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Comparative Study
. 2004 Aug;57(8):867-71.
doi: 10.1136/jcp.2003.015784.

Microvessel density and clinicopathological characteristics in hepatitis C virus and hepatitis B virus related hepatocellular carcinoma

Affiliations
Comparative Study

Microvessel density and clinicopathological characteristics in hepatitis C virus and hepatitis B virus related hepatocellular carcinoma

L Messerini et al. J Clin Pathol. 2004 Aug.

Abstract

Aims: To compare intratumorous microvessel density (MVD) and clinicopathological features in two different groups of hepatocellular carcinoma (HCC), namely: hepatitis B virus (HBV) related HCC (B-HCC) and HCV related HCC (C-HCC).

Methods: Fifty consecutive cases each of B-HCC and of C-HCC were studied. Microvessel numbers were assessed by staining for the antigen CD34; in each case, three areas with the highest numbers of microvessels were counted in both the intratumorous and the surrounding non-tumorous tissue; the mean value represented the final MVD.

Results: Patients with B-HCC were significantly younger than those with C-HCC (mean age, 60.1 (SD, 4.1) v 66.4 (4.3) years); no significant differences were seen for sex or Child's class distribution. The tumour diameter was larger in B-HCCs than in C-HCCs (mean, 5.6 (SD, 1.8) v 3.8 (1.8) cm). Tumour microsatellite formation was significantly higher in C-HCCs (12 v 4 cases). No differences were found for histological subtype, degree of differentiation, tumour encapsulation, and vascular invasion. The mean MVD value was significantly higher in tumorous (mean, 54 (SD, 13.8) v 38 (8.9)) and in the surrounding non-tumorous liver tissue (mean, 15 (SD, 4.3) v 7 (3.1)) of C-HCCs.

Conclusions: C-HCCs present as smaller tumours in older patients, with a higher incidence of tumour microsatellite formation and higher MVD values both in the tumorous and the non-tumorous areas, suggesting a link between HCV infection, angiogenesis, and hepatocarcinogenesis.

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Figures

Figure 1
Figure 1
Area of hepatitis C virus related hepatocellular carcinoma showing high density of microvessels as assessed by anti-CD34 immunostaining. Original magnification, ×200.

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References

    1. Kim CM, Koike K, Saito I, et al. HBx gene of hepatitis B virus induces liver cancer in transgenic mice. Nature 1991;351:317–20. - PubMed
    1. Trevisani F, D’Intino PE, Caraceini P, et al. Etiologic factors and clinical presentation of hepatocellular carcinoma. Differences between cirrhotic and noncirrhotic Italian patients. Cancer 1995;75:2220–32. - PubMed
    1. Salvucci M, Lemoine A, Saffroy R, et al. Microsatellite instability in European hepatocellular carcinoma. Oncogene 1999;18:181–7. - PubMed
    1. Moriya K, Fujie H, Shintani Y, et al. The core protein of hepatitis C virus induces hepatocellular carcinoma in transgenic mice. Nat Med 1998;4:1065–7. - PubMed
    1. Dutta U, Kench J, Byth H, et al. Hepatocellular proliferation and development of hepatocellular carcinoma: a case control study in chronic hepatitis C. Hum Pathol 1998;29:1279–84. - PubMed

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