Instead of directly targeting tumors, researchers have devised a way to cut the power to them by intervening with a cellular receptor that is overexpressed in cancer blood vessels, allowing them to regulate vascularization. The research was done by an international team of scientists from the University of Geneva (UNIGE) and Amsterdam UMC, and reported in the British Journal of Cancer.
From genomic screens, the researchers had observed that a receptor that normally serves as a receptor for insulin is overexpressed in the vasculature within a tumor. The receptor is called insulin receptor (INSR). Targeting this mechanism with anti-INSR antibodies both in vitro and in vivo in chicken chorioallantoic membrane (CAM) blocked blood vessel development. Furthermore, treatment with the inhibitor sunitinib showed reduction of INSR-A in both a preclinical mouse model as well as patient data.
Armed with this knowledge, the researchers hope to be able to develop a treatment suitable for clinical use. One of the primary benefits would be the ability to precisely target the tumor endothelium, while sparing healthy cells. Additionally, because this would be an indirect approach, there would potentially be less opportunity for the cancer to become resistant to the treatment.
Image: Immunohistochemical staining for the insulin receptor (INSR) in a microscopic section of human stomach cancer. A clear overexpression of this receptor (brown) is seen in the tumor tissue, while this is absent in non-cancerous stomach tissues. Image courtesy of UNIGE / DR.