Table 2.

Summary of the aforementioned studies that assessed the use of the CAM model for the assessment of tumor-induced angiogenesis in pancreatic cancer.

Study	Readout	Results
[58]	Hypoxia-induced de novo transcription of uPAR mRNA in pancreatic cancer cell lines	Tumor-induced angioinvasion of human pancreatic cancer cells in vitro and in vivo may depend on hypoxia
[59]	Depletion of PKD2 in the endothelium in sprouting assays and tumor xenografts inhibited tumor-induced angiogenesis of pancreatic cancer cells	PKD2 controls hypoxia-induced VEGF-A expression, secretion, and blood vessel formation of pancreatic and gastric tumors
[60]	The sst2-dependent upregulation of TSP-1 slowed down tumor cell-induced blood vessel formation by encapsulating VEGF and inactivated the endothelial effects of VEGFR2	TSP-1 and sst2 function as tumor suppressors and could suppress the proliferation of pancreatic cancer
[61]	Inhibition of EGFL7 expression restricted microvessel formation of pancreatic carcinoma by downregulation of VEGF and Ang-2	EGFL7 is a possible marker for prognosis and perhaps a therapeutic target of pancreatic carcinoma
[62]	Prognostic values and expression of Ezrin on Akt/mTOR pathway and YAP expression in pancreatic cancer and healthy pancreas tissue was assessed in different assays	Ezrin and YAP are overexpressed in pancreatic cancer and correspond with a poor prognosis