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Journal of Clinical Pathology 2005;58:1170-1174; doi:10.1136/jcp.2004.025536
Copyright © 2005 by the BMJ Publishing Group Ltd & Association of Clinical Pathologists.

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ORIGINAL ARTICLE

Tumour proliferation, angiogenesis, and ploidy status in human colon cancer

E Cristi1, G Perrone1, G Toscano2, A Verzì1, S Nori1, D Santini3, G Tonini3, A Vetrani4, A Fabiano2, C Rabitti1

1 Surgical Pathology, Campus Bio-Medico University, Via Emilio Longoni, Rome 83 00155, Italy
2 Surgical Pathology, Fatebenefratelli Hospital, Rome 00186, Italy
3 Oncology Unit, Campus Bio-Medico University, Rome 00155, Italy
4 Department of Anatomic Pathology and Cytopathology, University of Naples "Federico II", Naples 80131, Italy

Correspondence to:
Dr G Perrone
Campus Bio-Medico University, Via Emilio Longoni, 83 00155 Rome, Italy; g.perrone{at}unicampus.it Aims: Tumour angiogenesis is essential for carcinogenesis and facilitates the process of tumour development and metastasis. Vascular endothelial growth factor (VEGF) is a well characterised angiogenetic factor and is known to play a crucial role in new vessel development. To gain further insight into the effects of microvessel density and VEGF expression in colon cancer, their relation with tumour proliferation, ploidy status, and p53 expression was investigated in colon cancer.

Methods: Tissue samples of 50 archived colon cancers were analysed by immunohistochemistry for VEGF, p53, and the endothelial cell marker, von Willebrand factor (VWF), using specific antibodies. The same samples were re-cut for flow cytometric studies to obtain S phase fraction (SPF) and ploidy status.

Results: A positive significant correlation was found between SPF and angiogenesis. The median microvessel count in high SPF tumours was significantly higher than in low SPF ones. No association was found between VEGF expression and SPF. A positive correlation was found between ploidy status and p53 expression and microvessel count. Furthermore, a positive correlation was established between DNA ploidy, VEGF expression, and microvessel count.

Conclusion: This study provides evidence that in colon cancer, tumour growth may be stimulated by vascular supply, and the lack of a correlation between tumour cell proliferation and VEGF expression indicates that these two parameters may be regulated by separate mechanisms. Furthermore, the positive correlation between microvessel density, VEGF expression, and ploidy status provides more evidence that genetic alterations are involved in tumour angiogenesis.


Abbreviations: DI, DNA index; IQR, interquartile range; SPF, Sphase fraction; VEGF, vascular endothelial growth factor; VWF, von Willebrand factor

Keywords: angiogenesis; colon cancer; Sphase; ploidy; microvessel count







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