• Asian Pacific Journal of Cancer Prevention
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• 제17권8호
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• pp.3881-3885
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• 2016

Background: MicroRNAs (miRNAs) have fundamental roles in tumorigenesis. MiR-675 is upregulated in hepatocellular carcinoma(HCC) cells. However, the roles of miR-675 in hepatocellular carcinogenesis are still not fully elucidated. In this study, we focus on investigating the effect and mechanism of miR-675 in proliferation of HCC cells. Materials and Methods: The cell proliferation was measured by MTT assays after transfection with miR-675 inhibitor and miR-675 mimics in HCC cells. The expression level of miR-675 was detected by real-time quantitative reverse transcription polymerase chain reaction. Protein expression of Cdc25A was measured by western blotting analysis. Results: In MTT assays, overexpression of miR-675 promoted the proliferation of HCC cells(P<0.05. at 48 hours, P<0.01. at 72 hours) compared with the miR-675mimics control group. Downexpression of miR-675 inhibited the proliferation of HCC cells(P<0.05. at 48 hours, P<0.01. at 72 hours) compared with the miR-675inhibitor control group. In western blotting analysis, the expression level of Cdc25A was significantly increased (p<0.05) after treatment with miR-675 mimics. The expression level of Cdc25A was significantly decreased (p<0.05) after treatment with miR-675 inhibitor. Conclusions: Our results indicate that miR-675 promotes the proliferation in human hepatocellular carcinoma cells by associating with Cdc25A signaling pathway.

• Asian Pacific Journal of Cancer Prevention
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• 제17권2호
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• pp.473-478
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• 2016

Hepatocellular cancer is a very common cause of cancer related deaths worldwide. Only 30-40% of patients present with early-stage disease open to curative treatments, such as resection or transplantation, while others can only undergo local therapies or palliative care. Various trans-arterial approaches have been used for treatment of hepatocellular carcinoma in patients who need a down-staging to liver transplantation, and who are not candidates for transplantation or radiofrequency ablation. Transarterial chemoembolization (TACE), transarterial embolization (TAE), drug-eluting beads, and radioembolization have been used for locoregional control, and have been shown to prolong the overall survival when compared with supportive care. In this review, we discuss patient selection, pre- and post-procedure imaging, techniques, safety, and clinical outcomes related to these therapies. Newer advances with future directions in various fields related to trans-arterial therapies are also discussed.

• Journal of Yeungnam Medical Science
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• 제17권1호
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• pp.66-74
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• 2000

1991년 3월부터 1995년 3월까지 영남대학교 의과대학 부속병원 내과에서 입원해서 혈청학적, 방사선학적 및 조직학적으로 간세포함으로 진단받은 156명의 환자 중 진단당시부터 폐전이를 동반한 12명(7.7%)을 제외한 144명의 환자를 대상으로 최소한 5개월 이상을 추적관찰하여 폐전이를 동반한 경우와 동반하지 않은 경우로 나누어 나이, 성별, Child-Pugh 점수, 간경변증 동반유무, AFP치 및 간동맥 색전술여부 등을 조사하여 그 차이점을 비교 분석하여 다음과 같은 결과를 얻었다. 추적관찰 중 폐전이를 동반한 경우가 26례(18.0%)였는데 간동맥 색전술을 시행한 경우가 26례 중 24례(92.3%), 시행하지않은 경우가 26례 중 2례(7.7%)였다. 폐전이를 동반하지 않은 118례 가운데 간동맥 색전술을 시행한 경우가 78례, 시행하지 않은 경우가 40례였다. 따라서 간동맥 색전술 시행후 폐전이를 동반한 경우가 102례 중 24례(23.5%), 간동맥 색전술을 시행하지 않고 폐전이를 동반한 경우가 42례 중 2례(4.7%)로 나타나서 간동맥 색전술 이후 폐전이가 더 빈번함을 알 수 있었다(p<0.01). 그러나, 나이, 성별, Child-Pugh 접수, 간경변증 동반유무 및 AFP치는 차이를 보이지 않았다. 결론적으로 간세포암에서 간동맥 색전술 이후 폐전이가 보다 많이 동반됨을 알 수 있었고 이에 관련되는 근본적인 설명과 그외 관련인자들에 대한 보다 많은 연구가 필요할 것으로 사료된다.

• Journal of Yeungnam Medical Science
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• 제30권2호
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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).

• 대한약침학회지
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• 제20권3호
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• pp.207-212
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• 2017

Objectives: Study of the mechanisms involved in cancer progression suggests that cyclooxygenase enzymes play an important role in the induction of inflammation, tumor formation, and metastasis of cancer cells. Thus, cyclooxygenase enzymes could be considered for cancer chemotherapy. Among these enzymes, cyclooxygenase 2 (COX-2) is associated with liver carcinogenesis. Various COX-2 inhibitors cause growth inhibition of human hepatocellular carcinoma cells, but many of them act in the COX-2 independent mechanism. Thus, the introduction of selective COX-2 inhibitors is necessary to achieve a clear result. The present study was aimed to determine the growth-inhibitory effects of new analogues of chalcone epoxide as selective COX-2 inhibitors on the human hepatocellular carcinoma (HepG2) cell line. Methods: Estimation of both cell growth and the amount of prostaglandin E2 (PGE2) production were used to study the effect of selective COX-2 inhibitors on the hepatocellular carcinoma cell. Cell growth determination has done by MTT assay in 24 h, 48 h and 72 h, and PGE2 production has estimated by using ELYSA kit in 48 h and 72 h. Results: The results showed growth inhibition of the HepG2 cell line in a concentration and time-dependent manner, as well as a reduction in the formation of PGE2 as a product of COX-2 activity. Among the compounds those analogues with methoxy and hydrogen group showed more inhibitory effect than others. Conclusion: The current in-vitro study indicates that the observed significant growth-inhibitory effect of chalcone-epoxide analogues on the HepG2 cell line may involve COX-dependent mechanisms and the PGE2 pathway parallel to the effect of celecoxib. It can be said that these analogues might be efficient compounds in chemotherapy of COX-2 dependent carcinoma specially preventing and treatment of hepatocellular carcinomas.

• Tuberculosis and Respiratory Diseases
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• 제51권4호
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• pp.386-389
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• 2001

An endobronchial metastasis is defined as a subsegmental or a more proximal central bronchial metastasis of a nonpulmonary neoplasm in the bronchoscopically visible range. However, the frequencies of endobronchial metastasis range from 2 to 50% of pulmonary metastases from extrathoracic neoplasms by a different definition of an endobronchial metastasis. Primary neoplasms of an endobronchial metastasis including breast cancer, colon cancer, renal cell carcinoma, and ovarian cancer are relatively common. However, an endobronchial metastasis arising from thyroid cancer, parotid gland tumor, bone tumor, bladder cancer, and stomach cancer has only rarely been reported in the literature. Here we report a case of an endobrochial metastases from a hepatocellular carcinoma.

• Journal of Yeungnam Medical Science
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• 제32권1호
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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.

• Asian Pacific Journal of Cancer Prevention
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• 제13권11호
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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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• 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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• 제14권6호
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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.