• 대한핵의학회:학술대회논문집
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• 대한핵의학회 1992년도 제31차 춘계학술대회
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• pp.194.1-194.1
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• 1992

• 대한핵의학회:학술대회논문집
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• 대한핵의학회 1995년도 제34차 춘계학술대회 초록집
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• pp.201-201
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• 1995

• 대한핵의학회:학술대회논문집
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• 대한핵의학회 1991년도 제30차 춘계학술대회
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• pp.158.2-159
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• 1991

• Korean Journal of Radiology
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• 제24권1호
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• pp.6-9
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• 2023

• Korean Journal of Radiology
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• 제24권1호
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• pp.10-14
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• 2023

• Nuclear Medicine and Molecular Imaging
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• 제42권1호
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• pp.70-73
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• 2008

A 65 year-old man with hepatocellulcar carcinoma (HCC) admitted to treat left lower leg swelling and pus discharge suspecting osteomyelitis. MRI of his lower leg revealed the bone metastasis. Whole body FDG PET/CT additionally detected left shoulder and right ilium metastasis. Hematemesis suddenly developed in this patient after 3 weeks. Metastasis of right tonsil was histologically proven. When we reviewed his FDG PET/CT, there was asymmetric mild hypermetabolism in the right tonsil. When focal hypermetabolism is shown in the organ physiologically taking glucose up such as tonsil, we should cautiously assess whole body PET/CT in the examination of distant metastasis. We present a patient with multiple distant metastasis including tonsil from HCC showing increased FDG uptake with the literature review.

• Asian Pacific Journal of Cancer Prevention
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• 제13권9호
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• pp.4423-4426
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• 2012

Aim: XRCC1 and XPD are two major repair genes involved in nucleotide excision repair (NER), which is reported to be associated with risk of several cancers. We explored the association of XRCC1 and XPD polymorphisms with the risk of HCC. Methods: A total of 410 cases with HCC and 410 health controls were collected. XRCC1 Arg194Trp, XRCC1 Arg399Gln, XPD Lys751Gln and XPD Asp312Asn genotyping was performed by duplex polymerase-chain-reaction with the confronting-two-pair primer (PCR-CTPP) method. Results: XRCC1 194Trp/Trp was strongly significantly associated with an increased risk of HCC cancer when compared with the wide-type genotype (OR=2.26, 95% CI=(1.23-5.38). Individuals carrying the XRCC1 399Gln/Gln showed increased risk of HCC (OR=1.74, 95%CI=1.06-2.74). The XPD 751Gln/Gln and Gln allele genotype were associated with strong elevated susceptibility to HCC (OR=3.51 and 1.42, respectively). Conclusion: These results suggest that polymorphisms in XRCC1 and XPD may have functional significance in risk of HCC.

• Asian Pacific Journal of Cancer Prevention
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• 제16권5호
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• pp.1725-1728
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• 2015

Objective: To explore effects of paclitaxel-loaded poly lactic-co-glycolic acid (PLGA) particles on the viability of human hepatocellular carcinoma (HCC) HepG2 cells. Materials and Methods: The viability of HepG2 cells was assessed using MTT under different concentrations of prepared paclitaxel-loaded particles and paclitaxel (6.25, 12.5, 25, 50, and 100 mg/L), and apoptosis was analyzed using Hochest33342/Annexin V-FITC/PI combined with an IN Cell Analyzer 2000. Results: Paxlitaxel-loaded nanoparticles were characterized by narrow particle size distribution (158.6 nm average particle size). The survival rate of HepG2 cells exposed to paclitaxel-loaded PLGA particles decreased with the increase of concentration and time period (P<0.01 or P<0.05), the dose- and time-dependence indicating sustained release (P<0.05). Moreover, apoptosis of HepG2 cells was induced, again with an obvious dose- and time-effect relationship (P<0.05). Conclusions: Paclitaxel-loaded PLGA particles can inhibit the proliferation and induce the apoptosis of HCC HepG2 cells. This new-type of paclitaxel carrier body is easily made and has low cost, good nanoparticle characterization and sustained release. Hence, paclitaxel-loaded PLGA particles deserve to be widely popularized in the clinic.

• Asian Pacific Journal of Cancer Prevention
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• 제17권5호
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• pp.2699-2703
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• 2016

Background: Primary hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. MicroRNAs (miRNAs) have great HCC diagnostic potential and circulating miRNAs have been reported as promising biomarkers for various pathologic conditions. Aim: To explore the potential benefit of serum miR-126, miR-129, miR-155, miR-203 and miR-223 as non-invasive diagnostic markers of hepatitis C virus (HCV)-related HCC. Materials and Methods: The expression of miRNA was evaluated using real-time quantitative RT-PCR in 78 serum samples (30 $treatment-na{\ddot{i}}ve$ chronic HCV, 25 post-HCV compensated cirrhosis and 23 $treatment-na{\ddot{i}}ve$ HCC cases). Results: Comparing miRNA fold changes in the HCC group vs the non HCC groups, there was significant fold decrease in miR-126 (P= 0.034), miR-129 (P= 0.006), miR-155 (P= 0.011), miR-203 (P<0.001) and miR-223 (P= 0.013). The highest AUC to differentiate HCC patients from non-HCC was 0.76 for miR-203. Conclusions: Among studied miRNAs, serum miR-203 has the highest potential as a non-invasive biomarker of HCC.

• The Korean Journal of Physiology and Pharmacology
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• 제2권2호
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• pp.261-269
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• 1998

Concomitant administration of a single acute dose of ethanol (4 g/kg) protected mice from the hepatocellular injury observed upon administration of a large dose of acetaminophen (400 mg/kg). This was evidenced by the normal histological appearances of liver sections and by the lowered serum aminotransferase activities in mice treated with ethanol and acetaminophen together. In the mice treated with acetaminophen alone, along with the hepatic necrosis, the hepatic microsomal aminopyrine N-demethylase activity was decreased. However, co-administration of ethanol prevented this acetaminophen dependent inhibition on the microsomal mixed function oxidase activity. Pharmacokinetic studies indicated that the concentration of un-metabolized drug in the blood was increased in the ethanol treated mice. Furthermore, upon co-administration of ethanol, although the biliary levels of acetaminophen metabolites (glucuronide, sulfate and cysteine conjugates) were decreased, the level of unmetabolized acetaminophen was increased. Our findings suggest that co-administration of an acute dose of ethanol reduces the degree of hepatocellular necrosis produced by a large dose of acetaminophen and this ethanol dependent protection is, in major part, afforded by suppression of the hepatic microsomal mixed function oxidase activity catalyzing the metabolic activation of acetaminophen.