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RISS 인기검색어
- 검색키워드
- 저자 : ( Hoda El Aggan ) (검색결과 3 건)
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( Hoda El Aggan ),( Sabah Mahmoud ),( Nevine El Deeb ),( Amany Elyamany ),( Manar Attia ) 대한간학회 2017 춘·추계 학술대회 (KASL) Vol.2017 No.1
Aims: Hepatitis C virus (HCV) is a major risk of hepatocellular carcinoma (HCC), however, the molecular mechanism of HCV-related hepatocarcinogenesis is still unclear. The polycistronic microRNA (miR)-17~92 cluster, designated also as “OncomiR-1”, plays a role in tumorigenesis and is transactivated by c-MYC oncogene. The cluster negatively regulates phosphatase and tensin homolog (PTEN) and activates nuclear factor-kappa B (NF-κB). The present study was designed to evaluate plasma levels of miR-17 host gene (MIR17HG) protein, encoded by miR-17~92 cluster host gene, in patients with HCV-related HCC in relation to tumor c-MYC, PTEN and NF-κB expression. Methods: Forty five patients with chronic HCV infection [18 patients with chronic hepatitis C (CHC), 12 patients with cirrhosis and 18 patients with HCC] and 15 healthy subjects were enrolled in the study. The HCC stage was determined according to the Barcelona Clinic Liver Cancer (BCLC) staging system and Cancer of the Liver Italian Program (CLIP). Quantitative measurement of plasma MIR17HG protein levels was performed using an enzyme-linked immunosorbant assay kit. The HCC histologic grade was assessed according to Edmonson and Steiner scoring system. Immunohistochemical staining of liver specimens was done using anti-human antibodies against c-MYC, PTEN and NF-kB and was scored semiquatitatively. Results: Plasma MIR17HG protein levels showed significant increases in CHC and cirrhotic patients with and without HCC compared with healthy subjects and in patients with HCC compared with those without HCC (P < 0.001). By plotting ROC curve, the sensitivity and specificity of plasma MIR17HG protein levels in detecting HCC were 100% and 93.3% respectively at a cut-off level of 257.25 pg/ml [AUC = 0.996]. The HCC tissues showed a significant increase in c-MYC, and NF-kB expression and a significant decrease in PTEN expression compared with CHC, cirrhotic and surrounding non-neoplastic liver tissues (P < 0.05). The plasma MIR17HG protein levels were positively correlated with tumor size (P = 0.001), stage (P = 0.001) and HCC histological grade (P = 0.002) and c-MYC (P = 0.001) and NF-kB expression (P = 0.015) and were inversely correlated with PTEN expression (P = 0.001). Conclusions: Activation of miR-17~92 cluster induced by c-MYC may play an important role in the development and progression of HCV-related HCC, possibly, through inhibition of PTEN and activation of NF-kB and could provide a potential therapeutic target for HCC. Circulating MIR17HG protein could be a useful non-invasive biomarker for the detection of HCC in chronic HCV infection.
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( Hoda El Aggan ),( Nahla Farahat ),( Bassma Sabaa ),( Amany Elyamany ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1
Background: Bone marrow-derived stem cells (BMSCs) are pluripotent cells that can be mobilized into circulation and recruited to sites of inflammation to promote tissue repair. The present work was designed to study circulating hematopoietic stem cells (HSCs) and mesenchymal stem cells (MSCs) and serum stem cell factor (SCF) levels in patients with chronic hepatitis C (CHC) in relation to hepatic progenitor cells (HPCs) and hepatocyte proliferation. Methods: Thirty patients with CHC and 15 healthy subjects were included in the study. The HSCs and MSCs in blood samples were identified as CD34+CD45+CD117+ and CD34-CD45-CD106+ cells respectively using flow cytometry. Serum SCF levels were measured using enzyme linked immunosorbant assay kit. Liver biopsies were examined to assess METAVIR histological activity grade and fibrosis stage. Immunohistochemical staining was done using monoclonal antibodies against cytokeratin (CK)7 for HPCs, Ki-67 as proliferation marker and alpha-smooth muscle actin for activated hepatic stellate cells (HpSCs). Results: Patients with CHC showed significant increases in the percentages of HSCs and MSCs in peripheral blood and serum SCF levels compared with healthy subjects (P < 0.05). Numerous CK7+ HPCs were detected mostly lining bile ductules in the portal tracts. Hepatocyte proliferative activity was directly correlated with HPC expansion. The percentages of circulating HSCs and MSCs showed positive correlation with serum SCF levels and inverse correlations with HPC expansion, hepatocyte proliferative activity, histological activity grade, fibrosis stage and intensity of activated HpSCs (P < 0.05). Conclusions: CHC is associated with mobilization of BMSCs into the circulation in parallel with an increased SCF production, particularly when HPC activation and hepatocyte proliferative activity are impaired. Although mobilized BMSCs are not sufficient for hepatic repopulation, they may play a role in limiting HCV-induced liver damage.
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