Expression of vascular endothelial growth factor in hepatocellular carcinoma and the surrounding liver: correlation with MR imaging and angiographically assisted CT.
We summarize and discuss our previous research results on the correlation between findings on magnetic resonance (MR) imaging and angiographically assisted computed tomography (CT) and the intensity of vascular endothelial growth factor (VEGF) expression in hepatocellular carcinoma (HCC) and in the surrounding nontumorous liver. MR images (n = 22), CT during arterial portography (n = 20), and CT hepatic arteriography (n = 17) were retrospectively correlated quantitatively and qualitatively with VEGF expression in HCCs and in the surrounding liver assessed by western blotting. HCC-to-liver contrast-to-noise ratio correlated with VEGF expression index (VEGF(IND)) values of HCCs inversely on opposed-phase, T1-weighted, spoiled gradient recalled-echo (GRE) images, directly on T2-weighted, fast spin-echo images, and marginally and inversely on gadolinium-enhanced hepatic arterial-phase GRE images. On T2-weighted fast spin-echo images, standard deviation ratio of HCCs correlated directly with VEGF(IND) values of HCCs. By CT hepatic arteriography, the contrast-enhancement index of HCCs showed a moderate inverse correlation with VEGF(IND) values of HCCs, and the contrast-enhancement index of the liver showed marginal, moderate direct correlation with VEGF(IND) values in the liver. Heterogeneities of HCCs on images correlated directly with VEGF(IND) values of HCCs on opposed-phase T1-weighted GRE images, T2-weighted fast spin-echo images, hepatic arterial-phase GRE images, equilibrium-phase GRE images, and CT hepatic arteriogram. Our results may reflect that MR signal intensity, hepatic arterial vascularity, and heterogeneity of HCCs on CT or MR images are closely related to the intensity of VEGF expression in HCC as upregulated by hyper- or hypoxia in HCCs. Although the real effects of our results on radiologic practice are debatable at this moment, we believe that our results may help future radiologic practice in conjunction with biomolecular or genetic treatment for HCCs.
Kanematsu
M
M
Department of Radiology, Gifu University School of Medicine, 1-1 Yanagido, Gifu, 501-1193, Japan. masa-gif@umin.ac.jp
Osada
S
S
Amaoka
N
N
Goshima
S
S
Kondo
H
H
Moriyama
N
N
D006528:Carcinoma, Hepatocellular / Q000378:metabolism* / Q000473:pathology; D006499:Hepatic Artery / Q000000981:diagnostic imaging; D006801:Humans; D007089:Image Enhancement; D008099:Liver / Q000378:metabolism*; D008113:Liver Neoplasms / Q000378:metabolism* / Q000473:pathology; D008279:Magnetic Resonance Imaging; D011172:Portography; D014057:Tomography, X-Ray Computed / Q000379:methods*; D015854:Up-Regulation / Q000502:physiology; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*
D042461:Vascular Endothelial Growth Factor A