Table 1. Current treatment options for pancreatic NETs (PNETs).

Medical
	Biotherapy Somatostatin analogues e.g. octreotide, lanreotide, pasireotide α-interferon Mechanistic target of rapamycin (mTOR) inhibitors e.g. everolimus Receptor tyrosine kinase (RTK) inhibitors, including PDGFRa and VEGFRa inhibitors e.g. sunitinib and sorafenib VEGFAb antibodies e.g. bevacizumab
	Chemotherapy Alkylating agentsc e.g. streptozocin, temozolomide, cisplatin Anti-microtubule agentsc e.g. etoposide, docetaxel Topoisomerase inhibitorsc e.g. doxorubicin, irinotecan Antimetabolitesd e.g. 5’fluorouracil (capecitabinee), gemcitabine Cytotoxic antibodiesd e.g. actinomycin D, mitomycin C, doxorubicin, mitoxantrone Non-classical compounds
Surgery
	Curative
	Cytoreduction
Radiological
	Radiotherapy External beam Tumour targeted (e.g. Peptide Receptor Radionuclide Therapy (PRRT) using 90Y-DOTATOC, or 177Lu-DOTATE)
	Interventional Radiology Radiofrequency ablation (RFA) Transarterial embolisation (TAE) Transarterial chemoembolisation (TACE) Selective internal radiation therapy (SIRT)

^aPDGFR – platelet-derived growth factor receptor; and VEGFR – vascular endothelial growth factor receptor are both TKI inhibitors. Inhibitors may have multiple targets, for example sunitinib and sorafenib inhibit PDGFR and VEGFRs; imatinib inhibits PDGFRs, Abelson murine leukemia viral oncogene homolog 1 (vABl) and proto-oncogene c-Kit (c-kit); and vandetanib inhibits VEGFRs and epidermal growth factor receptors (EGFRs)

^bVEGFA – vascular endothelial growth factor A

^cNuclear targets

^dcytoplasmic targets; capecitabine is the orally administered pro-drug of 5’fluorouracil (5FU).