Witaya ThamavitChawalit PairojkulDanai TiwawechTomoyuki ShiraiNobuyuki ItoMahidol UniversityNational Cancer Institute ThailandKhon Kaen UniversityNagoya City University2018-02-272018-02-271994-01-01Teratogenesis, Carcinogenesis, and Mutagenesis. Vol.14, No.4 (1994), 169-17415206866027032112-s2.0-0028108038https://repository.li.mahidol.ac.th/handle/20.500.14594/9539Bile duct hyperplasia caused by proline is believed to represent a chemical effect of the liver fluke, Fasciola hepatica, and the resultant cell division might be expected to play a role as a tumor promoter. To investigate the potential promoting effect of proline on bile duct cancer development, Syrian hamsters were therefore divided into 8 treatment groups: dimethylnitrosamine (DMN) + proline intraperitoneally (i.p.); DMN + proline s.c.; DMN + saline i.p.; DMN + saline s.c.; proline i.p.; proline s.c.; saline i.p.; and saline s.c. DMN was injected i.p. at 20 mg/kg to the animals 2 weeks prior to commencement of proline treatment, whereby 1 ml of a 2 M solution was given by i.p. or s.c. injection 3 times a week for 20 weeks. At the end of week 42, assessment of preneoplastic lesion development did not reveal any significant modulating influence of proline on DMN‐initiated lesion development nor did it itself cause persistent bile duct hyperplasia. © 1994 Wiley‐Liss, Inc. Copyright © 1994 Wiley‐Liss, Inc., A Wiley CompanyMahidol UniversityBiochemistry, Genetics and Molecular BiologyEnvironmental ScienceMedicinePharmacology, Toxicology and PharmaceuticsArticleSCOPUS10.1002/tcm.1770140403