Comparison of 18F-FDG, 18F-Fluoroacetate, and 18F-FEPPA for Imaging Liver Fibrosis in a Bile Duct-Ligated Rat Model.

Developing sensitive diagnostic methods for a longitudinal evaluation of the status of liver fibrosis is a priority. This study is aimed at assessing the significance of longitudinal positron emission tomography (PET) imaging with 18F-labeling tracers for assessing liver fibrosis in a rat model with bile duct ligation (BDL). Twenty-one 6-week-old Sprague-Dawley male rats were used in this study. Longitudinal PET images using [18F]N-2-(2-fluoroethoxy)benzyl)-N-(4-phenoxypyridin-3-yl)acetamide ([18F]FEPPA) (n = 3), [18F]fluoroacetate ([18F]FAc) (n = 3), and 18F-fluoro-2-deoxy-D-glucose ([18F]FDG) (n = 3) were obtained at 0, 1, and 2 weeks after BDL. Biochemical assays, histological assays, immunohistochemical staining assays, and next generation sequencing analyses were also performed at 0 (n = 3), 1 (n = 3), 2 (n = 3), and 3 (n = 3) weeks after BDL, which demonstrated the severe damage in rat livers after BDL. Regarding [18F]FEPPA and [18F]FDG, there was a significantly higher uptake in the liver after BDL (both P < 0.05), which lasted until week 2. However, the uptake of [18F]FAc in the liver was not significantly different before and after BDL (P = 0.28). Collectively, both [18F]FEPPA and [18F]FDG can serve as sensitive probes for detecting the liver fibrosis. However, [18F]FAc is not recommended to diagnose liver fibrosis.

Methylenetetrahydrofolate reductase (MTHFR) genotype, smoking habit, metastasis and oral cancer in Taiwan.

The aim of this study was to evaluate the association and interaction of genotypic polymorphism in methylenetetrahydrofolate reductase (MTHFR) with smoking habits and oral cancer in Taiwan. Two well-known polymorphic variants of MTHFR, C677T (rs1801133) and A1298C (rs1801131), were analyzed in association with oral cancer risk, and their joint effects with individual smoking habits on oral cancer risk are discussed. In total, 620 oral cancer patients and 620 non-cancer controls in central Taiwan were recruited and genotyped. The MTHFR C677T genotype, but not the A1298C, was differently distributed between the oral cancer and control groups. The T allele of MTHFR C677T was significantly more frequently found in controls than in oral cancer patients. Joint effects of smoking and MTHFR C677T genotype significantly affected oral cancer susceptibility. The MTHFR C677T CT and TT genotypes in association with smoking conferred lower odds ratios of 0.66 and 0.54 (95% confidence interval=0.49-0.82 and 0.39-0.86), respectively. Those patients with MTHFR C677T CT and TT genotypes also had a lower risk of oral cancer metastasis. MTHFR C677T genotype may have joint effects with smoking on oral carcinogenesis, and may be a useful biomarker for prediction and prognosis of oral cancer.

Significant association of cyclin D1 single nucleotide polymorphisms with oral cancer in taiwan.

UNLABELLED: The cell cycle regulator cyclin D1 (CCND1) is thought to play a major role in the transition of the cell cycle from G(1) to S-phase. It is known that cancer cells have unbalanced cell cycle regulation. This study aimed to investigate the association of CCND1 single nucleotide polymorphisms A870G (rs9344) and C1722G (rs678653) with oral cancer risk and examine the interaction between CCND1 and smoking habit. MATERIALS AND METHODS: In this hospital-based case-control study, the CCND1 polymorphisms were investigated in 620 patients and 620 age- and gender-matched controls. RESULTS: Significant differences were shown between the oral cancer and control groups in the distribution of the genotypes (p=0.0014) and allelic frequency (p=0.0027) in the CCND1 rs9344 genotype. Individuals who carried at least one G allele (GG or AG) had a 0.64-fold decreased risk of developing oral cancer compared to those who carried the AA wild-type genotype (95% CI: 0.50-0.81). There was an obvious joint effect of CCND1 rs9344 genotype with smoking habit on oral cancer. CONCLUSION: Cell cycle regulation may play a role in oral carcinogenesis and CCND1 rs9344 polymorphism maybe a useful biomarker for oral oncology.

The joint effect of hOGG1 single nucleotide polymorphism and betel quid chewing on oral cancer in Taiwan.

AIM: To evaluate the association and interaction among hOGG1 genotypic polymorphism, betel quid chewing status and oral cancer risk in Taiwan. MATERIALS AND METHODS: The well-known polymorphic variants of hOGG1, codon 326, were analyzed in association with oral cancer susceptibility, and discussed regarding its joint effect with individual habits on oral cancer susceptibility. In total, 620 patients with oral cancer and 620 healthy controls recruited from the China Medical Hospital were analyzed by polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP). RESULTS: The hOGG1 codon 326 genotypes were differently distributed between the oral cancer and control groups (p=0.0266) and the C allele of hOGG1 codon 326 was significantly (p=0.0046) more frequently found in cancer patients than in controls. We further analyzed the joint effects of gene variants and habits on oral cancer risk and found an interaction between hOGG1 codon 326 genotype and betel quid chewing status. The association of the C allele for hOGG1 codon 326 with oral cancer risk was found to be significant only in the betel quid chewer group (p=0.0149), not in the non-chewer group (p=0.8028). CONCLUSION: Our results provide evidence that the C allele of hOGG1 codon 326 may have a joint effect with betel quid chewing on the development of oral cancer.

Association between DNA double strand break gene Ku80 polymorphisms and oral cancer susceptibility.

The DNA double strand break repair gene Ku80 is thought to play a major role in the caretaking of the overall genome stability. It is very possible that defective in double strand break repair capacity can lead to human carcinogenesis. Thus, the polymorphic variants of Ku80 were firstly investigated regarding their association with oral cancer susceptibility. In this hospital-based case-control study, the association of Ku80 promoter G-1401T (rs828907), promoter C-319T (rs11685387), and intron19 (rs9288518) polymorphisms with oral cancer risk in a Taiwanese population was investigated. 600 patients with oral cancer and 600 age- and gender-matched healthy controls recruited were genotyped and analyzed by PCR-RFLP method. There were significant differences between oral cancer and control groups in the distributions of their genotypes (P=0.0038) and allelic frequencies (P=0.0044) in the Ku80 promoter G-1401T polymorphism. In the other two polymorphisms, there was no difference between both groups in the distribution of either genotype or allelic frequency. There is a synergistic gene-environmental interaction between Ku80 and areca chewing. Compared with G/G genotype in Ku80 promoter G-1401T, the G/T plus T/T significantly enhanced the risk only in the areca chewers (odds ratio=1.603; 95% confidence interval=1.053-2.011), not in the non-areca chewers. In conclusion, the Ku80 promoter G-1401T is correlated with oral cancer susceptibility and this polymorphism may be a useful marker for oral cancer prevention and early detection.