• 약학회지
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• 제56권6호
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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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• 제13권2호
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• pp.302-307
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• 1996

급속조영 전산화단층촬영에서 다른 간종괴와 감별이 어려운 간세포암의 경우 AFP 수치의 상승과 HBsAg 양성은 간세포암을 시사하는 유용한 지표이며 종괴의 모양과 조영양상을 같이 고려한다면 간종괴의 감별진단에 많은 도움을 주리라 생각한다.

• Nuclear Medicine and Molecular Imaging
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• 제42권sup1호
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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.

• 대한방사선기술학회지:방사선기술과학
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• 제20권2호
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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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• 제13권10호
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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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• 제6권4호
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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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• 제14권2호
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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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• 제9권2호
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• pp.351-358
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• 1992

저자들은 최근 6년간 영남대학교 의과대학 부속병원에서 외과적 절제술로 치료한 간세포암 37례를 대상으로 그 조직병리학적 소견 및 임상적 소견을 관찰하여 다음과 같은 결론을 얻었다. 1. 환자들의 연령분포는 31세-74세(평균 53.1세로 40대(29.7%), 50대(35.1%)에 호발하였고 남녀비는 3 : 1이었으며 간의 우엽에 많이 생겼고(23/37) 30례(88.2%)에서 혈청 알파형 태아단백이 증가되었다. 2. 종양을 구성하는 세포는 전형적 세포형이 75.7%로 가장 많았고 조직학적 성장양상은 주형이 13례(35.1%), 혼합형이 11례(29.7%)였다. 종양세포의 분화도는 중분화도 종양 18례(48.6%), 저분화 종양 16례(43.2%)였다. 3. 주위 간 조직의 변화로서 19 례(51.4%)에서 간경화증이 동반되었고 6례(16.2%)에서 전 경화증의 소견이 있었다. 4. 종양의 분화도를 간경화증의 유무와 비교했을 때 고분화 종양이 통계학적으로 유의하게 경화성 간에 생기는 경향을 보였으나(p<0.05). 분화도와 종양의 크기에 있어서는 유의한 상관성을 나타내지 않았다. 알파형 태아단백수치는 종양의 분화도 및 크기와 비교했을 때도 통계학적으로 유의한 관계는 없었다. 그러나 이 관계에 대해서는 더 자세한 검사를 동반하여 좀 더 광범위한 집단을 대상으로 연구하여 보완되어야 하리라 생각되었다.

• Asian Pacific Journal of Cancer Prevention
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• 제13권9호
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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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• 제15권23호
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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.