Table 1.

Precision medicine: therapeutic targets in PC.

Target	Treatment	Estimated Prevalence
KRAS wild-type	EGFR inhibitors (e.g., panitumumab, cetuximab, erlotinib)	10–20% [24,28,29,30]
DNA repair pathway defects (BRCA1, BRCA2, PALB2, ATM)	DNA damaging agents (e.g., mitomycin C, platinums) PARP inhibitors (e.g., olaparib)	4–20% [22,24,30,31]
HER2 amplification	Anti-HER2 antibodies/tyrosine kinase inhibitors (e.g., trastuzumab/lapatinib)	10–30% [32,33]
MET activation (mutation, overexpression, amplification)	MET inhibitors	20% [34,35,36]
Mismatch repair gene deficits (MLH1, MSH2, MSH6, PMS2)	Immunotherapy	3–22% [37,38,39,40]
PIK3CA amplification/mutation +/− PTEN loss	mTOR inhibitors (e.g., everolimus)	15–20% [24,41,42]
CDKN2A loss	CDK4/6 inhibitors (e.g., palbociclib)	25% [22,43,44,45]
BRAF mutation	BRAF inhibitors (e.g., dabrafinib), MEK inhibitors (e.g., trametinib)	2% [19,24,27,42]
FGFR1 amplification	FGFR inhibitors	1% [27,30]