• Journal of Yeungnam Medical Science
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• v.32 no.1
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• pp.1-7
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• 2015

Over several decades, a hierarchical cancer stem cell (CSC) model has been established in development of solid cancers, including hepatocellular carcinoma(HCC). In terms of this concept, HCCs originate from liver CSCs. Clinically HCCs show a wide range of manifestations from slow growth to very aggressive metastasis. One of the reasons may be that liver CSCs originate from different cells. This review describes the basic concept of CSCs and the cellular origin of liver CSCs.

• Korean Journal of Radiology
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• v.1 no.4
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• pp.175-184
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• 2000

Although surgical resection remains the best option as potentially curative therapy for hepatocellular carcinoma, radiofrequency thermal ablation has begun to receive much attention as an effective minimally invasive technique for the local control of unresectable malignant hepatic tumors. Most recent radiofrequency devices equipped with a powerful generator and larger needle electrode permit larger thermal lesions, up to 5 cm in diameter, with a single ablation. In this article, the author reviews the technical developments and early clinical results obtained with radiofrequency ablation techniques.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.11
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• pp.5799-5804
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• 2012

Family with sequence similarity 189, member B (FAM189B), alias COTE1, a putative oncogene selected by microarray, for the first time was here found to be significantly up-regulated in hepatocellular carcinoma (HCC) specimens and HCC cell lines. mRNA expression of COTE1 in HCC samples and cell lines was detected by reverse transcription-polymerase chain reaction (RT-PCR) and real-time PCR, while protein expression of COTE1 in HCC tissues was assessed by immunohistochemistry. In addition, invasion of HCC cells was observed after overexpressing or silencing COTE1. In the total of 48 paired HCC specimens, compared with the adjacent non-cancer tissues, the expression of COTE1 was up-regulated in 31 (p<0.01). In HCC cell lines, COTE1 expression was significantly higher than in normal human adult liver (p<0.01). Overexpression of COTE1 enhanced HCC-derived LM6 and MHCC-L cellular invasion in vitro. In contrast, COTE1 knockdown via RNAi markedly suppressed these phenotypes, as documented in LM3 and MHCC-H HCC cells. Mechanistic analyses indicated that COTE1 could physically associate with WW domain oxidoreductase (WWOX), a tumor suppressor. COTE1 may be closely correlated with invasion of hepatocellular carcinoma (HCC) cells and thus may serve as an effective target for gene therapy.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.9
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• pp.4363-4368
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• 2012

The epidermal differentiation complex (EDC) contains a large number of gene products which are crucial for the maturation of the human epidermis and can contribute to skin diseases, even carcinogenesis. It is generally accepted that activation of oncogenes and/or inactivation of tumor suppressor genes play pivotal roles in the process of carcinogenesis. Here, NICE-3, a novel EDC gene, was found to be up-regulated in human hepatocellular carcinoma (HCC) by quantitative real-time RT-PCR. Furthermore, overexpression of exogenous NICE-3 by recombinant plasmids could significantly promote cell proliferation, colony formation and soft agar colony formation in Focus and WRL-68 HCC cell lines. Reversely, NICE-3 silencing by RNA interference could markedly inhibit these malignant phenotypes in YY-8103 and MHCC-97H cells. Moreover, cell cycle analysis of MHCC-97H transfected with siRNA by flow cytometry showed that NICE-3 knockdown may inhibit cell growth via arrest in G0/G1 phase and hindering entry of cells into S phase. All data of our findings indicate that NICE-3 may contribute to human hepatocellular carcinoma by promoting cell proliferation.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.6
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• pp.3819-3823
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• 2013

Background: Hepatocellular carcinoma (HCC) is a major cause of cancer mortality worldwide. The outcome of HCC depends mainly on its early diagnosis. To date, the performance of traditional biomarkers is unsatisfactory. Talins were firstly identified as cytoplasmic protein partners of integrins but Talin-1 appears to play a crucial role in cancer formation and progression. Our study was conducted to assess the diagnostic value of serum Talin-1 (TLN1) compared to the most feasible traditional biomarker alpha-fetoprotein (AFP) for the diagnosis of HCC. Methods: TLN1 was detected using enzyme linked immunosorbent assay (ELISA) in serum samples from 120 Egyptian subjects including 40 with HCC, 40 with liver cirrhosis (LC) and 40 healthy controls (HC). Results: ROC curve analysis was used to create a predictive model for TLN1 relative to AFP in HCC diagnosis. Serum levels of TLN1 in hepatocellular carcinoma patients were significantly higher compared to the other groups (p<0.0001). The diagnostic accuracy of TLN1 was higher than that of AFP regarding sensitivity, specificity, positive predictive value and negative predictive value in diagnosis of HCC. Conclusions: The present study showed for the first time that Talin-1 (TLN1) is a potential diagnostic marker for HCC, with a higher sensitivity and specificity compared to the traditional biomarker AFP.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.5
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• pp.2429-2434
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• 2016

Transforming growth factor-B1 ($TGF-{\beta}1$ )and its coreceptor endoglin (ENG) have been shown to contribute to hepatocellular tumor development and malignant progression. Our aim was to evaluate the serum expression levels of $ENG/TGF-{\beta}1$ mRNAs and risk of hepatocellular carcinoma in cirrhotic Egyptian patients. Our study included 77 subjects. Real time polymerase chain reaction was used to evaluate the expression level of ENG and $TGF-{\beta}1$mRNAs. The relative expression ratio of ENG mRNA was 0.82 (0.1 -3.2), 0.66 (0.15-5.3), 0.38(0.007-2.8) and 0.12 (0.00-0.22) and the relative expression ratio of $TGF-{\beta}1$mRNA was 1.4 (0.19 -6.2), 1.2 (0.22-4.3), 1.0 (0.15-4.4) and 0.6 (0.00-2.2) for cirrhotic HCC cirrhotic, HCC only and healthy control groups respectively. Increased ENG and $TGF-{\beta}1$ mRNA gene expression was correlated with TNM clinical stage. The expression ratio in TNM stage III-IV 1.1 (0.07-3.2), 1.55 (0.15-6.2) was statistically significantly higher than that in stage I-II 0.47 (0.007-2.8), 1.0 (0.31-4.4) (P<0.05). Our data suggested that increased ENG and $TGF-{\beta}1$ gene expression may participate in hepatocarcinogenesis and increased risk of HCC in individuals with cirrhosis. Early screening for evidence of cirrhosis and consideration of ENG and $TGF-{\beta}1$ as targets for therapy and treatment strategies are warranted.

• Journal of Chest Surgery
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• v.37 no.9
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• pp.809-812
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• 2004

Chest wall metastases from malignant tumors are rare and the majority of them are from adjacent structures such as the breast, lung, pleura, and mediastinum. Paticularly, chest wall metastases from distant organs are an even rarer event. There are few reports of chest wall metastasis with obscure or absent primary tumor. A 51-year-old man was diagnosed with metastatic hepatocellular carcinoma after an operation for a palpable mass on his left upper chest wall, At that time, there was no evidence of primary hepatocellular carcinoma in the liver after various examinations. We report a case of chest wall metastasis from unknown primary hepatocellular carcinoma.

• Journal of Yeungnam Medical Science
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• v.13 no.2
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• pp.302-307
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• 1996

Hepatic masses show different enhancing patterns in IV bolus computed tomography: Hepatocellular carcinoma shows high-attenuation in the early enhancing phase and low-attenuation in the late enhancing phase, hemangioma shows peripheral dot-like high-attenuation in the early enhancing phase and central high-attenuation in the late enhancing phase, and metastatic cancer and cholangiocelluar carcinoma show peripheral high-attenuation rim in the early enhancing phase and central portion gradulally high-attenuation in the late enhancing phase. but sometimes enhancing patterns of the hepatic masses are confuse. To evaluate the significance of the AFP level and HBsAg in differentiation of the hepatic masses, we retrospectively analyzed AFP level and HBsAg in 228 pathologically or radiologically confirmed hepatocellular carcinomas, and 137 pathologically nonhepatocellular cacinomas. The results were as follows : In hepatocellular carcinoma, AFP level above 20ng/ml was 77.8% and HBsAg positve was 72.6%. In nonhepatocellular carcinoma, AFP level above 20ng/ml was 3.7% and HBsAg positve was 16.1%. We concluded that AFP level and HBsAg are helpful to distinguish hepatocellular carcinoma from nonhepatocellular carcinoma, when IV bolus computed tomogram finding is uncertain.

• Journal of Yeungnam Medical Science
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• v.30 no.2
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• pp.152-155
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• 2013

Orbital metastasis from hepatocellular carcinoma is very rare, with only 14 biopsy-proven cases from hepa tocellular carcinoma cases reported in English literature and three cases reported in Korea. Common symptoms of orbital metastasis are proptosis, visual loss, ocular pain and oculomotor dysfunction. For its precise diagnosis, we can perform fine needle aspiration biopsy, orbit CT or MRI, and ultrasonography. Radiotherapy is the mainstay in the treatment of orbital metastasis. In addition, chemotherapy, hormonal therapy and surgical intervention can play a role in the treatment of orbital metastasis according to the primary cancer and symptoms. However, the prognosis of orbital metastasis is poor. We report herein a rare case of a patient with orbital metastasis from hepatocellular carcinoma, which was treated with various modalities that included resection, and who had good clinical and radiological responses to radiation therapy and sorafenib (Nexavar, Bayer HealthCare).

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.3
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• pp.237-243
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• 2016

Oleanolic acid (OA) has a wide variety of bioactivities such as hepatoprotective, anti-inflammatory and anti-cancer activity and is used for medicinal purposes in many Asian countries. In the present study, the effect of OA on induction of autophagy in human hepatocellular carcinoma HepG2 and SMC7721 cells and the related mechanisms were investigated. MTT assay showed that OA significantly inhibited HepG2 and SMC7721 cells growth. OA treatment enhanced formation of autophagic vacuoles as revealed by monodansylcadaverine (MDC) staining. At the same time, increasing punctuate distribution of microtubule-associated protein 1 light chain 3 (LC3) and an increasing ratio of LC3-II to LC3-I were also triggered by OA incubation. In addition, OA-induced cell death was significantly inhibited by autophagy inhibitors 3-methyladenine (3-MA) and chloroquine (CQ) pretreatment. And we found out that OA can suppress the PI3K/Akt1/mTOR signaling pathway. Furthermore, our data suggested that OA-triggered autophagy was ROS-dependent as demonstrated by elevated cellular ROS levels by OA treatment. When ROS was cleared by N-acetylcysteine (NAC), OA-induced LC3-II convertsion and cell death were all reversed. Taken together, our results suggest that OA exerts anticancer effect via autophagic cell death in hepatocellular carcinoma.