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Clinical significance of vascular endothelial growth factor in hepatitis C related hepatocellular carcinoma in Egyptian patients

Authors Atta MM, Atta H, Gad M, Rashed L, Said E, Hassanien S, Kaseb A

Received 16 April 2015

Accepted for publication 7 October 2015

Published 14 June 2016 Volume 2016:3 Pages 19—24


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3

Editor who approved publication: Dr Ravi Murthy

Mohamed Magdi El-Sadek Ali Atta,1,2 Hazem Mahmoud Atta,3,4 Magdy Abdel-Mawgoud Gad,2 Laila Ahmad Rashed,4 Ebada M Said,2 Sharaf El-Sayed Ali Hassanien,2 Ahmed O Kaseb5

1Department of Medicine, Rabigh Faculty of Medicine, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia; 2Department of Hepatology, Gastroenterology and Infectious Diseases, Faculty of Medicine, Benha University, Benha, Egypt; 3Department of Clinical Biochemistry, Rabigh Faculty of Medicine, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia; 4Department of Medical Biochemistry and Molecular Biology, Faculty of Medicine, Cairo University, Cairo, Egypt; 5Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA

Background and aims: Several angiogenic factors are involved in the development and progression of hepatocellular carcinoma (HCC), a hypervascular tumor. Vascular endothelial growth factor (VEGF) is a primary driving force for angiogenesis, and its overexpression has been reported in HCC. However, the significance of plasma and tissue VEGF levels in HCC in Egyptian patients with chronic hepatitis C (CHC) infection is understudied. The aim of this study was to evaluate the role of VEGF (measured in plasma and liver tissue) in patients with hepatitis C virus-related HCC and to assess its significance in the diagnosis and prognosis of HCC.
Materials and methods: A total of 90 subjects were studied. Among 90 subjects, 60 with CHC were examined and were subdivided into two groups: 30 patients with CHC-related HCC (HCC group) and 30 patients with CHC without HCC (non-HCC group). Thirty apparently healthy subjects served as the control group. VEGF was estimated in plasma by enzyme-linked immunosorbent assay and its expression in liver tissue was evaluated by real-time polymerase chain reaction. VEGF expression level and its relationship to tumor parameters, patients' liver function profile, and patients' clinical parameters were also investigated.
Results: Plasma VEGF levels in the HCC group were significantly higher than those of the non-HCC group, and both groups had significantly higher plasma VEGF levels than did the control group. Liver tissue VEGF expression was significantly higher in the HCC group than in the non-HCC group and positively correlated with plasma VEGF in the HCC group. The plasma VEGF levels were positively correlated with patients' age, aspartate aminotransferase levels, serum alpha-fetoprotein levels, the presence of portal vein thrombosis, and the number of hepatic focal lesions in the HCC group. However, plasma VEGF levels were not significantly correlated with the Child-Pugh score, alanine aminotransferase levels, the size of focal lesions, and Okuda stage. Using both the VEGF and alpha-fetoprotein levels to detect HCC maximizes the sensitivity and specificity.
Conclusion: Plasma levels of VEGF may be a useful diagnostic and prognostic marker for HCC in patients who have been diagnosed with CHC.

VEGF, hepatocellular carcinoma, hepatitis C virus

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