Vascular endothelial growth factor (VEGF) signaling in tumor progression

Roskoski, Robert

doi:10.1016/j.critrevonc.2007.01.006

Cited by 539 publications

(502 citation statements)

References 270 publications

(463 reference statements)

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“…VEGF receptor signalling has been shown to have effects on endothelial cell proliferation, migration, survival and vascular permeability (Roskoski, 2007). In addition, urokinase plasminogen activator, tissue plasminogen activator and matrix metalloproteinases are induced by upregulation of VEGF.…”

Section: Discussionmentioning

confidence: 99%

“…These proteins function to degrade the basement membrane and extracellular matrix, providing a scaffold for proliferating, migrating and extravasating endothelial cells (Ferrara et al, 2003). The result of tumour angiogenesis is a newly formed vasculature with 'leaky', disorganised vessels, increased interstitial pressure and chaotic blood flow, which decreases the efficiency of radiotherapy (Willett et al, 2006;Roskoski, 2007). In 1971, Folkman (1971 hypothesised that blocking angiogenesis in tumours could be used a method of treatment for patients with cancer.…”

Section: Discussionmentioning

confidence: 99%

“…In 1971, Folkman (1971 hypothesised that blocking angiogenesis in tumours could be used a method of treatment for patients with cancer. Pharmacological agents designed to block VEGF or VEGF receptor signalling are currently in various phases of clinical trials and have demonstrating promising results (Kowanetz and Ferrara, 2006;Roskoski, 2007;Willett et al, 2007). The VEGF blockade results in A B Figure 1 Representative immunostains of VEGF (A) and EGFR (B) from pretreatment rectal tumour biopsies.…”

Section: Discussionmentioning

confidence: 99%

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Combined analysis of VEGF and EGFR predicts complete tumour response in rectal cancer treated with preoperative radiotherapy

et al. 2008

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The ability to predict complete pathologic response or sensitivity to radiation before treatment would have a significant impact on the selection of patients for preoperative radiotherapy or chemo-radiation therapy schedules. The aim of this study was to determine the value of epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF), p53, Bcl-2 and apoptosis proteaseactivating factor-1 (APAF-1) as predictors of complete pathologic tumour regression in patients undergoing preoperative radiotherapy for advanced rectal cancer. Pretreatment tumour biopsies from predominantly cT3 patients undergoing a preoperative high-dose-rate brachytherapy protocol were immunostained for EGFR, VEGF, p53, Bcl-2 and APAF-1. Immunoreactivity was evaluated by three pathologists. Cut-off scores for tumour marker positivity were obtained by receiver-operating characteristic (ROC) curve analysis. The association of marker expression with complete pathologic response was analysed in univariate and multivariable analysis. Multi-marker phenotypes of the independent protein markers were evaluated. In multivariable analysis, loss of VEGF (P-value ¼ 0.009; odds ratio (OR) (95% CI) ¼ 0.24 (0.08 -0.69)) and positive EGFR (P-value ¼ 0.01; OR (95% CI) ¼ 3.82 (1.37 -10.6)) both demonstrated independent predictive value for complete pathologic response. The odds of complete response were 12.8 for the multi-marker combination of VEGF-negative and EGFR-positive tumours. Of the 34 EGFR-negative-and VEGFpositive cases, 32 (94.1%) had no complete pathologic response. The combined analysis of VEGF and EGFR is predictive of complete pathologic response in patients undergoing preoperative radiotherapy. In addition, the findings of this study have identified a subgroup of simultaneous EGFR-negative and VEGF-positive patients who are highly resistant to radiotherapy and should perhaps be considered candidates for innovative neoadjuvant combined modalities.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Combined analysis of VEGF and EGFR predicts complete tumour response in rectal cancer treated with preoperative radiotherapy

et al. 2008

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“…Bevacizumab prevents the binding of VEGF-A to its receptor VEGF-R1 (Flt-1) and R2 (Flt-2 or KDR). Although the function of VEGF-R2 in tumor angiogenesis has been characterized thoroughly, the function of VEGF-R1 is not yet well defined (9). Bevacizumab has been found clinically active in many solid tumors, such as colon, non-small cell lung, metastatic renal cell carcinoma, or glioblastoma (10)(11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

Akt-Activated Endothelium Constitutes the Niche for Residual Disease and Resistance to Bevacizumab in Ovarian Cancer

Guerrouahen

Pasquier

Kaoud

et al. 2014

Molecular Cancer Therapeutics

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“…Tumors and metastases usually arise as small avascular masses that subsequently induce neovascularization in order to acquire nutrients for further growth and metastatic spread (1)(2)(3).…”

Section: Introductionmentioning

confidence: 99%

Construction and expression of a lentivirus expression vector carrying the VEGF165-EGFP fusion gene in breast cancer MCF-7 cells

Luo¹,

Huang²,

Hou³

et al. 2017

Oncology Letters

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Abstract. Vascular endothelial growth factor (VEGF)165 is one of the most abundant and potent angiogenic factors in both physiological and pathological conditions. However, the function and mechanism of VEGF165 in tumors and their environment remain to be elucidated. In the present study, a lentivirus vector (LV) that contained the VEGF165-enhanced green fluorescent protein (EGFP) fusion gene was constructed and transfected into the human breast cancer cell line MCF-7. Following transfection, the expression of VEGF165 in MCF-7 cells was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting. Further cellular localization of VEGF165 was observed through fluorescence microscopy. The titer of the recombinant lentivirus was 5.44x10 7 TU/ml in the LV-VEGF165-EGFP group and 5.00x10 8 TU/ml in the LV-EGFP negative control group. RT-qPCR and western blotting demonstrated that the expression of VEGF165 was significantly increased in the LV-VEGF165-EGFP group compared with the control group. The present study lays the foundation for in vitro and in vivo studies on tumor cell derived-VEGF165. Furthermore, the present fusion gene expression vector may provide a potential approach for gene therapy treatment of cancer and other diseases that require regulation of angiogenesis.

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Vascular endothelial growth factor (VEGF) signaling in tumor progression

Cited by 539 publications

References 270 publications

Combined analysis of VEGF and EGFR predicts complete tumour response in rectal cancer treated with preoperative radiotherapy

Combined analysis of VEGF and EGFR predicts complete tumour response in rectal cancer treated with preoperative radiotherapy

Akt-Activated Endothelium Constitutes the Niche for Residual Disease and Resistance to Bevacizumab in Ovarian Cancer

Construction and expression of a lentivirus expression vector carrying the VEGF165-EGFP fusion gene in breast cancer MCF-7 cells

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