• YAKHAK HOEJI
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• v.56 no.6
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• pp.352-357
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• 2012

FGFR3 is a member of the fibroblast growth factor receptor family which interacts with fibroblast growth factors, setting in motion a cascade of downstream signals, ultimately influencing mitogenesis and differentiation. This particular family member binds acidic and basic fibroblast growth hormone and plays a role in bone development and maintenance. Accumulated evidence suggests that aberrant regulation of FGFR3 and genetic alterations are implicated in the development and progression of various cancers. Despite a high incidence of FGFR3 over-expression, no such investigation has been performed in hepatocellular carcinoma. Thus, we investigated genetic alterations of the FGFR3 gene in 73 cases of hepatocellular carcinoma by single-strand conformational polymorphism (SSCP) and sequencing. One silent mutation (A369A) was found in the extracellular domain of FGFR3, and one genetic alteration in the immunoglobulin-like III domain of FGFR3 appeared to be polymorphism. Taken together, we concluded that over-expression of FGFR3 in hepatocellular carcinoma is not associated with genetic alterations of FGFR3 gene, and we suggest that there could be another underlying mechanism of aberrant FGFR3 expression in 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.

• Nuclear Medicine and Molecular Imaging
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• v.42 no.sup1
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• pp.60-65
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• 2008

Hepatocellular carcinoma is the most common primary tumor in the liver. FDG PET has been applied for staging and treatment planning of hepatocellular carcinoma. It could reflect tumor prognosis because glucose metabolism assessed by FDG PET is known to have correlations with the differentiation and aggressiveness of the tumor. Although the ability of FDG PET to detect well-differentiated or low grade tumors and intra-hepatic lesions is not good, it is expected to playa major role in pre-surgical assessments for liver transplantation because it is useful in detecting extra-hepatic lesions and unexpected distant metastases with a better diagnostic performance than other conventional imaging modalities. Additionally, FDG PET has an advantage to screen other cancers through whole body scanning. As a new tracer for PET, Acetate demonstrates higher sensitivity and specificity to FDG in evaluating hepatocellular carcinoma. It thus seems that simultaneous use of Acetate PET with FDG PET could be helpful in diagnosis, especially detecting extra-hepatic metastases.

• 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.

• KSII Transactions on Internet and Information Systems (TIIS)
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• v.13 no.10
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• pp.5179-5196
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• 2019

To explore an effective non-invasion medical imaging diagnostics approach for hepatocellular carcinoma (HCC), we propose a method based on adopting the multiple technologies with the multi-parametric data fusion, transfer learning, and multi-scale deep feature extraction. Firstly, to make full use of complementary and enhancing the contribution of different modalities viz. multi-parametric MRI images in the lesion diagnosis, we propose a data-level fusion strategy. Secondly, based on the fusion data as the input, the multi-scale residual neural network with SPP (Spatial Pyramid Pooling) is utilized for the discriminative feature representation learning. Thirdly, to mitigate the impact of the lack of training samples, we do the pre-training of the proposed multi-scale residual neural network model on the natural image dataset and the fine-tuning with the chosen multi-parametric MRI images as complementary data. The comparative experiment results on the dataset from the clinical cases show that our proposed approach by employing the multiple strategies achieves the highest accuracy of 0.847±0.023 in the classification problem on the HCC differentiation. In the problem of discriminating the HCC lesion from the non-tumor area, we achieve a good performance with accuracy, sensitivity, specificity and AUC (area under the ROC curve) being 0.981±0.002, 0.981±0.002, 0.991±0.007 and 0.999±0.0008, respectively.

• Genomics & Informatics
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• v.6 no.4
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• pp.192-201
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• 2008

Erythropoietin-producing human hepatocellular carcinoma receptor B1 (EPHB1) is a member of the Eph family of receptor tyrosine kinases that mediate vascular system development. Eph receptor overexpression has been observed in various cancers and is related to the malignant transformation, metastasis, and differentiation of cancers, including hepatocellular carcinoma (HCC). Eph receptors regulate cell migration and attachment to the extracellular matrix by modulating integrin activity. EphrinB1, the ligand of EPHB1, has been shown to regulate HCC carcinogenesis. Here, we sought to determine whether EPHB1 polymorphisms are associated with hepatitis B virus (HBV)-infected liver diseases, including chronic liver disease (CLD) and HCC. We genotyped 26 EPHB1 single nucleotide polymorphisms (SNPs) in 399 Korean CLD, HCC, and LD (CLD+HCC) cases and seroconverted controls (HBV clearance, CLE) using the GoldenGate assay. Two SNPs (rs6793828 and rs11717042) and 1 haplotype that were composed of these SNPs were associated with an increased risk for CLD, HCC, and LD (CLD+HCC) compared with CLE. Haplotypes that could be associated with HBV-infected liver diseases by affecting downstream signaling were located in the Eph tyrosine kinase domain of EPHB1. Therefore, we suggest that EPHB1 SNPs, haplotypes, and diplotypes may be genetic markers for the progression of HBV-associated acute hepatitis to CLD and HCC.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.2
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• pp.747-752
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• 2013

Oncostatin M (OSM) is a multifunctional cellular regulator acting on a wide variety of cells, which has potential roles in the regulation of gene activation, cell survival, proliferation and differentiation. Previous studies have shown that OSM can induce morphological and/or functional differentiation and maturation of many tumor cells. However, the action of OSM on the induction of differentiation of human hepatocellular carcinoma (HCC) has not been reported. Here, we investigated the effects of different concentrations of OSM on human HCC cell line SMMC-7721 growth, proliferation, cell cycling, apoptosis and differentiation in vitro. Cell growth was determined via MTT assay, proliferation by cell cycle analysis, apoptosis by flow cytometry, morphology by transmission electronic microscopy, and cell function by detection of biochemical markers. Our results demonstrated that OSM strongly inhibited the growth of SMMC-7721 cells in a dose-dependent manner, associated with decreased clonogenicity. Cell cycle analysis revealed a decreased proportion of cells in S phase, with arrest at G0/G1. The apotosis rate was increased after OSM treatment compared to the control. These changes were associated with striking changes in cellular morphology, toward a more mature hepatic phenotype, accompanied by significant reduction of the expression of AFP and specific activity of ${\gamma}$-GT, with remarkable increase in secretion of albumin and ALP activity. Taken together, our findings indicate that OSM could induce the differentiation and reduce cell viability of SMMC-7721 cells, suggesting that differentiation therapy with OSM offers the opportunity for therapeutic intervention in HCC.

• Journal of Yeungnam Medical Science
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• v.9 no.2
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• pp.351-358
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• 1992

Hepatocellular carcinoma represents approximately 90% of the primary liver cancers. Recently, its incidence tends to be increased. Thirty seven cases from 1986 to 1991 diagnosed as hepatocellular carcinoma by resection were analized to know their histopathologic features and related clinical findings. The average age at the time of resection was 53.1 years, with frequent occurrence in third and fourth decades. Microscopically, the trabecular type was the most frequent growth pattern(35.1%) and classic hepatocyte-like cell type was the most frequent cell type(75.7%). The tumors are mainly moderately differentiated and frequently associated with liver cirrhosis. In comparison of cytologic differentiation with liver cirrhosis, there was a tendency for well-differentiated tumors to arise in cirrhotic livers more often than poorly differentiated tumors, and the tendency was statistically significant. But differentiation and tumor size did not show significant correlation. Also statistically significant correlation were not observed between the level of alpha-fetoprotein and tumor size, and between the level of alpha-fetoprotein and differentiation.

• 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.15 no.23
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• pp.10085-10089
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• 2015

Background: The insulin-like growth factor (IGF) system comprises a group of proteins that play key roles in regulating cell growth, differentiation, and apoptosis in a variety of cellular systems. The aim of this study was to investigate the role of insulin-like growth factor binding protein 3 (IGFBP3) in hepatocellular carcinoma. Materials and Methods: Expression of IGF2, IGFBP3, and PTEN was analyzed by qRT-PCR. Lentivirus vectors were used to overexpress IGFBP3 in hepatocellular carcinoma cell (HCC) lines. The effect of IGFBP3 on proliferation was investigated by MTT and colony formation assays. Results: Expression of IGF2, IGFBP3, and PTEN in several HCC cell lines was lower than in normal cell lines. After 5-aza-2'-deoxycytidine/trichostatin A treatment, significant demethylation of the promoter region of IGFBP3 was observed in HCC cells. Overexpression of IGFBP3 induced apoptosis and reduced colony formation in HUH7 cells. Conclusions: Expression of IGF2, IGFBP3, and PTEN in several HCC cell lines was lower than in normal cell lines. After 5-aza-2'-deoxycytidine/trichostatin A treatment, significant demethylation of the promoter region of IGFBP3 was observed in HCC cells. Overexpression of IGFBP3 induced apoptosis and reduced colony formation in HUH7 cells.