• Asian Pacific Journal of Cancer Prevention
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• v.14 no.8
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• pp.4509-4513
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• 2013

Chronic hepatitis B virus (HBV) infection has long been the most common cause of hepatocellular carcinoma (HCC). However, some aspects of the pathogenesis of HBV infection and genesis of hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) are still inconclusive. An increasing number of published studies indicate that hepatitis B virus mutations are associated with risk of HCC. These variations include, in particular, mutations in ORF S,C,X gene regions. This mini-review summarizes results of clinical studies and molecular mechanisms on the possible relations of HBV mutations with the development of hepatocellular carcinoma.

• Molecules and Cells
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• v.21 no.2
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• pp.224-228
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• 2006

Glypican-3 (GPC3) is a member of the glypican family, which encodes cell-surface heparan-sulfate proteoglycans, and is frequently upregulated in hepatocellular carcinoma (HCC). We have recently reported that blocking endogenous GPC3 expression promotes the growth of HCC cell lines, suggesting that GPC3 plays a negative role in HCC cell proliferation. Here, we report that forced expression of GPC3 reduced the growth of HCC cells. We also found that FGF2-mediated cell proliferation was inhibited by GPC3. In addition, we observed that the adhesion of HCC cells to collagen type I and fibronectin was decreased by GPC3, whereas cellular migration and invasiveness were stimulated. Collectively, these results suggest that progression of hepatocellular carcinoma is associated with upregulation of GPC3.

• Korean Journal of Radiology
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• v.24 no.7
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• pp.660-667
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• 2023

• The Korean Journal of Nuclear Medicine
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• v.23 no.1
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• pp.27-33
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• 1989

The relationship between angiographic findings and those of $^{67}Ga$ scan was evaluated in 30 patients with primary hepatocellular carcinoma diagnosed by either pathological examination or laboratory, radiologic findings. Twenty-three cases revealed hot activities on $^{67}Ga$ scan and definite tumor stains on angiography. Main findings of $^{67}Ga$ scans of 7 cases were isoactivity in 5 and cold area in 2, 5 of which revealed faint or no tumor stain on angiography. Cold areas within the primary hepatocellular carcinoma were noted in 9 cases by $^{67}Ga$ scan. In 6 cases these were due to tumor necrosis. Remaining 3 cases had arterioportal shunt, portal vein thrombosis and one had necrosis as well. These results indicate that gallium uptake of primary hepatocellular carcinoma seems to be relatively correlated with tumor stains on angiography. It is well known that the necrotic portion of primary hepatocellular carcinoma does not uptake gallium and it's the main cause of cold areas on $^{67}Ga$ scan. And we suspect that the hemodynamic changes of primary hepatocellular carcinoma such as large arterioportal shunt, portal vein thromosis may cause the decreased activity on $^{67}Ga$ scan.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.6
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• pp.2503-2509
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• 2012

Considerable research has been conducted concerning galectin-9 and carcinomas, but little information is available about any relation with the hepatocellular carcinoma. In this study, we employed a small interfering RNA (siRNA) targeting galectin-9 to down-regulate the expression in HepG2 cells. As a result, after galectin-9 expression was reduced, cell aggregation was suppressed, while other behaviour such as the proliferation, adhesion and invasion to ECM, cell-endothelial adhesion and transendothelial invasion of the cells were markedly enhanced. When tumors of 200 patients with hepatocellular carcinoma were tested for galectin-9 expression by immunohistochemistry, binding levels demonstrated intimate correlations with the histopathologic grade, lymph node metastasis, vascular invasion and intrahepatic metastasis (P<0.05). Moreover, survival analysis indicated that patients with galectin-9 expression had much longer survival time than those with negative lesions, and the Log-rank test indicated that this difference was statistical significant (P<0.0001). The Cox proportional hazards model suggested that negative galectin-9 expression in hepatocellular carcinoma represented a significant risk factor for patient survival. We propose that galectin-9 might be a new prognostic factor with antimetastatic potential in patients with hepatocellular carcinoma.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.6
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• pp.2565-2570
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• 2014

H19 is an imprinted oncofetal gene, and loss of imprinting at the H19 locus results in over-expression of H19 in cancers. Aflatoxin B1(AFB1) is regarded as one of the most dangerous carcinogens. Exposure to AFB1 would most easily increase susceptibility to diseases such as hepatocellular carcinoma(HCC) but any possible relationship between AFB1 and H19 is not clear. In present study, we found that AFB1 could up-regulate the expression of H19 and promote cell growth and invasion by hepatocellular carcinoma HepG2 cells. Knocking down H19 RNA co ld reverse the effects of AFB1 on cell growth and invasion. In addition, AFB1 induced the expression of E2F1 and its knock-down could down-regulate H19 expression and suppress cell growth and invasion in hepatocellular carcinoma HepG2 cells. Furthermore, E2F1 over-expression could up-regulate H19 expression and promote cell growth and invasion, with binding to the H19 promoter being demonstrated by chromatin immunoprecipitation assays (ChIP). In summary, our results suggested that aflatoxin B1could promote cell growth and invasion in hepatocellular carcinoma HepG2 cells through actions on H19 and E2F1.

• The Korean Journal of Cytopathology
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• v.2 no.2
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• pp.90-97
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• 1991

Liver is generally known as an organ which is most commonly involved by the metastic tumors. According to the tendency of using fine needle aspiration in the diagnosis of hepatic tumors, the differentital diagnosis between hepatocellular carcinoma and metastatic carcinoma frequently has been a main issue in the poorly differentitated cases, especially to the pathologists of Korea, an endemic area of hepatocellular carcinoma. Until now the problem has been usually solved by the comparison of cytologic characteristics of their tumor cells but not by background cytologic features which rarely have been studied. We observed the background cytologic features helpful for the differential diagnosis through the analysis of 20 cases who had confirmed primary cancer and were diagnosed as metastatic carcinomas in the liver by fine needle aspiration cytology. Twenty cases included 9 adenocarcinomas, 7 spuamous cell carcinomas, 1 small cell carcinoma, 1 carcinoid, 1 adenoid cystic carcinoma, and 1 renal cell cacinoma. Analysis of background cytologic features revealed that 77% of adenocacinoma cases showed benign mesenchymal components and hepatocytes and spuamous cell carcinoma cases disclosed benign mesenchymal tissue (71%) and necrosis (57%), Remaining cases showed variable combinations of benign mesenchymal component, necrosis, hepatocytes, and bile duct epithelial cells. No case revealed atypical hepatocytic naked nuclei, a useful cytologic finding of hepatocellular carcinoma. In summary, the background cytologic features more commonly observed in metastatic carcinomas than in the hepatocellular carcinoma were benign mesenchymal components, hepatocytes, necrosis, and bile duct epithelium. The endothelial cells and hepatocytic naked nuclei, two relatively specific findings of hepatocellular carcinoma were not observed except for renal ceil carcinoma. Above background cytologic features are thought to be helpful for the differential diagnosis between the hepatocellular carcinoma and various metastatic carcinomas in the poorly differentiated cases.

• Journal of radiological science and technology
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• v.20 no.2
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• pp.73-78
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• 1997

The goal of this paper is that we know the usefulness of echo-planar imaging(EPI) for discriminate between hepatocellular carcinoma(HCC) and hemangioma. We get a time signal intensity curve for liver diseases from the dynamic contrast enhancement images and compared and analyze both the contrast ratio(CR) and the contrast to noise ratio(CNR) using echo planar imaging. The obtained results are follows : 1. Hepatocellular carcinoma was shown the best contrast after about 20 seconds when Is the earlist time in the main artery, and then reduced. The center where is disease was shown the characteristic that the best contrast is appeared after about 35-45 seconds and then slowly reduced. Liver parenchyma was shown the best contrast and reduced after 60 seconds. 2. The peripheral nodular of hemangioma was shown the better contrast soon. On the other hend, the contrast of center where is disease started to increase after 60 seconds and was equal to that of liver parenchyma. Increasing of the contrast continued after. 3. Turbo SE technic was used, the average of CR for hepatocellular carcinoma was $36.7{\pm}1.2$ and the average of CNR was $2.4{\pm}3.2$, while the average of CNR for hemangioma was $54.9{\pm}1.0$ and the average of CNR was $9.7{\pm}1.3$. 4. EPI technic was used, the average of CR for hepatocellular carcinoma was $47.8{\pm}1.2$ and the average of CNR was $3.4{\pm}2.1$, while the average of CNR for hemangioma was $75.7{\pm}2.2$ and the average of CNR was $9.5{\pm}1.1$. According to above we can find that hemangioma is more bright than hepatocellular carcinoma and the difference of brightness between hepatocellular carcinoma and hemangioma is useful sequence.

• The Journal of Internal Korean Medicine
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• v.41 no.3
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• pp.447-456
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• 2020

Objectives: This review aimed to present the characteristics of hepatocellular cancer patients treated by Korean medicine. Methods: Sixty hepatocellular cancer patients in a Korean medicine hospital from July 2012 to December 2019 were studied. We evaluated the general characteristics, overall therapies, and chief complaints of the patients. Results: Of the patients, 55% were stage IV, and Korean medicine was accompanied by conventional treatments, such as chemotherapy, operation, and transarterial chemoembolization. An average number of hepatocellular cancer patients had admitted to the hospital. The patients' chief complaints were dyspnea, general weakness, abdominal discomfort, and cancer-related pain. Conclusions: This study illustrates the general characteristics of hepatocellular cancer patients on Korean medicine treatments. These findings suggest that further investigations with a rigorous study design and more participants are needed.

• Nutrition Research and Practice
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• v.2 no.2
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• pp.80-84
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• 2008

Beneficial effects of dehydroepiandrosterone (DHEA) supplement on age-associated chronic diseases such as cancer, cardiovascular disease, insulin resistance and diabetes, have been reported. However, its mechanism of action in hepatocellular carcinoma in vivo has not been investigated in detail. We have previously shown that during hepatocellular carcinogenesis, DHEA treatment decreases formation of preneoplastic glutathione S-transferase placental form-positive foci in the liver and has antioxidant effects. Here we aimed to determine the mechanism of actions of DHEA, in comparison to vitamin E, in a chemically-induced hepatocellular carcinoma model in rats. Sprague-Dawley rats were administered with control diet without a carcinogen, diets with 1.5% vitamin E, 0.5% DHEA and both of the compounds with a carcinogen for 6 weeks. The doses were previously reported to have anti-cancer effects in animals without known toxicities. With DHEA treatment, cytosolic malate dehydrogenase activities were significantly increased by ${\sim}5$ fold and glucose 6-phosphate dehydrogenase activities were decreased by ${\sim}25%$ compared to carcinogen treated group. Activities of Se-glutathione peroxidase in the cytotol was decreased siguificantly with DHEA treatment, confirming its antioxidative effect. However, liver microsomal cytochrome P-450 content and NADPH-dependent cytochrome P-450 reductase activities were not altered with DHEA treatment. Vitamin E treatment decreased cytosolic Se-glutathione peroxidase activities in accordance with our previous reports. However, vitamin E did not alter glucose 6-phosphate dehydrogenase or malate dehydrogenase activities. Our results suggest that DHEA may have decreased tumor nodule formation and reduced lipid peroxidation as previously reported, possibly by increasing the production of NADPH, a reducing equivalent for NADPH-dependent antioxidant enzymes. DHEA treatment tended to reduce glucose 6-phosphate dehydrogenase activities, which may have resulted in limited supply for de novo synthesis of DNA via inhibiting the hexose monophophaste pathway. Although both DHEA and vitamin E effectively reduced preneoplastic foci in this model, they seemed to fimction in different mechanisms. In conclusion, DHEA may be used to reduce hepatocellular carcinoma growth by targeting NADPH synthesis, cell proliferation and anti-oxidant enzyme activities during tumor growth.