Serum levels of vascular endothelial growth factor in patients with head and neck cancer

Abstract

Angiogenesis is now considered to be crucial for tumor growth and metastasis. In several tumors, microvascular density has been shown to be correlated with metastasis and aggressiveness. Vascular endothelial growth factor (VEGF) is a secreted endothelial cell-specific mitogen, which is induced by hypoxia and is angiogenic in vivo. VEGF has been identified in a wide variety of malignancies including head and neck squamous cell carcinomas (HNSCC). We investigated the circulating level of VEGF in sera from patients with various head and neck squamous cell carcinomas (n = 71) as well as from healthy normal controls (n = 47). Serum VEGF concentrations were determined as serum immunoreactivity by using a quantitative sandwich enzyme immunoassay technique. For statistical analysis, the Wilcoxon 2-sample test and Kruskal-Wallis test were performed. The majority of the patients with HNSCC were found to have high concentrations of serum VEGE The levels of VEGF in the sera of patients with cancer ranged from below the detection limit to 937.1 pg/ml (mean, 144.5 pg/ml). In contrast, the VEGF serum levels in 47 healthy individuals ranged from below the detection limit to 168.1 pg/ml (mean, 32.7 pg/ml), VEGF serum concentration being significantly higher in HNSCC patients (P = < 0.001). These findings indicate that a positive angiogenesis regulator such as VEGF might function as an endocrine growth factor, particularly for solid HNSCC tumors and may be a useful marker for clinical monitoring.

Serum Vascular Endothelial Growth Factor-A (VEGF-A) as a Biomarker in Squamous Cell Carcinoma of Head and Neck Patients Undergoing Chemoradiotherapy

“…In our study, serum VEGF-A level was found to be significantly higher (p=0.001) in SCCHN patients as compared to healthy controls. A similar study previously done by Riedel et al (2000), De Schutter et al (2005) and Hong et al (2009) found that serum VEGF-A level is elevated in head and neck cancer patients as compared to healthy controls.…”

Excessive tumor-elaborated VEGF and its neutralization define a lethal paraneoplastic syndrome

“…Others have also described the development of peliosis in the setting of known malignancies, including renal cell carcinoma, pancreatic cancer, and Wilm's tumor (28)(29)(30). With respect to VEGF as a mediator of this particular paraneoplastic syndrome, it has been well established that many human cancers secrete VEGF, and that in some instances, elevated levels of VEGF can be detected in sera of patients with advanced malignancy (31)(32)(33)(34). Moreover, there seems to be a correlation between serum VEGF levels and prognosis (33,(35)(36)(37).…”

Chemotherapeutic alteration of VEGF-/PDGF- and PDGF-Rα/β expression by imatinib in HPV-transformed squamous cell carcinoma compared to HPV-negative HNSCC in vitro

“…One strategy in novel approaches to cancer therapy is the inhibition of angiogenesis of malignant tumors. Various studies detect the induced angiogenic response in vivo, and the correlation between high microvessel counts and recurrent or metastatic disease in HNSCC (51,52). A variety of angiogenic factors released from tumor cells and the extracellular matrix regulate the induction of tumor vascularization.…”

“…Enhanced expression of VEGF has been detected in a number of malignant human tumors, including HNSCC (49,50). VEGF expression in HNSCC tumors is strongly correlated with tumor angio genesis and is inversely correlated with apoptosis (51,52), which illustrates the anti-apoptotic potential of VEGF. For example, VEGF expression could be induced by loss or inactivation of tumor suppressor genes or overexpression of oncogenes.…”

“…Several studies demonstrate that HPV16 oncoproteins E6 and E7 strongly stimulate various pro-angiogenic factors, including VEGF (53). Tumor angiogenesis, microvessel density and VEGF expression have been associated with poor prognosis of head and neck cancers (50)(51)(52). Inhibition of angiogenesis by blocking angiogenic cytokines or their pathways has become a major target not only in experimental cancer therapies.…”