EvidencePancreatic ductal adenocarcinoma

The IHC 3+ subgroup result is why the tumour-agnostic label is written at 3+ and not 2+, and why a gallbladder cancer with a strong HER2 stain now has two on-label choices (zanidatamab, trastuzumab deruxtecan) after chemotherapy. Lung toxicity again ran higher than in breast cancer.

For someone offered the test, these are the numbers that describe what a result means in an NHS population: about 1 in 100 tests came back positive each year, between 46 and 58 in 100 positives were cancer, and a negative result left about 1 in 100 with an undetected cancer within the year. The test found between a quarter and a third of all cancers diagnosed in a screening round, and about half to two thirds of the 12 cancer types it was designed to find. Whether finding them this way reduces late-stage diagnoses is the primary question, and this paper says only that the answer was no; the primary-endpoint paper had not appeared on Europe PMC by 23 September 2026.

Every KRAS wild-type pancreatic cancer should be tested for NRG1 fusions because a specific, approved antibody now exists; zenocutuzumab is the first targeted drug approved for a pancreatic cancer driver.

The current international standard for deciding which pancreatic cysts to operate on, which to watch and for how long.

Upfront surgery followed by adjuvant chemotherapy remains standard for clearly resectable pancreatic cancer; neoadjuvant treatment belongs in trials or borderline disease.

This series is the standard reference for US cancer numbers and the source of most headlines about cancer in younger adults. The gap between falling mortality and rising incidence is the argument for both continued treatment advances and stronger prevention and screening.

Sotorasib is a guideline-listed later-line option for the 1 to 2 percent of pancreatic cancers with KRAS G12C, and the proof that KRAS in pancreatic cancer is druggable; the larger opportunity lies with inhibitors of G12D and pan-RAS drugs.

Supports neoadjuvant therapy, preferably chemotherapy, for borderline resectable pancreatic cancer while larger trials define the regimen.

ESPAC5 supports neoadjuvant chemotherapy over immediate surgery in borderline resectable disease and points to FOLFIRINOX as the regimen to build on.

Adagrasib joins sotorasib as a later-line option for KRAS G12C pancreatic cancer in guidelines; both drugs are the template for the G12D and pan-RAS inhibitors now in pancreatic trials.

For fit patients with newly diagnosed metastatic pancreatic cancer, a FOLFIRINOX-type regimen is now proven to be better than gemcitabine plus nab-paclitaxel, settling a long-standing debate. The absolute gain is about two months of median survival, and the regimen is more toxic for the gut. Whether liposomal irinotecan adds anything over conventional irinotecan (standard FOLFIRINOX) has never been tested head-to-head.

Pancreatic cancer was thought to be immunologically inert because of its low mutation burden; this study showed that with the right vaccine platform its few neoantigens can still be targeted. It is the strongest human evidence so far that personalised cancer vaccines can generate durable, tumour-specific immunity, and it justifies the randomised trials now running in pancreatic cancer and melanoma. Benefit is not yet proven, because responders may simply have had more immunogenic tumours.

Neoadjuvant modified FOLFIRINOX without routine radiotherapy became the reference approach for borderline resectable disease in North America; radiotherapy is reserved for selected patients or trials.

Olaparib maintenance remains a standard option because of its progression-free benefit, tolerability and long-term survivors, but patients should know that it has not been shown to extend average survival.

Neoadjuvant treatment is now the standard for borderline resectable pancreatic cancer, and PREOPANC is the trial guidelines cite; the follow-on PREOPANC-2 tested FOLFIRINOX in the same setting.

Every pancreatic cancer should be tested for mismatch repair deficiency because the 1 percent who have it can receive pembrolizumab, but responses in pancreatic cancer are less frequent and less durable than in other MSI-high cancers.

Gemcitabine plus cisplatin is a validated platinum doublet for BRCA or PALB2 carriers, and the trial explains why PARP inhibitors are used as maintenance after platinum rather than concurrently with it.

Together with the German MASTER report, this paper is why guidelines recommend comprehensive profiling with fusion detection in KRAS wild-type pancreatic cancer.

Germline testing for every pancreatic cancer patient, platinum first line for BRCA carriers, and olaparib maintenance for those who respond are all downstream of POLO.

CONCORD is the evidence base for national cancer plans and for the statement that where you live changes your chance of surviving cancer. Its country tables are the benchmark health systems use to judge early diagnosis and treatment access.

European centres manage pancreatic cysts by this guideline; its lifelong surveillance stance is the main point of difference from the American and Kyoto guidelines.

KRAS wild-type status should trigger fusion testing, ideally by RNA sequencing, because NRG1 fusions can be targeted by HER-family inhibitors and now by zenocutuzumab.

Guidelines recommending universal mismatch repair testing in pancreatic cancer, by immunohistochemistry or sequencing rather than PCR alone, rest on this and similar series.

Modified FOLFIRINOX is the adjuvant standard for patients who recover well from a pancreatic resection and can tolerate combination chemotherapy; gemcitabine-based regimens remain for those who cannot.

Gemcitabine plus capecitabine became the adjuvant standard after resection and remains the option for patients unfit for modified FOLFIRINOX.

Gemcitabine plus capecitabine became the adjuvant regimen for patients unfit for modified FOLFIRINOX, and remains the comparator in European trials of adjuvant treatment.

This paper established a new regulatory paradigm: a drug approved for a molecular feature regardless of organ. It made MSI/MMR testing standard across advanced cancers and remains the clearest example of a biomarker that works across histologies. It also anchored the idea that mutation load, via neoantigens, is what makes tumours visible to T cells.

Most radiology reports and surgical decisions on pancreatic cysts still follow the Fukuoka criteria or their 2024 Kyoto revision.

Maintaining a healthy weight is now established cancer prevention for over a dozen cancer types. For clinicians and policymakers, obesity belongs alongside tobacco and alcohol in prevention strategy. Whether intentional weight loss in adulthood reverses risk is still being studied, including in trials of GLP-1 drugs.

Consolidation chemoradiotherapy is optional in locally advanced pancreatic cancer, used for local control rather than survival; erlotinib has no role.

Systemic chemotherapy is the backbone for locally advanced pancreatic cancer; consolidation chemoradiotherapy is an option to control local symptoms or as a bridge to surgery rather than a survival treatment.

Acinar cell carcinoma should be sequenced: RAF fusions and DNA repair defects offer targeted and platinum or PARP inhibitor options that ductal adenocarcinoma rarely has.

This paper reframed pancreatic and liver cancer as the coming burden and is cited in most arguments for investing in them. Its pancreatic cancer projection has been tracking close to reality in the years since.

Adjuvant chemotherapy is standard after pancreatic cancer resection; gemcitabine alone remains the option for patients who cannot tolerate combinations.

With FOLFIRINOX this trial defined the two chemotherapy standards for metastatic pancreatic cancer that still apply, and the gemcitabine and nab-paclitaxel backbone is the comparator in most current first-line pancreatic trials.

The most frequently mutated oncogene in cancer stopped being undruggable, and patients with KRAS G12C lung and bowel cancers now have targeted pills. The approach, exploiting a mutation-created chemical handle and an inactive-state pocket, has become a template for other hard targets.

The paper underpins the WHO diagnostic criteria for acinar cell carcinoma and its variants and supports aggressive surgery for localised disease.

The EXPeRT recommendations, surgery when feasible and PLADO chemotherapy for unresectable or metastatic disease, remain the treatment framework for childhood pancreatoblastoma.

FOLFIRINOX and, soon after, gemcitabine plus nab-paclitaxel ended the era of single-agent gemcitabine for metastatic pancreatic cancer. The regimen's modified form later improved survival after surgery in PRODIGE 24, and its toxicity is why fitness, not just stage, decides which treatment a patient is offered.

Either regimen was acceptable adjuvant therapy in 2010, with gemcitabine preferred for tolerability; combination regimens (ESPAC-4, PRODIGE 24) have since superseded both.

Acinar cell carcinoma justifies an aggressive surgical approach, including for larger tumours and selected metastatic disease, because the natural history is far better than ductal adenocarcinoma.

The review is the usual citation for the natural history of pancreatoblastoma and for the recommendation of resection with chemotherapy for advanced disease.

Smoking is the single largest preventable cause of cancer death, and quitting at any age helps, with the greatest gain from quitting young. Cessation support belongs in every cancer service, including lung screening programmes.

This is the study most often cited for the size of the obesity and cancer link, and it broadened the list of weight-related cancers well beyond the few known before. It underlies weight management advice in cancer prevention guidance and the current interest in whether GLP-1 drugs change cancer risk.

This trial introduced a patient-centred composite endpoint and a drug that remained the backbone of pancreatic cancer treatment for a generation. Its small survival gain also shows how low the bar was, which is the context for the FOLFIRINOX and MPACT trials that followed.

Pathologists diagnose pancreatoblastoma by the criteria set out here, and the paper established that the paediatric and adult forms behave differently.

This series defined the diagnostic criteria still used for acinar cell carcinoma and established that it should be classified and treated as a distinct disease from ductal adenocarcinoma.