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MEK inhibitors cobimetinib and trametinib, regressed a gemcitabine-resistant pancreatic-cancer patient-derived orthotopic xenograft (PDOX)

Authors
 Kei Kawaguchi  ;  Kentaro Igarashi  ;  Takashi Murakami  ;  Tasuku Kiyuna  ;  Thinzar M. Lwin  ;  Ho Kyoung Hwang  ;  Jonathan C. Delong  ;  Bryan M. Clary  ;  Michael Bouvet  ;  Michiaki Unno  ;  Robert M. Hoffman 
Citation
 Oncotarget, Vol.8(29) : 47490-47496, 2017 
Journal Title
 Oncotarget 
Issue Date
2017
Keywords
PDOX ; drug-response ; nude mice ; orthotopic ; pancreatic cancer
Abstract
A pancreatic ductal adenocarcinoma (PDAC), obtained from a patient, was grown orthotopically in the pancreatic tail of nude mice to establish a patient-derived orthotopic (PDOX) model. Seven weeks after implantation, PDOX nude mice were divided into the following groups: untreated control (n = 7); gemcitabine (100 mg/kg, i.p., once a week for 2 weeks, n = 7); cobimetinib (5 mg/kg, p.o., 14 consecutive days, n = 7); trametinib (0.3 mg/kg, p.o., 14 consecutive days, n = 7); trabectedin (0.15 mg/kg, i.v., once a week for 2 weeks, n = 7); temozolomide (25 mg/kg, p.o., 14 consecutive days, n = 7); carfilzomib (2 mg/kg, i.v., twice a week for 2 weeks, n = 7); bortezomib (1 mg/kg, i.v., twice a week for 2 weeks, n = 7); MK-1775 (20 mg/kg, p.o., 14 consecutive days, n = 7); BEZ-235 (45 mg/kg, p.o., 14 consecutive days, n = 7); vorinostat (50 mg/kg, i.p., 14 consecutive days, n = 7). Only the MEK inhibitors, cobimetinib and trametinib, regressed tumor growth, and they were more significantly effective than other therapies (p < 0.0001, respectively), thereby demonstrating the precision of the PDOX models of PDAC and its potential for individualizing pancreatic-cancer therapy.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/161278
DOI
10.18632/oncotarget.17667
Appears in Collections:
1. Journal Papers (연구논문) > 1. College of Medicine (의과대학) > Dept. of Surgery (외과학교실)
Yonsei Authors
황호경(Hwang, Ho Kyoung)
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