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VEGFR-2 expression in malignant tumours of the canine mammary gland: a prospective survival study

Authors

  • A. Santos,

    1. Faculty of Veterinary Medicine, University Lusófona of Humanites and Technologies, Lisbon, Portugal
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  • C. Lopes,

    1. Department of Molecular Pathology and Immunology, Biomedical Sciences Institute of Abel Salazar (ICBAS), University of Porto, Porto, Portugal
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  • F. Gärtner,

    1. Department of Molecular Pathology and Immunology, Biomedical Sciences Institute of Abel Salazar (ICBAS), University of Porto, Porto, Portugal
    2. Institute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Porto, Portugal
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  • A. J. F. Matos

    Corresponding author
    1. Department of Veterinary Clinics, Biomedical Sciences Institute of Abel Salazar (ICBAS), University of Porto, Porto, Portugal
    2. Animal Science and Study Centre/Food and Agrarian Sciences and Technologies Institute (CECA/ICETA), University of Porto, Porto, Portugal
    • Correspondence address:

      A. J. F. Matos

      Department of Veterinary Clinics

      Biomedical Sciences Institute of Abel Salazar (ICBAS)

      Rua de Jorge Viterbo Ferreira no. 228

      4050-313 Porto, Portugal

      e-mail: ajmatos@icbas.up.pt

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Abstract

Vascular endothelial growth factor receptor-2 (VEGFR-2) is the main receptor activated by vascular endothelial growth factor -A (VEGF-A) to promote tumour angiogenesis. Its clinical prognostic value has not been studied in canine mammary tumours (CMTs). Dogs with mammary cancer were enrolled in a survival study and the immunohistochemical expressions of VEGFR-2 and VEGF-A were analysed and associated with clinicopathological features. VEGFR-2 expression was associated with VEGF immunoreactivity in cancer cells, supporting the presence of an autocrine loop that may be involved in CMTs growth and survival. VEGFR-2 was also expressed by endothelial cells from tumour vasculature and positively associated with stromal matrix metalloproteinase-9 (MMP-9), suggesting the existence of a link between endothelial cells activation and up-regulation of matrix degrading proteins. Carcinosarcomas exhibited high VEGFR-2 expression suggesting that it may be one of the activated molecular pathways in this aggressive histological type and that VEGFR-2 inhibitors may constitute a potential treatment to improve the prognosis of these patients. Both VEGF and VEGFR-2 immunoreactivities were independent of patients' overall survival (OS) and disease-free survival (DFS).

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