highly controversial.
authors.affiliation: Department of Digestive Surgery and Surgical Oncology, Yamaguchi University Graduate School of Medicine.
authors.forename: Shoichi
authors.initials: S
authors.lastname: Hazama
authors.forename: Masaaki
authors.initials: M
authors.lastname: Oka
mesh_terms: D000970:Antineoplastic Agents / Q000009:adverse effects / Q000378:metabolism / Q000627:therapeutic use; D002166:Camptothecin / Q000009:adverse effects / Q000031:analogs & derivatives* / Q000378:metabolism / Q000627:therapeutic use; D006801:Humans; D000077146:Irinotecan; D009369:Neoplasms / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism; D011110:Polymorphism, Genetic / Q000235:genetics
chemical_list: D000970:Antineoplastic Agents; D000077146:Irinotecan; D002166:Camptothecin