fig1

Figure 1. Schematic representation of the over activation of TKRs involved in enhancing the growth and survival in the tumor cell, promoting angiogenesis in the endothelial cell, and the inhibition of killing effect of the T cell on tumor cell. VEGFR 1/2: Vascular endothelial growth factor receptor 1/2; PDGFR: platelet-derived growth factor receptor; EGFR: epidermal growth factor receptor; RET: rearranged during transfection; MET: hepatocyte growth factor receptor; KIT: mast/stem cell growth factor receptor; RAS: rat sarcoma; RAF: v-raf murine sarcoma viral oncogene homolog; MEK: mitogen activated protein kinase; ERK: extracellular signal-regulated kinases; PI3K: phosphoinositide 3-kinase; pTEN: phosphatase and tensin homolog; AKT: protein kinase B; mTOR: mammalian target of rapamycin; MHC: major histocompatibility complex; TCR: T cell receptor; PD1: programmed cell death protein 1; PD-L1: programmed death ligand 1; CTLA-4: cytotoxic T-lymphocyte antigen 4; APC: antigen presenting cell.