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

Kitahashi, Tsukasa; Tsujiuchi, Toshifumi; Satoh, K.; Ohtsuki, Kozo; Konishi, Yoichi; Tsutsumi, Masahiro

doi:10.1016/j.etp.2004.08.001

Cited by 4 publications

(1 citation statement)

References 19 publications

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“…The transcription deletion of FHIT was detectable in intrahepatic cholangiocellular carcinomas induced by N-nitrosobis (2-oxopropyl) amine in female Syrian golden hamsters [ 11 ]. FHIT -deficient mice easily developed forestomach tumors and invasive bladder carcinoma after the treatment with N-nitrosomethylbenzylamine and N-butyl-N- (4-hydroxybutyl) nitrosamine respectively [ 12 , 13 ].…”

Section: Introductionmentioning

confidence: 99%

FHIT down-regulation was inversely linked to aggressive behaviors and adverse prognosis of gastric cancer: a meta- and bioinformatics analysis

Zheng

Liu

2017

Oncotarget

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FHIT (fragile histine triad) acts as diadenosine P1, P3-bis (5'-adenosyl)-triphosphate adenylohydrolase involved in purine metabolism, and induces apoptosis as a tumor suppressor. We performed a systematic meta- and bioinformatics analysis through multiple online databases up to March 14, 2017. The down-regulated FHIT expression was found in gastric cancer, compared with normal mucosa and dysplasia ( p < 0.05). FHIT expression was negatively with depth of invasion, lymph node metastasis, distant metastasis, TNM staging and dedifferentiation of gastric cancer ( p < 0.05). A positive association between FHIT expression and favorable overall survival was found in patients with gastric cancer ( p < 0.05). According to Kaplan-Meier plotter, we found that a higher FHIT expression was negatively correlated with overall and progression-free survival rates of all cancer patients, even stratified by aggressive parameters ( p < 0.05). These findings indicated that FHIT expression might be employed as a potential marker to indicate gastric carcinogenesis and subsequent progression, even prognosis.

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Section: Introductionmentioning

confidence: 99%

FHIT down-regulation was inversely linked to aggressive behaviors and adverse prognosis of gastric cancer: a meta- and bioinformatics analysis

Zheng

Liu

2017

Oncotarget

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Inverse correlation of aberrant expression of fragile histidine triad (FHIT) protein with cyclin D1 protein and prognosis in Chinese patients with cholangiocarcinoma

Zhao

Zhong

et al. 2008

Acta Oncologica

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Suppression of N-nitrosobis(2-oxopropyl)amine-induced pancreatic carcinogenesis in hamsters by pioglitazone, a ligand of peroxisome proliferator-activated receptor γ

Takeuchi¹,

Takahashi²,

Sakano³

et al. 2007

Carcinogenesis

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Fat intake and obesity are positively correlated with pancreatic cancer in humans. N-nitrosobis(2-oxopropyl)amine (BOP) induces pancreatic ductal adenocarcinomas limited to Syrian golden hamsters, other rodents not being susceptible. In the present study, we found markedly high levels of serum triglycerides (TGs) and total cholesterol (TC) in Syrian golden hamsters, but not C57BL/6 mice, ICR mice, F344 rats and Wistar rats. Consistent with this, lipoprotein lipase (LPL) activities in the liver were lower in hamsters compared with mice and rats. To examine effects of pioglitazone, a peroxisome proliferator-activated receptor gamma (PPARgamma) ligand, on LPL expression, serum lipid levels and pancreatic cancer development, 6-week-old female Syrian golden hamsters were subcutaneously injected with BOP (10 mg/kg body wt) four times in a week and thereafter fed a diet containing 800 p.p.m. pioglitazone for 22 weeks. The treatment elevated LPL mRNA expression in the liver and significantly improved hyperlipidemia with serum levels of TG and TC being decreased to 62 and 71%, respectively, of the control values. Concurrently, the incidence and multiplicity of pancreatic ductal adenocarcinomas were significantly decreased by pioglitazone in comparison with the controls (38 versus 80%, P < 0.01 and 0.55 +/- 0.15 versus 1.37 +/- 0.22, P < 0.01, respectively). The suppression rates were greater in invasive adenocarcinomas than non-invasive ones. The incidence of cholangiocellular carcinomas was also reduced. Thus, suppression of pancreatic adenocarcinoma development by pioglitazone is possibly associated with improvement in the serum lipid profile, and hyperlipidemia could be an enhancing factor for development of pancreatic cancer in hamsters.

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

Cited by 4 publications

References 19 publications

FHIT down-regulation was inversely linked to aggressive behaviors and adverse prognosis of gastric cancer: a meta- and bioinformatics analysis

FHIT down-regulation was inversely linked to aggressive behaviors and adverse prognosis of gastric cancer: a meta- and bioinformatics analysis

Inverse correlation of aberrant expression of fragile histidine triad (FHIT) protein with cyclin D1 protein and prognosis in Chinese patients with cholangiocarcinoma

Suppression of N-nitrosobis(2-oxopropyl)amine-induced pancreatic carcinogenesis in hamsters by pioglitazone, a ligand of peroxisome proliferator-activated receptor γ

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