Table 1.

Genetic subtypes.

		Collisson et al., 2011
Subtype	Genetic signature	Histology	Clinical implications
Classical	Adhesion-associated and epithelial genes; GATA6hi	Highly differentiated	Sensitive to erlotinib
QM-PDA*	Mesenchymal Genes	Poorly differentiated	Sensitive to gemcitabine
Exocrine-like	Digestive enzyme genes	ELA3A+ and CFTR+	-
		Moffitt et al., 2015
Subtype	Genetic Signature	Histology	Clinical implications
Classical	GATA6hi and SMAD4hi	>10% mucin expression	1 year survival of 70%
Basal-like	Laminins and Keratins	<10% mucin expression	1 year survival of 44%
Stromal factors	Collisson's mesenchymal genes and stroma histology likely from CAF° cells not neoplastic cells		Activated stroma = worse prognosis for both classical and basal-like subtypes
Exocrine factors	Similar to normal exocrine pancreas, not considered a tumor subtype
		Bailey et al., 2016
Subtype	Genetic signature	Histology	Clinical implications	COMPASS Trial
Pancreatic progenitor	high PDX1, MUC1 and MUC5AC expression	Includes mucinous non-cystic (colloid) and mucinous IPMN		Responsive to FOLFIRINOX
Squamous	TP53, KDM6A, TP63 N mutations	Includes adeno-squamous carcinomas	Poor prognostic factor	Resistant to FOLFIRINOX
ADEX#	Endocrine and exocrine pancreas genes, subclass of pancreatic progenitor	Includes rare acinar cell carcinomas
Immunogenic	B and T cell genes, upregulation of CTLA4 and PD1	Includes mucinous non-cystic (colloid) and mucinous IPMN	Potential responsiveness to immune modulators
		Cancer Genome Atlas Network, 2017
Subtype	Genetic signature	Histology	Clinical implications
Classical/ pancreatic progenitor	GNAS mutations common; high EVADR, DEANR1, and GATA6-AS1 lncRNAs
Squamous/ basal-like	TP53 mutations common; high CAV1, low miR-192-5p and miR-194-5p
ADEX#	Genetic signature may be due to non-neoplastic infiltrate rather than unique neoplasm	Low neoplastic cellularity
Immunogenic

*Quasi-mesenchymal-pancreatic ductal adenocarcinoma

°cancer associated fibroblast

^#aberrantly differentiated endocrine exocrine.