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Pancreatic ductal adenocarcinoma is characterised by KRAS, TP53, CDKN2A and SMAD4 alterations in most cases. The value of comprehensive profiling lies in identifying the minority of tumours with DNA repair deficiency, a fusion, mismatch repair deficiency or an uncommon KRAS variant. Germline testing is discussed for all patients, not only those with a family history.
Also called Pancreatic ductal adenocarcinoma, PDAC.
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Most pancreatic cancer carries the same small set of alterations, none of which is easily targetable, which makes the profiling discussion about finding the minority with something actionable rather than expecting to.
Pancreatic ductal adenocarcinoma is characterised by KRAS, TP53, CDKN2A and SMAD4 alterations in most cases. The value of comprehensive profiling lies in identifying the minority of tumours with DNA repair deficiency, a fusion, mismatch repair deficiency or an uncommon KRAS variant. Germline testing is discussed for all patients, not only those with a family history.
01Before any molecular question
Usually established first: whether the tumour is resectable, borderline resectable, locally advanced or metastatic. This resectability classification, rather than stage alone, organises the treatment discussion. Biliary obstruction and nutritional status are often immediate practical concerns.
Usually already established
02
The divisions below are not labels. Each one changes what the treatment discussion is actually about.
Resectable
Surgery is potentially curative, and the sequencing of treatment around it is the main discussion.
Borderline resectable
A category defined by the tumour’s relationship to nearby blood vessels, where treatment may be given first to make surgery possible.
Locally advanced, unresectable
Systemic treatment leads, with radiation discussed in some settings.
Metastatic
The setting where profiling most often changes the treatment discussion, in the minority with an actionable finding.
03What is discussed
KRAS alteration is present in the large majority, most commonly G12D, G12V or G12R, with G12C being uncommon in this disease. TP53, CDKN2A and SMAD4 alterations are also frequent and are not directly actionable. The findings that change the discussion are less common: BRCA1, BRCA2, PALB2 and other homologous recombination genes; NTRK, NRG1, ALK and RET fusions; mismatch repair deficiency; and, in the small group that lacks KRAS alteration entirely, a markedly higher chance of an actionable finding. That last point is worth knowing: KRAS wild-type pancreatic cancer is the group where comprehensive profiling is most likely to change something.
KRAS
Altered in most cases. Its absence is itself informative and prompts a wider search.
BRCA1, BRCA2, PALB2
DNA repair genes. Relevant both as tumour findings and as inherited risk.
MMR / MSI
Uncommon, but changes the discussion substantially where present.
NTRK, NRG1, ALK, RET
Fusions. Rare, enriched in KRAS wild-type tumours, and need a panel that reads fusions.
TP53, CDKN2A, SMAD4
Frequent and characteristic. Descriptive rather than actionable.
This is not an exhaustive list, and which markers are relevant depends on the individual case. Not every marker listed is assessed in every patient.
04What is tested, and from what
Comprehensive profiling and germline testing are both discussed for advanced disease. The practical difficulty is tissue: pancreatic diagnoses are often made on a fine needle aspirate that yields very little material, and profiling failures from insufficient tissue are common. Plasma testing is a frequent alternative or complement for that reason. Timing matters because treatment usually needs to start promptly.
Germline testing is discussed for all patients with pancreatic ductal adenocarcinoma regardless of family history, because the prior probability is high enough that family history is an unreliable filter. Relevant genes include BRCA1, BRCA2, PALB2, ATM, CDKN2A, the Lynch syndrome genes and STK11. A finding changes the patient’s treatment discussion and opens surveillance options for relatives, which in this disease is a meaningful offer given how late it is usually found.
Cancer genetics and hereditary riskPlasma testing is used where tissue is inadequate, which is common in this disease. Pancreatic cancer can shed relatively little ctDNA, so a negative plasma result needs to be read with that in mind rather than as evidence of absence.
More on ctDNA monitoring05The timing question
Testing that arrives after the decision it was meant to inform has already been made is a common and avoidable problem. This is the sequence in which molecular information tends to become relevant.
06Take these to your team
When a decision is being made
Questions worth raising with a treating team.
At progression, recurrence or resistance
The molecular picture at diagnosis is not always the molecular picture later.
07What shapes eligibility
Trial activity is substantial and includes KRAS-directed agents, DNA repair approaches, stromal and immune strategies. Performance status is frequently a limiting eligibility criterion in this disease, which is an argument for considering trials earlier rather than later.
| Term | What it means |
|---|---|
| Resectable and borderline resectable | Categories describing whether surgery is possible, based on the tumour’s relationship to nearby blood vessels. |
| Fine needle aspirate | A sampling method that yields cells rather than a tissue core. Often too little material for genomic profiling. |
| KRAS wild-type | Pancreatic cancer without a KRAS alteration. Uncommon, and much more likely to have an actionable finding. |
| Performance status | A measure of how well someone is functioning day to day. It strongly influences what treatment is feasible. |
These are the services most often relevant to this cancer. Which of them applies is a clinical question, not an automatic one.
This entry is educational. It describes what is commonly discussed in this cancer, not what should happen for any individual. Which of it applies depends on the specific diagnosis, stage, prior treatment and the person themselves. Nothing here is a recommendation, and no list of biomarkers here is exhaustive. Decisions belong with a treating team who know the whole case.
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