. Author manuscript; available in PMC: 2017 Dec 11.

Published in final edited form as: J Gastrointest Surg. 2015 Nov 18;20(1):53–65. doi: 10.1007/s11605-015-2985-y

Table 1.

Features of the proposed and previously established mouse models of pancreatic cancer (PDAC)

	Proposed model	Existing models
	STIM	Genetically engineered KPC⁸	KPC cell line implantation Model^4,23	Human PDAC cell line xenograft²³	Patient derived tumor xenograft (PDX)¹⁹
Mouse genetic background	C57BL/6J (wild type)	C57BL/6J (wild type)	C57BL/6J (wild type)	Athymic/SCID/NSG	Athymic/SCID/NSG
Immune background	Immunocompetent	Immunocompetent	Immunocompetent	Immunodeficient (lacks functional adaptive immunity)	Immunodeficient (lacks functional adaptive immunity)
Mutation profile	Mutations present only in implanted tumor tissue	Mutations present throughout pancreas	Mutations present only in implanted cells	Mutations present only in implanted cells	Mutations present only in implanted tumor tissue
Species	Mouse tumor	Mouse tumor	Mouse cell line	Human cell lines	Human tumor
Stromal content	High stromal content (ECM, fibroblasts and activated stellate cells)	High stromal content (ECM, fibroblasts and activated stellate cells)	Low stromal content	Absent stroma	High stromal content (ECM, fibroblasts and activated stellate cells)
Variability	Less variability in time to invasive disease ( within 2 weeks)	High variability in time to invasive disease (Range, 47–355 days)	Less variability in time to invasive disease (within 2 weeks)	Less variability in time to invasive disease (2–3 weeks); depends on cell line	Variability in time to tumor development (2–12 months ); depends on primary tumor
Predictability	Predictable course of disease progression	Unpredictable course of disease progression	Predictable course of disease progression	Predictable course of disease progression	Predictable course of disease progression and variable engraftment rates (23–75%)
Tumor milieu	Tumor growth is in natural milieu (pancreas)	Tumor growth is in natural milieu (pancreas)	Tumor growth is in natural milieu (pancreas)	Tumor growth is in unnatural (subcutaneous) milieu or natural (orthotopic) milieu	Tumor growth is in unnatural (subcutaneous) milieu or natural (orthotopic) milieu
Metastatic disease	Metastatic and loco-regional disease present after 2 months of implantation	Metastatic and loco-regional disease develops at variable time.	Metastatic and loco-regional disease present, but concerns of confounding due to cell spillage during orthotopic implantation	Metastatic and loco-regional disease absent in subcutaneous models and present in orthotopic.	Metastatic and loco-regional disease absent in subcutaneous models and present in orthotopic.
Tumor pathology	Well differentiated to poorly differentiated tumors (depends on parent tumor)	Well differentiated to poorly differentiated tumors	Poorly differentiated tumors	Variable	Variable

Tumor microenvironment	Robust desmoplastic reaction, collagen and vimentin content, immune infiltration, and stellate cells	Robust desmoplastic reaction, collagen and vimentin content, immune infiltration, and stellate cells	Paucity of desmoplastic reaction, less collagen, vimentin and stellate cells, and less immune infiltration	Paucity of desmoplastic reaction as well as infiltrating immune cells	Robust desmoplastic reaction without infiltrating adaptive immune cells
Surrounding pancreas	Adjacent normal/wild type pancreas	Adjacent mutant Kras-p53 pancreas	Adjacent normal/wild type pancreas	No surrounding pancreatic tissue (subcutaneous) or adjacent immunodeficient pancreas (orthotopic)	No surrounding pancreatic tissue (subcutaneous) or adjacent immunodeficient pancreas (orthotopic)

STIM: Syngeneic Tumor Implanta3on Model; SCID: Severe combined immunodeficiency; NSG: Non-obese diabe3c (NOD) SCID gamma mice; ECM: Extracellular matrix STIM Syngeneic Tumor Implantation Model, SCID severe combined immunodeficiency, NSG non-obese diabetic (NOD) SCID gamma mice, ECM extracellular matrix