As recommended by the guidelines of the National Comprehensive Cancer Network, patients were allocated to FU-based treatment. FOLFIRI , irinotecan (Camptosar; Pfizer) 180 mg/m2 intravenous (IV) infusion over 30–90 minutes, day 1; leucovorin 400 mg/m2 IV infusion to match the duration of irinotecan infusion, day 1; 5-FU 400 mg/m2 IV bolus, day 1; then 1200 mg/m2/day × 2 days (total 2400 mg/m2 over 46–48 hours) continuous infusion; repeat every 14 days or mCapeIRI 35 (link) regimen (irinotecan 125 mg/m2, days 1 and 8; capecitabine (Xeloda; Roche)825–1000 mg/m2, twice daily on days 1–14; repeat every 21 days) or FOLFOX (oxaliplatin 80 mg/m2 IV infusion over 2 hours, day 1; leucovorin 400 mg/m2 IV over 2 hours, day 1; 5-FU 400 mg/m2 IV bolus, day 1; then 1200 mg/m2/day × 2 days continuous infusion; repeat every 14 days) or CapeOX (Oxaliplatin 130 mg/m2 day 1, capecitabine 825–1000 mg/m2, twice daily on days 1–14; repeat every 21 days) or single-agent chemotherapy of capecitabine (1250 mg/m2 twice daily on days 1–14; repeat every 21 days). All patients accepted 5-hydroxytryptamine receptor antagonist (5 mg once a day) 30–60 minutes before irinotecan or oxaliplatin. The chemotherapy continued until disease progressed or intolerable toxicities came out or patients asked to withdrew due to any reason.
Irinotecan
Manufactured by Roche
Sourced in France
Irinotecan is a laboratory equipment product used for research and analytical purposes. It is a topoisomerase I inhibitor that can be utilized in various scientific investigations. The core function of Irinotecan is to enable researchers to study and analyze specific cellular processes and mechanisms.
Automatically generated - may contain errors
2 protocols using irinotecan
1
Metastatic Colorectal Cancer Treatment
2
Investigating p53 Mutant Effects on HCT116 Cells
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For transfection experiments, HCT116 cells were grown onto 6-well plates (500 000 cells per well) and transfected with 3 µg of either pCMV-Neo-Bam p53 wt, pCMV-Neo-Bam p53 V143A, pCMV-Neo-Bam p53 R248W, pCMV-Neo-Bam p53 R249 S, pCMV-Neo-Bam p53 R175 H, pCMV-Neo-Bam p53 R273 H, or pCMV-Neo-Bam (Addgene, Cambridge, MA) using JetPEI™ reagent (PolyPlus Transfection, Illkirch, France) according to the manufacturer’s instructions. RNA was extracted at different time intervals (6 h, 48 h, 3 days or 4 days) after transfection. For the 4 days time point of analysis, cells were re-transfected at day 3.
Five different MISSIONR lentiviral shRNA clones for human TP53 and a non-target shRNA control lentivirus (Sigma-Aldrich, St Louis, MO) were tested in a first round in HCT116 cells. Populations of lentiviral HCT116 infected cells were selected using 1 µg/ml puromycin (Invitrogen, France). Efficiency of TP53 inhibition was determined by RT-qPCR. Two stable HCT116 sh-TP53(1) and sh-TP53(2) cell lines showing an inhibition of p53 expression of 86% and 92% respectively were selected for further experiments. Cells were treated with irinotecan (20 µM, 48 h; Roche Diagnostics, Meylan, France) and RNA extracted for determination of LAMA1 transcripts by RT-qPCR.
Five different MISSIONR lentiviral shRNA clones for human TP53 and a non-target shRNA control lentivirus (Sigma-Aldrich, St Louis, MO) were tested in a first round in HCT116 cells. Populations of lentiviral HCT116 infected cells were selected using 1 µg/ml puromycin (Invitrogen, France). Efficiency of TP53 inhibition was determined by RT-qPCR. Two stable HCT116 sh-TP53(1) and sh-TP53(2) cell lines showing an inhibition of p53 expression of 86% and 92% respectively were selected for further experiments. Cells were treated with irinotecan (20 µM, 48 h; Roche Diagnostics, Meylan, France) and RNA extracted for determination of LAMA1 transcripts by RT-qPCR.
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