Molecular advances in pancreatic cancer: A genomic, proteomic and metabolomic approach

Table 1 Summary of molecular subtyping studies

Ref.	Subtypes	Clinical significance
	Genomic
Waddell et al[11]	Stable, locally re-arranged, scattered and unstable	High BRCA mutational signature in the unstable subtype, sensitizing to PARPi and PBC.
Singhi et al[12]	-	Real time genetic sequencing. 17% of specimens found to have sensitivities to available treatments. Potential therapeutic targets.
Aguirre et al[13]	SigA, SigB and SigC	Potential targets in 40% of patients. 48% eligible for trials/off-label use. Of 24% enrolled onto a clinical trial.
	Proteomic
Law et al[14]	Inflammatory, proliferative, progenitor-like and metabolic	↓Risk of death in metabolic and progenitor-like subtypes treated with FOLFIRINOX+Gemcitabine. ↑Survival in progenitor-like subtype treated with gemcitabine. SHMT1 a potential mediator of gemcitabine resistance.
Humphrey et al[15]	TKCC subtypes 1, 2 and 3	Subtypes 3 in both cohorts showed increased sensitivity to erlotinib, potentially mediated by tyrosine phosphorylation of RTK sites.
	ATCC subtypes 1, 2 and 3
	Metabolomic
Daemen et al[16]	Slow proliferating, glycolytic and lipogenic	Glycolytic subtype sensitive to inhibitors of aerobic glycolysis, glutaminolysis, γ-glutamylcysteine and Xct. Lipogenic subtype sensitive to lipid synthesis inhibitors.

BRCA; Breast cancer gene; RTK: Receptor tyrosine kinase; PBC: Platinum-based chemotherapy; PARPi: Poly (ADP-ribose) polymerase inhibitors; xCT: Cystine transporter; SHMT1: Serine hydroxymethyltransferase 1.