Here, we demonstrate that stimulation of human colorectal cancer cell lines with G-gly increases the expression of the proangiogenic factor VEGF at the mRNA and protein levels.
The aim of this study was to investigate the association between the risk for colorectal cancer and single nucleotide polymorphisms (SNP) of matrix metalloproteinase-2 (MMP2) -1306C/T, vascular endothelial growth factor (VEGF) 936C/T and hypoxia inducible factor-1α (HIF1A) 1772C/T.
Targeted therapies in the form of monoclonal antibodies directed against the endothelial growth factor receptor or the vascular endothelial growth factor have met with success, and have demonstrated the advantages of molecularly targeted therapy in colorectal cancer.
Our meta-analysis indicated that VEGF-2578C/A polymorphism was associated with the risk of colorectal cancer under homozygote comparison (OR=0.70, 95% CI=0.53-0.92), dominant model (OR=0.72, 95% CI=0.57-0.92), and recessive model (OR=0.82, 95% CI=0.67-1.01), although no evidence of association between VEGF-2578C/A polymorphism and cancer risk was observed as we compared in the pooled analyses (homozygote comparison: OR=0.97, 95% CI=0.81-1.16).
We sought to determine whether such genetic variability in VEGF contributes to susceptibility of colorectal adenoma (CRA), a presumably precancerous state of colorectal cancer.
The Colorectal Oral Novel therapy For the Inhibition of angiogenesis and Retarding of Metastases (CONFIRM)-randomized trials, investigating the role of the VEGF-receptor inhibitor PTK787/ZK 222584 (vatalanib) in colorectal cancer (FOLFOX 4 ± vatalanib), showed some benefit in patients with high serum lactate dehydrogenase (LDH) levels.
This review summarizes the current knowledge about the splice isoforms of VEGFA, UGT1A, PXR, cyclin D1, BIRC5 (survivin), DPD, K-RAS, SOX9, SLC39A14 and other genes, which may be possible therapeutic targets for colorectal cancer.
In oncological practice, angiogenesis inhibition, mainly through the blockade of the VEGF family and its receptors, has been robustly demonstrated to produce clinical benefits and, in specific disease subsets such as colorectal cancer, to extend the overall survival of treated patients.
Loss of phosphatase and tensin homologue (PTEN) expression may be prognostic in colorectal cancer (CRC) and may have a correlation with vascular endothelial growth factor (VEGF) expression via hypoxia-inducible factor 1 (HIF-1) alpha, and the PI3K/mTOR pathways.