Advancements in medical treatment for pancreatic neuroendocrine tumors: A beacon of hope

Figure 1 Mechanism of action various medical therapeutics. Everolimus by inhibiting mammalian target of rapamycin pathway can decrease cell proliferation as well as insulin action by supressing AKT. Somatostatin analog can supress hormone release by inhibiting Calcium channel and decrease proliferation by supressing Mitogen activated protein kinase. Temozolomide being an alkylating agent cause DNA damage. Capecitabine augment its activity by reducing methylguanine-DNA methyltransferase which is a DNA repair enzyme. Red lines are used to show inhibition and blue lines are used to show stimulation. GLUT 4: Glucose transporter 4, HIF-1a: Hypoxia inducible factor 1 alpha; 5-HTTP: 5 hydroxytryptophan; 5-HT: 5 hydroxy tryptamines; MAPK: Mitogen activated protein kinase; MGMT: Methylguanine-DNA methyltransferase; mTOR: Mammalian target of rapamycin; PD-1: Programmed cell death-1; TKR: Tyrosine kinase receptor; TPH: Tryptophan hydroxylase; VEGF: Vascular endothelial growth factor; SSA: Somatostatin analog.

Figure 2 Approach to medical therapy in pancreatic neuroendocrine tumors. SSA: Somatostatin analog; PPI: Proton pump inhibitor; Pan-NET: Pancreatic neuroendocrine tumor; PRRT: Peptide receptor radionuclide therapy.