Vascular Endothelial Growth Factor Receptor 2 (VEGFR2) Expression in Squamous Cell Carcinomas of the Head and Neck

Neuchrist, Csilla; Erovic, Boban M.; Handisurya, Alessandra; Steiner, Georg; Rockwell, Patricia; Gedlicka, Claudia; Burian, Martin

doi:10.1097/00005537-200110000-00031

Cited by 59 publications

(37 citation statements)

References 42 publications

(48 reference statements)

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“…before by Neuchrist et al (2001). Taken together, it seems likely that two overlapping systems are involved in the tumorigenicity and tumour angiogenesis with autocrine/paracrine loops using VEGF and VEGFR2.…”

Section: Discussionmentioning

confidence: 96%

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Combined effects of bevacizumab with erlotinib and irradiation: a preclinical study on a head and neck cancer orthotopic model

et al. 2008

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Clinical benefit has been demonstrated in patients with head and neck tumours receiving an anti-epidermal growth factor receptor (EGFR) agent in combination with radiotherapy (RT). Recent preclinical and clinical studies suggest beneficial effects from combining anti-angiogenic drugs with RT. To investigate the effect of combining these approaches, we evaluated in vivo the anti-tumour efficacy of the anti-angiogenic compound bevacizumab, a highly specific monoclonal antibody directed against the vascular endothelial growth factor (VEGF), erlotinib, an EGFR tyrosine kinase inhibitor, and irradiation given alone and in combination. Investigations were performed using a VEGF-secreting human head and neck tumour cell line, CAL33, with a high EGFR content, injected as orthotopic xenografts into the mouth floor of nude mice. Three days after tumour cell injection, bevacizumab (5 mg kg À1 , 5 days a week, i.p.), erlotinib (100 mg kg À1 , 5 days a week, orally) and irradiation (6 Gy, 3 days a week) were administered alone and in combination for 10 days. As compared with the control, concomitant administration of drugs produced a marked and significant supra-additive decrease in tumour mass; the addition of irradiation almost completely abolished tumour growth. The drug association markedly reduced the number of metastatic nodes and the triple combination significantly reduced the total number of pathologically positive lymph nodes as compared with controls. The RT-induced proliferation, reflected by Ki67 labelling, was reduced to control level with the triple combination. Radiotherapy induced a strong and very significant increase in tumour angiogenesis, which was no longer observed when combined with erlotinib and bevacizumab. The efficacy of the combination of bevacizumab þ erlotinib and RT may be of clinical importance in the management of head and neck cancer patients.

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Section: Discussionmentioning

confidence: 96%

“…The key VEGF receptor present on endothelial cells is VEGFR2. In addition, the presence of VEGFR2 has been reported on tumour cells themselves, particularly in head and neck cancer (Neuchrist et al, 2001). For this reason, we analysed VEGFR2 expression both on endothelial cells and on tumour cells.…”

mentioning

confidence: 99%

Combined effects of bevacizumab with erlotinib and irradiation: a preclinical study on a head and neck cancer orthotopic model

et al. 2008

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“…Recently, it has been reported that VEGF and VEGFR-2 were coexpressed in various types of solid tumors [6, 19, 20]. These data have suggested the presence of an autocrine growth pathway involving VEGF and VEGFR-2.…”

Section: Discussionmentioning

confidence: 99%

Autocrine Vascular Endothelial Growth Factor/Vascular Endothelial Growth Factor Receptor-2 Growth Pathway Represents a Cyclooxygenase-2-Independent Target for the Cyclooxygenase-2 Inhibitor NS-398 in Colon Cancer Cells

Kim¹,

Seo²,

Lee

et al. 2005

Oncology

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Objectives: Coexpression of vascular endothelial growth factor (VEGF) and vascular endothelial growth factor receptor-2 (VEGFR-2) has been reported in tumor cells, suggesting the presence of an autocrine VEGF/VEGFR-2 growth pathway in solid tumors. Thus, we hypothesize that the presence of this autocrine pathway in colon cancer cells may be a COX-2-independent target of COX-2 inhibitors and a mechanism behind the antitumor effects of these agents. Methods: COX-2-positive (Caco2, HT-29) and COX-2-negative colon cancer cells (DLD-1, Hct-15) were used. Expression of VEGFR-2 was evaluated by Western blot and reverse transcriptase-polymerase chain reaction and VEGF production was measured from culture supernatant by enzyme-linked immunosorbent assay. Growth inhibition and the expression of VEGF and VEGFR-2 were compared after treatment with the COX-2 inhibitor, NS-398 at doses ranging from 5 to 100 µM. Results: VEGF and VEGFR-2 were expressed in all four colon cancer cells and a blockade of VEGFR-2 with anti-VEGFR-2 antibody treatment induced growth inhibition of colon cancer cells, supporting the presence of autocrine VEGF/VEGFR-2 growth pathway. NS-398 suppressed the growth of colon cancer cells, independent of COX-2 expression. VEGFR-2 expression of tumor cells was reduced after NS-398 treatment at 100 µM, the concentration at which maximal growth inhibition was induced. The amount of VEGF in culture supernatant was increased by NS-398 at 100 µM, suggesting increased secretion of VEGF in compensation for reduced VEGFR-2 expression. Conclusion: The autocrine VEGF/VEGFR-2 growth pathway could be a COX-2-independent target of the COX-2 inhibitor, NS-398, in colon cancer cells.

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“…25 Our results also implicate the significance of VEGF-C and VEGFR3 in tumor-dependent angiogenesis, which in turn is closely associated with tumor growth and metastases. 4 In HNSCCs, evidence of angiogenesis has been provided (ie, increased microvessel density, 26 upregulated VEGF, 7,8,27 VEGFR1, 28 VEGFR2, 13,29 and bFGF). 30,31 Nobody has previously featured details about lymph angiogenesis in HNSCC, tumors with a predilection for locoregional lymphatic metastasization.…”

Section: Vegf-c Expression In Hnsccmentioning

confidence: 99%

Vascular endothelial growth factor C and vascular endothelial growth factor receptor 3 expression in squamous cell carcinomas of the head and neck

et al. 2003

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Vascular Endothelial Growth Factor Receptor 2 (VEGFR2) Expression in Squamous Cell Carcinomas of the Head and Neck

Cited by 59 publications

References 42 publications

Combined effects of bevacizumab with erlotinib and irradiation: a preclinical study on a head and neck cancer orthotopic model

Combined effects of bevacizumab with erlotinib and irradiation: a preclinical study on a head and neck cancer orthotopic model

Autocrine Vascular Endothelial Growth Factor/Vascular Endothelial Growth Factor Receptor-2 Growth Pathway Represents a Cyclooxygenase-2-Independent Target for the Cyclooxygenase-2 Inhibitor NS-398 in Colon Cancer Cells

Vascular endothelial growth factor C and vascular endothelial growth factor receptor 3 expression in squamous cell carcinomas of the head and neck

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