Gastric adenocarcinoma is the second leading cause of cancerrelated death world- wide, but the overall survival rate from the disease
still remains poor due to the lack of effective treatment strategies, especially in advanced situations. Approximately 650 000 people die
worldwide from gastric cancer every year. Epidemiological and interventional studies in humans, as well as experiments in rodents,
have strongly linked H. pylori infection to the development of both types of distal gastric cancer. Surgery, i.e. gastrectomy with
extended lymphadenectomy is the only curative option in early stages of gastric adenocarcinomas, and this treatment option is reasonable
when the tumor has exceeded the mucosal layer. Tumor prognosis is favourable only in early stages of gastric cancer, and recent studies
have revealed that tumors limited to the mucosa (T1m stages) can be resected endoscopically, since lymph nodes metastasis at this stage are
extremely rare. A key role for gastric micro vascularisation during cancer progression is the vascular growth factor VEGF-A. Vascular
endothelial growth factor (VEGF) is a multifunctional cellular factor which can induce neovascularization and increase capillary
permeability. VEGF-A regulates important steps in angiogenesis and physiological vascularisation and controls a number of physiological
processes like wound healing, ovulation, menstruation and pregnancy. There are four active isoforms of the VEGF-A molecule generated
by differential splicing of which VEGF-A165 is the most common. The biological activity of VEGF-A is mediated by binding on VEGFR-1 and
VEGFR-2 receptors, that are expressed on vascular endothelial cells; but also by binding on neuropilins located on vascular endothelium
or neurons.
Last date updated on April, 2025