Vol 65, No 5 (2015)
Research paper (original)
Published online: 2015-11-18

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Significance of VEGF and VEGFR factors for clinical evaluation of hepatocellular carcinoma patients

Włodzimierz Otto, Maria Król, Ewa Wilczek, Janusz Sierdziński, Magdalena Feliksbrot-Bratosiewicz, Urszula Wilkowojska, Marek Krawczyk
DOI: 10.5603/NJO.2015.0078
Nowotwory. Journal of Oncology 2015;65(5):404-410.

Abstract

Aim. VEGF factor is the most active promotor of angiogenesis that supports HCC development. This study aimed to evaluate the relationships between expression of circulating and tumour VEGF and VEGFR factors, tumour pathomorphologic characteristics and the clinical stage of tumour development in HCC patients receiving surgery.

Material and methods. The study reports on 146 patients that were qualified for liver resection (Group A, N = 53), liver transplantation (Group B, N = 49), and palliation (Group C, N = 44), according to standard systems of clinical evaluation. The samples of 2 mL of venous blood was collected and immediately evaluated by flow cytometer for the endothelial progenitor cells enumeration (EPCs). The samples of 8 mL of venous blood was centrifuged for serum and the measurement of serum VEGF concentration by ELISA. The tissue samples of HCC were examined for tumour grading and architectural growth pattern, and for the expression of VGEF/VEGFR-2 by using anty-VEGF/anty-VEGFR antibodies for immunohistochemical staining. The factors expression was evaluated by morphometric analysis (Da­koCitomation). The data were analysed statistically; p-values < 0.05 were considered as significant.

Results. Patients differed by the tumour architectural growth pattern (chi-squared = 13.44, p < 0.001), and tumour microvascular invasion (chi-squared = 9.43, p < 0.01), but not by the stage of tumour differentiation. They presented with significant differences in the rate of circulating EPCs (chi-squared = 30.55, p < 0.001), and the level of tumour VEGF/VEGFR concentration (chi-squared = 9.67, p < 0.008). The tumour growth pattern, the maturity and microva­scular invasion were not influenced by the rate of circulating EPCs and serum/tumour VEGF/VEGFR concentration.

Conclusions. The rate of circulating EPCs and the level of VEGF/VEGFR tumour tissue concentration corresponded to the tumour potential of angiogenesis and indicated the stage of tumour development. Only the enumeration of circulating EPCs provide useful information prior the treatment decision denoting angiogenesis factors may be beneficial in the course of patients’ clinical evaluation.