Elevated Vascular Endothelial Growth Factor (VEGF) levels in the blood serum of dogs with malignant neoplasms of the oral cavity

Abstract

Angiogenesis plays an essential role in the development of a neoplastic tumour by conditioning both its growth and the formation of metastases. The induction of blood vessel growth occurs under the influence of proangiogenic factors, among which Vascular Endothelial Growth Factor (VEGF) seems to be the most important. The aim of this research was to study the level of VEGF measured by ELISA in the serum of dogs with neoplasms of the oral cavity. The study material comprised samples of neoplastic tissue from 17 operated dogs and the serum of the examined animals as well as of dogs from the control group. The tissue samples were taken from dogs of different breeds, aged 6–14 years. The tumour type was determined in accordance with the applicable WHO classification. Blood samples taken from sick dogs and from animals of the control group were centrifuged, and immunoenzymatic labelling of VEGF was performed in the obtained serum using ELISA and R&D system reagents (Quantikine Canine VEGF). All stages of VEGF labelling were performed according to the recommendation of the test manufacturer. The median of VEGF in the serum of the dogs with neoplasms of the oral cavity was 40.64 pg/mL. The lowest value of 14.26 pg/mL was observed in the case of fibrosarcoma, and the highest value of 99.19 pg/mL in the case of squamous cell carcinoma. The VEGF median in the control group amounted to 11.14 pg/mL whereas the VEGF value in the groups of animals diagnosed with benign tumours ranged between 2.30 and 19.74 pg/mL. Elevated VEGF in the blood serum, in comparison with the benign tumour group and the control group, was observed in all examined neoplasms of the oral cavity. It was suggested that overexpression of VEGF can have a prognostic value and is useful in the early detection of neoplasms.

Immunohistochemical expression of vascular endothelial growth factor in canine oral squamous cell carcinomas

“…This was indicated by a high number of VEGF-positive cells associated with the accumulation and consequent loss of cytoplasmic polarization of VEGF granules in less differentiated tumours. These results are in agreement with those of Sobczyńska-Rak et al (15), who studied the level of VEGF in the serum of dogs with OSCC by ELISA, and identified an elevated presence of VEGF in the blood serum of all examined malignant tumours compared with the benign tumours and control tissues, confirming a significant role of VEGF in the disease progression of canine oral tumours. Upregulation of VEGF, which is particularly found in moderately or poorly differentiated tumours, may be induced mainly by HIF-1α under the hypoxic conditions present in the necrotic compartments of tumours (40).…”

“…Angiogenic switch is determined by the net balance of natural inhibitors and angiogenic stimulators, out of which vascular endothelial growth factor (VEGF), also termed VEGF-A, is considered to be the major stimulator responsible for tumour angiogenesis (6,7). Although extensive data are available on the role of VEGF and VEGF receptors in the biology and development of a variety of human and animal invasive malignant tumours (8)(9)(10)(11)(12)(13)(14), little information exists concerning oral canine tumours (15).…”

Treatment of oral squamous cell carcinoma in a horse by surgical debulking followed by metronomic chemotherapy

“…Recently, significantly higher values of VEGF have been reported in dogs with oral neoplasms and among them, SCCs showed the highest levels (Sobczyńska‐Rak et al . ). There do not appear to be any studies evaluating serum VEGF values in control or diseased horses.…”

Oncolytic Viruses for Canine Cancer Treatment

“…GLV-5b451 derived from the LIVP 6.1.1 strain contains the GLAF-1 gene encoding for a single chain of anti-canine VEGF antibody [ 142 ]. In dogs, VEGF overexpression was correlated with tumor malignancy and poor prognosis [ 143 , 163 , 164 , 165 , 166 ]. In in vitro studies, GLV-5b451 effectively infected, replicated, and killed canine cells from mammary carcinoma, mammary adenoma, prostatic carcinoma, and STS, inducing at least 60% cell death.…”