scholarly journals Methylene tetrahydrofolate reductase (MTHFR) and vascular endothelial growth factor (VEGF) polymorphisms in Brazilian patients with Hepatitis C virus (HCV)-related hepatocellular carcinoma (HCC)

Clinics ◽  
2021 ◽  
Vol 76 ◽  
Author(s):  
Sylene C.R. Carvalho ◽  
Luydson R.S. Vasconcelos ◽  
Leonardo da Fonseca ◽  
Rodrigo F. Carmo ◽  
Michele T. Tomitão ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Vascular Endothelial Growth Factor ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Growth Factor ◽  
Vascular Endothelial ◽  
Methylene Tetrahydrofolate Reductase ◽  
Methylene Tetrahydrofolate ◽  
Endothelial Growth Factor ◽  
Vegf Polymorphisms

scholarly journals Effect of directly acting anti-viral agents on immunological imprints in chronic HCV-4a patients: interleukin-10 and vascular endothelial growth factor genes expression level

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Iman S. Naga ◽  
Amel Abdel Fattah Kamel ◽  
Said Ahmed Ooda ◽  
Hadeer Muhammad Fath Elbab ◽  
Rania Mohamed El-Sharkawy
Keyword(s):  
Gene Expression ◽  
Vascular Endothelial Growth Factor ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Growth Factor ◽  
Angiogenic Factor ◽  
Vascular Endothelial ◽  
Wide Range ◽  
Chronic Hcv ◽  
Endothelial Growth Factor

Abstract Background Hepatitis C virus infection is a global health challenge with Egypt being one of the highly affected countries. IL-10 has been suggested as a suitable marker to assess necroinflammation and to monitor the progression of liver damage. Vascular endothelial growth factor (VEGF) is a potent angiogenic factor playing a central role in many physiological as well as pathological processes. Several factors can be predictive of the response to treatment and achievement of SVR; some of which are host-related, and others are virus-related. The gene expression of IL-10 and VEGF have multiple effects for treatment response. The aim of the present work was to study the effect of treatment with directly acting agents (DAA) on the expression of VEGF and IL-10 genes in chronic hepatitis C virus-infected Egyptian genotype-4a patients. Twenty-five HCV subjects where evaluated for IL-10 and VEGF gene expression before and after treatment with DAA. Results IL-10 expression was downregulated in 92% of the cases. VEGF expression was heterogeneous showing spreading of values along a wide range with 64% of the cases being downregulated. Conclusion DAAs do not completely reverse the immunological imprints established upon chronic HCV infection.

scholarly journals Vascular endothelial growth factor in relation to the development of hepatocellular carcinoma in hepatitis C virus patients treated by direct-acting antivirals

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ahmed Mohamed ElGhandour ◽  
Essam Mohamed Bayoumy ◽  
Wesam Ahmed Ibrahim ◽  
Moataz Mohamed Sayed ◽  
Ashraf Bekheet Salama ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Vascular Endothelial Growth Factor ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Vascular Endothelial ◽  
Direct Acting Antivirals ◽  
Group I ◽  
End Of Treatment ◽  
Direct Acting ◽  
Endothelial Growth Factor

Abstract Background Hepatocellular carcinoma (HCC) comprises 5.6% of all cancers worldwide representing the sixth most common cancer. It is also the fourth most common cause of cancer-related mortality. Angiogenesis is a main factor in the development of HCC. Vascular endothelial growth factor (VEGF) is considered as the force for physiological and pathological angiogenesis, and overexpression of VEGF is prominent in HCC. We aimed to study the effect of direct-acting antivirals (DAAs) on VEGF considered as the key regulator of angiogenesis in HCC. This cross-sectional study involved fifty patients who were divided into two groups: group I—twenty-five chronic hepatitis C virus (HCV) patients as (cases) subjected to treatment with direct-acting antiviral drugs for 3 months; group II—twenty-five chronic HCV patients developed HCC as (controls). Serum VEGF level was measured in of group I at baseline, at end of treatment, and 3 months after the end of treatment by sofosbuvir 400 mg plus daclatasvir 60 mg for 3 months in the HCV patient group, also VEGF was assessed in group II with HCC. Results Serum VEGF was high in both groups, but it was higher in the HCC group with a statistically significant difference (p < 0.001), also serum VEGF in the HCV group decreased after 3 months at the end of DAA treatment from 209.5 ± 137.6 to 44.1 (31.8–55.3) mg/ml, and all patients who received DAAs achieved sustained virologic response (SVR). Conclusion We found that change in serum VEGF in HCV patients treated with DAAs in this study cannot explain the risk of HCC after treatment by DAAs.

scholarly journals Hepatitis C Virus Stabilizes Hypoxia-Inducible Factor 1α and Stimulates the Synthesis of Vascular Endothelial Growth Factor

2007 ◽  
Vol 81 (19) ◽  
pp. 10249-10257 ◽  
Author(s):  
Md Nasimuzzaman ◽  
Gulam Waris ◽  
David Mikolon ◽  
Dwayne G. Stupack ◽  
Aleem Siddiqui
Keyword(s):  
Gene Expression ◽  
Vascular Endothelial Growth Factor ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Growth Factor ◽  
Hypoxia Inducible Factor ◽  
Hcv Infection ◽  
Vascular Endothelial ◽  
Hypoxia Inducible Factor 1Α ◽  
Endothelial Growth Factor

ABSTRACT Hepatitis C virus (HCV) infection is one of the major causes of chronic hepatitis, liver cirrhosis, which subsequently leads to hepatocellular carcinoma (HCC). The overexpression of the angiogenic factors has been demonstrated in HCC. In this study, we investigated the potential of HCV gene expression in inducing angiogenesis. Our results show that HCV infection leads to the stabilization of hypoxia-inducible factor 1α (HIF-1α). We further show that this stabilization was mediated via oxidative stress induced by HCV gene expression. The activation of NF-κB, STAT-3, PI3-K/AkT, and p42/44 mitogen-activated protein kinase was necessary for HIF-1α stabilization. HIF-1α induction in turn led to the stimulation of vascular endothelial growth factor. By using the chick chorioallantoic membrane assay, we show that HCV-infected cells released angiogenic cytokines, leading to neovascularization in vivo. These results indicate the potential of HCV gene expression in angiogenesis.

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