Vascular Endothelial Growth Factor Expression is Increased in Renal Cell Carcinoma

Nicol, David; Hii, S. I.; Walsh, Michael D.; Teh, Bin Tean; Thompson, Les; Kennett, Colin; Gotley, D. C.

doi:10.1016/s0022-5347(01)65028-6

Cited by 110 publications

(24 citation statements)

References 20 publications

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“…A number of EGFR are presently in clinical trials (Fabbro et al 2002). Likewise, overproduction of VEGF is common in renal cell carcinoma and likely contributes to tumor angiogenesis in this setting (Walke et al 1991; Brown et al 1993; Takahashi et al 1994; Nicol et al 1997; Ramp et al 1997). Drugs directed against VEGF or its receptors are also being tested in humans (Fabbro et al 2002).…”

Section: Resultsmentioning

confidence: 99%

Inhibition of HIF2α Is Sufficient to Suppress pVHL-Defective Tumor Growth

et al. 2003

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Biallelic inactivation of the von Hippel–Lindau tumor suppressor gene (VHL) is linked to the development of hereditary (VHL-associated) and sporadic clear-cell renal carcinomas as well as other abnormalities. The VHL gene product, pVHL, is part of an E3 ubiquitin ligase complex that targets the α subunits of the heterodimeric transcription factor HIF (hypoxia-inducible factor) for degradation in the presence of oxygen. Here we report that a HIF2α variant lacking both of its two prolyl hydroxylation/pVHL-binding sites prevents tumor inhibition by pVHL in a DNA-binding dependent manner. Conversely, downregulation of HIF2α with short hairpin RNAs is sufficient to suppress tumor formation by pVHL-defective renal carcinoma cells. These results establish that tumor suppression by pVHL is linked to regulation of HIF target genes.

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Section: Resultsmentioning

confidence: 99%

Inhibition of HIF2α Is Sufficient to Suppress pVHL-Defective Tumor Growth

et al. 2003

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“…In addition to having proangiogenic effects, VEGF has several important functions that are independent of vascular processes, including autocrine effects on tumor cell function (survival, migration, invasion), immune suppression, and homing of bone marrow progenitors to ‘prepare’ an organ for subsequent metastasis (56). Higher angiogenesis and VEGF expression have been detected in various human cancers including colorectal cancer (57), breast cancer (58), non small cell lung cancer (59), renal cell cancer (60), glioblastoma multiforme (61) and other tumors than corresponding nonmalignant normal tissue. Among patients with the highest levels of VEGF expression, survival was significantly worse than in patients with negative or lower levels of VEGF expression (62).…”

Section: Vascular Endothelial Growth Factor (Vegf)mentioning

confidence: 99%

Vascular Endothelial Growth Factor as an Anti-Angiogenic Target for Cancer Therapy

Niu¹,

Chen²

2010

CDT

351

257

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New blood vessel formation (angiogenesis) is fundamental to tumor growth, invasion, and metastatic dissemination. The vascular endothelial growth factor (VEGF) signaling pathway plays pivotal roles in regulating tumor angiogenesis. VEGF as a therapeutic target has been validated in various types of human cancers. Different agents including antibodies, aptamers, peptides, and small molecules have been extensively investigated to block VEGF and its pro-angiogenic functions. Some of these agents have been approved by FDA and some are currently in clinical trials. Combination therapies are also being pursued for better tumor control. By providing comprehensive real-time information, molecular imaging of VEGF pathway may accelerate the drug development process. Moreover, the imaging will be of great help for patient stratification and therapeutic effect monitoring, which will promote effective personalized molecular cancer therapy. This review summarizes the current status of tumor therapeutic agents targeting to VEGF and the applications of VEGF related molecular imaging.

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“…Several hypoxia-inducible genes are induced by this process, including VEGF [65]. Examination of RCC tumours for VEGF (mRNA transcripts and/or VEGF protein) has demonstrated VEGF overexpression in the vast majority of samples [66].…”

Section: Renal Cell Cancer (Rcc)mentioning

confidence: 99%

Vascular Endothelial Growth Factor (VEGF) as a Target of Bevacizumab in Cancer: From the Biology to the Clinic

Ranieri¹,

Patruno²,

Ruggieri³

et al. 2006

CMC

282

192

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Angiogenesis is important in the growth and progression of solid tumours. The main pro-angiogenic factor, namely vascular endothelial growth factor (VEGF), also known as vascular permeability factor, is a potent angiogenic cytokine that induces mitosis and also regulates the permeability of endothelial cells. The soluble isoform of VEGF is a dimeric glycoprotein of 36-46 kDa, induced by hypoxia and oncogenic mutation and it binds to two specific tyrosine-kinase receptors: VEGF-1 (flt-1) and VEGF-2 (KDR/flk1). An increase in VEGF expression in tumour tissue or some blood compartments (i.e. serum or plasma) has been found in solid and haematological malignancies of various origins and is associated with metastasis formation and poor prognosis. Bevacizumab, a recombinant humanised monoclonal antibody developed against VEGF, binds to soluble VEGF, preventing receptor binding and inhibiting endothelial cell proliferation and vessel formation. Pre-clinical and clinical studies have shown that bevacizumab alone or in combination with a cytotoxic agent decreases tumour growth and increases median survival time and time to tumour progression. Bevacizumab is the first anti-angiogenetic treatment approved by the American Food and Drug Administration in the first-line treatment of metastatic colorectal cancer. It has shown preliminary evidence of efficacy for breast, non-small-cell lung, pancreatic, prostate, head and neck and renal cancer as well as haematological malignancies. Common toxicities associated with bevacizumab include hypertension, proteinuria, bleeding episodes and thrombotic events. This review summarises the critical role of VEGF and discusses the data available on bevacizumab, from the humanisation of its parent murine monoclonal antibody (mAb) A.4.6.1 to its use in cancer clinical trials.

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Vascular Endothelial Growth Factor Expression is Increased in Renal Cell Carcinoma

Abstract: VEGF expression is increased in RCC and may have a paracrine effect in these tumours in stimulating angiogenesis.

Cited by 110 publications

References 20 publications

Inhibition of HIF2α Is Sufficient to Suppress pVHL-Defective Tumor Growth

Inhibition of HIF2α Is Sufficient to Suppress pVHL-Defective Tumor Growth

Vascular Endothelial Growth Factor as an Anti-Angiogenic Target for Cancer Therapy

Vascular Endothelial Growth Factor (VEGF) as a Target of Bevacizumab in Cancer: From the Biology to the Clinic

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