EGF stimulation of glioma cells induced the phosphorylation of tyrosine 221 of the CrkII protein, which correlates with its dissociation from the EGFR.
However, in the stratified analysis by ethnicity, the EGF+61G/A polymorphism had a higher risk of glioma development among Asians, but a lower risk among Caucasians.
Overall, there was a significant association between EGF +61A>G polymorphism and glioma risk in the allele model (OR = 1.419, 95% CI = 1.144-1.759, P = 0.001).
This meta-analysis suggests that the EGFG61A polymorphism most likely contributes to decreased susceptibility to cancers among Asians and Americans, and A allele may be a protective factor for gastric cancer, esophageal cancer, hepatoma and glioma.
TSCs of glioma were enriched from U87 and two primary cells (SHG62, and SHG66) using serum-free medium supplemented with growth factors, including bFGF, EGF and B27.
Loss of the tumor-suppressor PTEN and activation of the receptor tyrosine kinases (RTKs) EGF receptor, c-Met, PDGF receptor and VEGF receptor are among the most common molecular dysfunctions associated with glioma malignancy.
In this study, we have investigated whether the molecular motor myosin II represents such a target by examining glioma invasion in a series of increasingly complex models that are sensitive to platelet-derived growth factor, epidermal growth factor, or both.Our results lead to two conclusions.
In conclusion, the results suggest that there is a significant association between EGFrs4444903 polymorphism and glioma risk, and genotypes of EGFrs4444903 mutation contribute to increased host susceptibility to glioma.