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%).
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.
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.
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.
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.
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.