Finding itPancreatic ductal adenocarcinoma

• CA 19-9 (prognosis and monitoring)
• KRAS mutation subtype (G12D about 40%, G12V about 32%, G12R about 16%, Q61 about 7%, G12C 1 to 2%; cohort ranges in the molecular table; wild-type triggers fusion testing)
• Germline panel (BRCA1/2, PALB2, ATM, CDKN2A, STK11, Lynch)
• HRD / platinum sensitivity
• GATA6 (classical vs basal-like)
• ctDNA (KRAS-mutant cfDNA) for MRD and response
• FAPI PET avidity (investigational)
• CLDN18.2 IHC (trials)
• CA 19-9 with Lewis status : falsely low in the 5 to 10 percent who are Lewis-negative; above 500 U/mL counts as biological borderline resectability
• Resectability class on pancreas protocol CT (degrees of arterial contact; venous contact and reconstructability), reported on a standard template
• Resection margin by the 1 mm rule (R0 more than 1 mm; R1 within 1 mm; R1 direct), the strongest surgeon- and pathologist-controlled prognostic factor
• KRAS activating mutation (any allele): 88-94%
• KRAS G12D g12d allele (share of kras mutation records): 39-41%
• KRAS G12V g12v allele (share of kras mutation records): 28-37%
• KRAS G12R g12r allele (share of kras mutation records): 12-21%
• KRAS Q61 q61h, q61r, q61l or q61k allele (share of kras mutation records): 5-8%
• KRAS G12C g12c allele (share of kras mutation records): 1-2%
• KRAS wild-type no kras mutation (fusion and alternative-driver search): 6-12%
• NRG1 gene fusion (atp1b1-nrg1, cd44-nrg1 and others): 0.3-1%
• BRAF mutation (v600e, in-frame deletion) or fusion: 1-3%
• ALK gene fusion (eml4-alk, strn-alk): 0.2%
• NTRK1 / NTRK3 gene fusion (etv6-ntrk3, ctrc-ntrk1): 0.4%
• FGFR2 gene fusion : 0.2%
• TP53 mutation : 66-76%
• CDKN2A mutation or deep deletion (with cdkn2b and mtap co-deletion): 37-48%
• SMAD4 (DPC4) mutation or deep deletion: 17-33%
• BRCA2 germline pathogenic variant : 1.4-2%
• BRCA1 germline pathogenic variant : 0.4-1%
• PALB2 germline or somatic pathogenic variant : 0.2-0.6%
• ATM germline pathogenic variant (somatic in a further 3 to 4%): 1.2-2.3%
• Any germline susceptibility gene pathogenic germline variant (multigene panel): 4-10%
• Homologous recombination deficiency hrd (core or biallelic hr gene mutation, unstable genome or signature 3): 11-19%
• MLH1 / MSH2 / MSH6 / PMS2 mismatch repair deficiency or microsatellite instability : 0.5-2%
• Tumour mutational burden tmb 10 or more mutations per megabase : 1-2%
• GNAS r201 hotspot mutation (ipmn-derived tumours): 2-4%
• RNF43 inactivating mutation : 5-8%
• KDM6A inactivating mutation or structural disruption : 3-4%
• MYC amplification : 4-13%
• ARID1A inactivating mutation (swi/snf and chromatin genes): 5-9%
• GATA6 amplification (classical lineage marker): 15-17%
• ERBB2 (HER2) amplification (mutation in a further 1%): 1-5%

What each tumour test looks for → · Biomarker matrix →