Aberrant transcription of FHIT gene in intrahepatic cholangiocellular carcinomas induced by N-nitrosobis(2-oxopropyl)amine in hamsters.

Abstract	Aberrant transcription of the fragile histidine triad (FHIT) gene was investigated in intrahepatic cholangiocellular carcinomas (ICCs) induced by N-nitrosobis(2-oxopropyl)amine (BOP) in female Syrian golden hamsters. The animals received 70 mg/kg of BOP followed by repeated exposure to an augmentation pressure regimen consisting of a choline-deficient diet combined with DL-ethionine and then L-methionine and administration of 20 mg/kg BOP. A total of 14 ICCs were obtained 10 weeks after the beginning of the experiment and total RNAs were extracted from each for assessment of aberrant transcription of the FHIT gene by reverse transcription-polymerase chain reaction analysis. Aberrant transcripts were detected in four out of 14 ICCs (28.6%), as absence in the regions of nucleotides (nt) -75 to 279, nt -75 to 348 and nt -75 to 447. These results suggest that alteration of the FHIT gene may play a role in a small fraction of ICCs induced by BOP in the hamster.
Authors	Tsukasa Kitahashi, Toshifumi Tsujiuchi, Kenji Satoh, Kozo Ohtsuki, Yoichi Konishi, Masahiro Tsutsumi
Journal	Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie (Exp Toxicol Pathol) Vol. 56 Issue 3 Pg. 153-7 (Dec 2004) ISSN: 0940-2993 [Print] Germany
PMID	15625784 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	Carcinogens Neoplasm Proteins Nitrosamines RNA, Messenger fragile histidine triad protein nitrosobis(2-oxopropyl)amine Acid Anhydride Hydrolases
Topics	Acid Anhydride Hydrolases (genetics, metabolism) Animals Bile Duct Neoplasms (chemically induced, genetics, pathology) Bile Ducts, Intrahepatic (metabolism, pathology) Carcinogens (toxicity) Cholangiocarcinoma (chemically induced, genetics, pathology) Cricetinae Disease Models, Animal Female Gene Expression Regulation, Neoplastic Mesocricetus Neoplasm Proteins (genetics, metabolism) Nitrosamines (toxicity) RNA, Messenger Reverse Transcriptase Polymerase Chain Reaction Transcription, Genetic (drug effects)

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