After stratifying by tumor molecular subtype, SNP associations observed for colon cancer were: VEGFArs2010963 with CIMP+ colon tumors; FLT1 rs4771249 and rs7987649 with TP53; FLT1 rs3751397, rs7337610, rs7987649, and rs9513008 and KDR rs10020464, rs11941492, and rs12498529 with MSI+ and CIMP+/KRAS2-mutated tumors.
Vascular endothelial growth factor polymorphisms -1154 G/A and -460 C/T are not associated with VEGF mRNA expression and susceptibility to sporadic colon cancer.
In RAS-BRAF wild type left colon tumors, Turkish oncologists mostly use chemotherapy and anti-EGFR therapy (90.1%) for the first-line treatment, while on the right side, oncologists favored anti-VEGF therapy in combination with chemotherapy (65.5%).
Both Del1-shRNA and VEGF-shRNA gene therapies exhibited anti-tumor activities and they also showed a synergistic effect in suppressing growth of colon tumors by anti-angiogenesis and anti-proliferation.
Activation of beta-adrenoceptors and the subsequent stimulation of COX-2, PGE(2), and VEGF expression is perhaps an important mechanism in the tumorigenic action of nicotine on colon tumor growth.
Although these results are consistent with the known role of wild-type p53 in down-regulating VEGF, no association was found between a mutation in p53 and VEGF or bFGF levels in all colonic neoplasms.
Our results showed that biglycan overexpression notably up-regulated the levels of VEGF in colon cancer cells, which was further confirmed by immunohistochemistry analysis in the xenograft colon tumors.