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Pancreas

C25WHO Vol. 1
Digestive System

Key facts

New cases and deaths (US, 2026 est.)
67,530 new cases and 52,740 deaths estimated (SEER)
5-year relative survival
13.7% overall; 43.6% localized, 17.0% regional, 3.4% distant (SEER 2016–2022)
Stage at diagnosis
51% found after distant spread; only 15% while still localized (US SEER)
Main risk factors
Smoking, excess body weight, diabetes, chronic pancreatitis, family history and hereditary syndromes (NCI PDQ)
Detection
Usually symptomless early; diagnosed with CT/MRI/PET, endoscopic ultrasound, biopsy and the CA 19-9 blood marker (NCI PDQ)
Typical age
Median age at diagnosis: 71 (US SEER)

Pancreatic cancer forms in the tissues of the pancreas, a gland behind the stomach that produces digestive juices and hormones such as insulin. About 95% of cases are exocrine tumors — most often adenocarcinoma arising from the cells that make digestive juices — while pancreatic neuroendocrine tumors form a rarer, distinct group. Early disease usually causes no symptoms; later signs can include jaundice, light-colored stools and dark urine, pain in the upper abdomen or back, unexplained weight loss, loss of appetite, and fatigue. Because early symptoms are absent or resemble other illnesses, and the pancreas lies hidden behind other organs, the disease is often found at an advanced stage — in the United States, about half of cases (51%) are diagnosed only after distant spread. Diagnosis relies on imaging (CT, MRI, PET), endoscopic ultrasound with biopsy, and blood tests including the CA 19-9 tumor marker.

Prognosis

The outlook in pancreatic cancer depends strongly on the stage at diagnosis and on whether the tumor can be completely removed by surgery; the NCI notes that the disease "can be controlled only if it is found before it has spread." In US SEER data (2016–2022), 5-year relative survival is 13.7% overall: 43.6% when the cancer is still localized, 17.0% for regional disease, and 3.4% after distant spread. These are population statistics drawn from many thousands of patients treated in past years — they describe groups, not individuals, and cannot predict the course of any one person's illness; individual outcomes also depend on overall health, response to treatment, and access to newer therapies. Because most cases are detected only after the cancer has spread, the overall averages look severe, yet the outlook for tumors found while still localized is markedly better — stage at detection is the single most important factor behind these numbers.

🔬 Histological Types

📚 Latest Research

2026-09-08

Australian Pancreatic Cyst Registry: protocol for a prospective national clinical quality registry of intraductal papillary mucinous neoplasms.

Poh AR, et al

Australia has launched the Australian Pancreatic Cyst Registry (APCR), a prospective, multicentre national clinical quality registry designed to enrol up to 10,000 individuals with intraductal papillary mucinous neoplasms (IPMNs) — common pancreatic precancer lesions with malignant potential — over a five-year recruitment period. The registry addresses a critical evidence gap caused by existing data being derived predominantly from retrospective surgical cohorts that over-represent high-risk cases and offer limited insight into the outcomes of conservatively managed patients. Operating under an opt-out model across both public and private healthcare settings, the APCR will collect standardised clinical, imaging, and outcome data aligned with the 2024 Kyoto guidelines to evaluate surveillance pathways, guideline adherence, and the predictive performance of established risk stratification frameworks. Findings are expected to directly inform evidence-based IPMN management and reduce variation driven by differing international guideline recommendations.

BMJ open

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2026-09-08

EPHA2 and WNT reciprocally regulate MAPK-dependent gene expression in a pancreatic cancer model.

Wadia SR, et al

A new study in JCI Insight reveals that the receptor tyrosine kinase EPHA2 suppresses EGFR and ERK activation in pancreatic cancer xenografts, and that loss of EPHA2 renders tumors more sensitive to both erlotinib and Wnt pathway inhibitors. Using phosphotyrosine-targeted mass spectrometry, researchers discovered that blocking Wnt signaling triggers robust phosphorylation of EPHA2 and EGFR, yet the resulting ERK hyperactivation remains transcriptionally silent — failing to increase MAPK target gene expression — unless Wnt is simultaneously inhibited, suggesting the transcription factor GATA3 acts as a Wnt-controlled gatekeeper of MAPK output. Critically, while Wnt-high, KRAS-mutant pancreatic cancers are resistant to the EGFR inhibitor erlotinib alone, combining it with a Wnt inhibitor overcomes this resistance. These findings expose actionable therapeutic vulnerabilities in Wnt-addicted pancreatic tumors even in the traditionally intractable EGFR-inhibitor-resistant, RAS-mutant setting.

JCI insight

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2026-09-06

An atypical case with recurrent episodes of pancreatitis: is eosinophilic pancreatitis a diagnosis or a mimic in the spectrum of IgG4-related diseases? A case-based review : Eosinophilic pancreatitis or IGG4-releated disease.

Okyar B, et al

A case report reveals that eosinophilic pancreatitis (EP) can closely mimic both pancreatic malignancy and IgG4-related disease (IgG4-RD), making careful clinicopathological correlation essential to avoid misdiagnosis. A 43-year-old man underwent distal pancreatectomy in 2016 for suspected cancer and subsequently suffered three episodes of acute pancreatitis; re-evaluation of the archival surgical specimen in 2024, triggered by a serum IgG4 level of 304 mg/dL (reference range 3–201 mg/dL) and persistent monocytosis, revealed dense eosinophilic infiltration with microabscesses and non-storiform fibrosis alongside only sparse IgG4-positive plasma cells, ultimately favoring EP over type 1 autoimmune pancreatitis. Critically, the patient lacked peripheral eosinophilia, demonstrating that EP can present atypically and that re-examination of previously resected tissue may be indispensable to establish the correct diagnosis and prevent unnecessary treatment delays.

Clinical journal of gastroenterology

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💊 Therapies

Surgery
Radiation Therapy
Chemotherapy
Targeted therapies

🥗 Diet

Nutritional support during cancer treatment Nutrition in cancer cachexia Sugar and cancer - what the evidence shows Excess body fatness and cancer risk Nutritional support around gastrointestinal cancer surgery Enteral and parenteral nutrition (tube feeding and intravenous feeding) Refeeding syndrome

🫙 Supplements

Omega-3 fatty acids (EPA and DHA) High-dose vitamin C (including intravenous infusions) Mistletoe (Viscum album) Cannabis and cannabinoids (THC, CBD, CBD oils) L-carnitine for cancer-related fatigue

🧪 Tumor markers

Cancer antigen 19-9 Gastrin

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🩺 Centers for this diagnosis

Show all centers for this diagnosis (18) ›
See all › Outpatient clinics for this diagnosis (11) ›

Sources

  1. NCI SEER Cancer Stat Facts: Pancreatic Cancer ↗
  2. NCI PDQ: Pancreatic Cancer Treatment (Patient Version) ↗