Vandetanib is a multikinase inhibitor that is a target of drug treatments for non-small cell lung cancer. In this study, researchers determine the cellular and biological effects of vandetanib on Calu-6 cells. Results showed that vandetanib inhibits Calu-6 cell migration and invasiveness. Vandetanib also induces autophagy in Calu-6 cells by increasing the level of reactive oxygen species (ROS). These findings show that vandetanib produces a double effect in some NSCLC cells, which presents vandetanib as a potential agent for treatment of Calu-6 cells. [LINK]
Tumors are characterized by either tumor vessel or stromal vessel phenotypes, which reportedly define how tumors responds to VEGFR2 antibody treatment. In this study, researchers seek to understand whether the tumor phenotypes associate with vascular response to VEGFR tyrosine kinase inhibitors (TKI) or if changes in vascular function are associated with changes in tumor size. Stromal vessel phenotype Calu-3 and tumor vessel phenotype Calu-6 cells were treated with cediranib for 5 days. Following treatment, cediranib decreased Calu-3 tumor perfusion and hypoxia significantly increased; however, neither of these factors were affected in Calu-6 tumors. These findings suggest that tumor stromal phenotypes associate more with acute tumor vascular response to VEGFR TKI. [ LINK ]
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