Comparative analysis of microvessel density quantified through the immunohistochemistry expression of CD34 and CD105 in rectal cancer

Vol. 56 No. 2 Suppl., 2015
This supplement was not sponsored by Outside Organizations.


Dan Silviu Goldis, Mircea Florin Sferdian, Cristian Tarta, Lazar Octavian Fulger, Bogdan Dan Totolici, Carmen Neamtu

Endothelial cells are highlighted using a variety of endothelial markers. One of the best known markers is CD34, a surface antigen. The most used immunohistochemical marker for identification of activated endothelial cells is CD105. We chose to compare these two markers in order to evaluate angiogenesis of the rectal cancers by determining the microvessel density (MVD). Our study included 31 patients with rectal cancer between 2010-2014, who underwent rectal resection at Arad and Timisoara Counties Hospitals, Romania. We used MVD quantification by highlighting the tumor blood vessels with two different endothelial markers using the immunohistochemical protocols. The CD34 evaluation of MVD was 37 vessels/field/x200 peritumoral (PT), compared with normal rectal mucosa with 17 vessels/field/x200. Intra-tumoral (IT) MVD for CD34 positive vessels was between 7 and 120 vessels/field/x200. Average IT MVD CD105+ was 13.7 vessels/field/x200, the PT MVD CD105+ was 10 vessels/field/x200. Usually, IT MVD CD105 is smaller than PT MVD CD105, a pattern that was not respected in our study. There was a statistical significant correlation between IT MVD CD34 and PT MVD CD34 with p=0.008, also IT MVD CD34 and IT MVD CD105 with p=0.009, PT MVD CD34 with PT MVD CD105, p=0.001. PT MVD CD34 had a statistical significant correlation with T, p=0.004. IT MVD CD105 associated with T, p=0.004, and with N, p=0.004. The evaluation of both CD34-CD105 showed the role of angiogenesis in the cancer proliferation and local spread, the angiogenesis level being maintained high even in the advanced stages of the disease. There was observed a difference between the intratumoral and peritumoral MVD, the study of this difference possibly leading to a better assessment of prognosis and adjusted therapies in the future.

Corresponding author: Bogdan Dan Totolici, MD; e-mail:

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Amr K. Elfayomy, Shaima M. Almasry, Ghalia M. Attia, Fawzia A. Habib

This case-control study aimed to investigate the expression of natural killer cells (NKCs) and the integrated optical density (IOD) of vascular endothelial growth factor (VEGF) and to quantify microvascular density (MVD) in endometrial biopsies from women with endometrial hyperplasia (EH) relative to normal subjects. Histological data from four groups were analyzed. The study population included 30 women with simple EH without atypia, 25 patients with complex EH without atypia, 25 with complex EH with atypia and 25 healthy women with non-hyperplastic endometrium (control group). Paraffin sections were immunostained with antibodies against CD56, VEGF-A and CD34 using an Avidin-Biotin-Peroxidase technique. The evaluation of NKC density and IOD of VEGF expression and measurement of MVD were performed using light microscopy examination and image analysis techniques. Increased numbers of NKCs were documented in cases of complex EH with atypia compared with the other groups (p<0.001). The number of NKCs was lower in cases of hyperplasia without atypia compared with the controls, but the difference was not significant. The IOD of VEGF-A and MVD increased significantly with progression from the non-hyperplastic endometrium through the three groups of EH (p<0.001). We observed a significant correlation between the MVD and the IOD of VEGF-A in the studied groups (r=0.434; p<0.001). Additionally, NKCs density was correlated significantly with IOD of VEGF-A (r=0.661; p<0.001) and with the MVD (r=0.473; p<0.001). These results suggest that NKC-count, IOD of VEGF and endometrial MVD are all related to the histological changes of the endometrium and that endometrial hyperplasia exhibits distinct immunological backgrounds in the context of NKC infiltration and VEGF production.

Corresponding author: Shaima Mohamad Almasry, MD, PhD; e-mail:

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