• Asian Pacific Journal of Cancer Prevention
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• 제15권6호
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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.

• BMB Reports
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• 제51권12호
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• pp.630-635
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• 2018

C-X-C motif chemokine ligand 2 (CXCL2) is a small secreted protein that exhibits a structure similar to the proangiogenic subgroup of the CXC chemokine family. Recently, accumulating evidence suggests that chemokines play a pivotal role in cancer progression and carcinogenesis. We examined the expression levels of 7 types of $ELR^+$ CXCLs messenger RNA (mRNA) in 264 clinical samples. We found that CXCL2 expression was stably down-regulated in 94% of hepatocellular carcinoma (HCC) specimens compared with paired adjacent normal liver tissues and some HCC cell lines. Moreover, CXCL2 overexpression profoundly attenuated HCC cell proliferation and growth and induced apoptosis in vitro. In animal studies, we found that overexpressing CXCL2 by lentivirus also apparently inhibited the size and weight of subcutaneous tumours in nude mice. Furthermore, we demonstrated that CXCL2 induced HCC cell apoptosis via both nuclear and mitochondrial apoptosis pathways. Our results indicate that CXCL2 negatively regulates the cell cycle in HCC cells via the ERK1/2 signalling pathway. These results provide new insights into HCC and may ultimately lead to the discovery of innovative therapeutic approaches of HCC.

• Korean Journal of Radiology
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• 제23권4호
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• pp.491-491
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• 2022

• Clinical Endoscopy
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• 제56권6호
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• pp.802-811
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• 2023

Background/Aims: Covered self-expandable metallic stents (cSEMS) have become popular for endoscopic ultrasound-guided hepaticogastrostomy with transmural stenting (EUS-HGS). We compared the time to recurrent biliary obstruction (TRBO), complications, and reintervention rates between EUS-HGS using plastic stent (PS) and cSEMS in patients with unresectable malignancies at multicenter institutions in Japan. Methods: Patients with unresectable malignant biliary obstruction who underwent EUS-HGS between April 2015 and July 2020 at any of the six participating facilities were enrolled. Primary endpoint: TRBO; secondary endpoints: rate of complications other than recurrent biliary obstruction and technical success rate of reintervention were evaluated. Results: PS and cSEMS were used for EUS-HGS in 109 and 43 patients, respectively. The TRBO was significantly longer in the cSEMS group than in the PS group (646 vs. 202 days). Multivariate analysis identified two independent factors associated with a favorable TRBO: combined EUS-guided antegrade stenting with EUS-HGS and the use of cSEMS. No significant difference was observed in the rate of complications other than recurrent biliary obstruction between the two groups. The technical success rate of reintervention was 85.7% for PS and 100% for cSEMS (p=0.309). Conclusions: cSEMS might be a better option for EUS-HGS in patients with unresectable malignancies, given the longer TRBO.

• 대한핵의학회지
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• 제29권3호
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• pp.313-318
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• 1995

통상적인 Tc-99m DISIDA 스캔도중 우연하게 위장역류가 발견되는 경우가 있는데 이의 임상적 의의를 알아보고자 1991년 12월부터 1995년 6월까지 충남대학교병원에서 통상적인 Tc-99m DISIDA 스캔을 시행한 1,553명의 환자들중 우연하게 위장부위로 방사능역류를 보인 36명의 환자들을 대상으로 후향적으로 이러한 환자들의 검사당시 임상상을 알아보았다. 1) 연구기간동안 시행한 Tc-99m DISIDA 스캔상 위장 역류는 2.3%에서 발견되었다. 2) 위장역류를 보인 대상환자중 위장관 및 담도계에 수술을 받은 과거 병력이 있는 경우는 19% 이었으며 역류가 없었던 환자들에서보다 의미있게 많았다(p<0.01). 3) 역류가 발견되는 시점은 Tc-99m DISIDA 정맥주사 후 30분에서 60분 사이가 50%로 가장 많았으며 60분에서 90분 사이가 23% 이었다. 4) 위장 역류를 보인 환자중 87%에서 위내시경 검사상 위염, 위궤양, 십이지장궤양, 위암등의 병변을 보였다. 이상에서 저자들은 Tc-99m DISIDA 스캔상 위-십이지장 역류를 보이는 경우는 역류가 없는 경우보다 위장관이나 담도계에 수술을 받은 병력이 있는 경우가 의미있게 많았으며 이들 중 상당수가 위-십이지장에 질환을 가지고 있음을 알 수 있었다.

• Asian Pacific Journal of Cancer Prevention
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• 제13권9호
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• pp.4627-4630
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• 2012

Purpose: Methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms have been reported to be associated with pancreatic cancer, but the published studies have yielded inconsistent results. This study assessed the relationship between MTHFR gene polymorphisms and the risk for pancreatic cancer using a meta-analysis approach. Methods:A search of Google scholar, PubMed, Cochrane Library and CNKI databases before April 2012 was performed, and then associations of the MTHFR polymorphisms with pancreatic cancer risk were summarized. The association was assessed by odds ratios (ORs) with 95% confidence intervals (CIs). Publication bias was also calculated. Results: Four relative studies on MTHFR gene polymorphisms (C667T and A1298C) were included in this meta-analysis. Overall, C667T (TT vs. CC:OR=1.61,95%CI=0.78-3.34; TT vs. CT: OR=1.41,95%CI=0.88-2.25; Dominant model:OR=0.68,95%CI=0.40-1.17; Recessive model: OR=0.82,95%CI=0.52-1.30) and A1298C (CC vs. AA:OR=1.01,95%CI=0.47-2.17; CC vs. AC: OR=0.99,95%CI=0.46-2.14; Dominant model:OR=1.01, 95%CI=0.47-2.20; Recessive model: OR=1.01,95%CI=0.80-1.26) did not increase pancreatic cancer risk. Conclusions: This meta-analysis indicated that MTHFR polymorphisms (C667T and A1298C) are not associated with pancreatic cancer risk.

• Asian Pacific Journal of Cancer Prevention
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• 제13권12호
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• pp.6349-6355
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• 2012

Previous studies showed that Math1 homologous to human Hath1 can cause mouse goblet cells to differentiate. In this context it is important that the majority of colon cancers have few goblet cells. In the present study, the potential role of Hath1 in colon carcinogenesis was investigated. Sections of paraffin-embedded tissues were used to investigate the goblet cell population of normal colon mucosa, mucosa adjacent colon cancer and colon cancer samples from 48 patients. Hath1 and Muc2 expression in these samples were tested by immunohistochemistry, quantitative real-time reverse transcription -PCR and Western blotting. After the recombinant plasmid, pcDNA3.1(+)-Hath1 had been transfected into HT29 colon cancer cells, three clones were selected randomly to test the levels of Hath1 mRNA, Muc2 mRNA, Hath1, Muc2, cyclin D1 and p27 by quantitative real-time reverse transcription-PCR and Western blotting. Moreover, the proliferative ability of HT29 cells introduced with Hath1 was assessed by means of colony formation assay and xenografting. Expression of Hath1, Muc2, cyclin D1 and p27 in the xenograft tumors was also detected by Western blotting. No goblet cells were to be found in colon cancer and levels of Hath1 mRNA and Hath1, Muc2 mRNA and Muc2 were significantly down-regulated. Hath1 could decrease cyclin D1, increase p27 and Muc2 in HT29 cells and inhibit their proliferation. Hath1 may be an anti-oncogene in colon carcinogenesis.

• Asian Pacific Journal of Cancer Prevention
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• 제16권2호
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• pp.661-666
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• 2015

Background: Postoperative carbohydrate antigen 19-9 (CA19-9) is an independent predictor of survival for pancreatic ductal adenocarcinoma (PDAC), and more powerful than preoperative CA19-9. However, making decisions just dependent on postoperative CA19-9 may result in necessary treatments not being performed. Materials and Methods: A total of 178 patients with resected PDAC were eligible for this retrospective study, classified into two corresponding subgroups according to postoperative CA19-9. Prognostic significance of all clinicopathologic factors was evaluated by univariate and multivariate analyses. Results: Postoperative CA19-9, preoperative CA125 and lymph node status were independent predictors. Better predictive performances for overall survival (OS) and recurrence-free survival (RFS) were achieved by postoperative CA19-9 compared to preoperative CA125 and lymph node status. Particularly, preoperative CA125 was associated with poor OS (p<0.001 for the normalized CA19-9 patients, p=0.012 for the elevated) and RFS (p=0.005 for the normalized, p=0.004 for the elevated). Moreover, preoperative CA125 levels related with survival in double-negative patients. Conclusions: Normalization of CA19-9 is not tantamount to be cured. Preoperative CA125 is a critical predictor for PDAC patients, especially in double-negative patients.

• 대한자기공명의과학회:학술대회논문집
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• 대한자기공명의과학회 2006년도 제11차 학술대회
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• pp.56-56
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• 2006

• 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.