Immunophenotype

— neuroendocrine: chromogranin, synaptophysin, CD56.

— hormonal: specific peptides—insulin, glucagon, gastrin, pancreatic polypeptide, VIP, ACTH, somatostatin.

— exocrine carcinoma: cytokeratins (including CK7, CK8, CK18, CK19, ±CK20), CEA, CA19-9, CA-125, MUC I—expressed in >80% of ductal pT1 < 2 cm pT1 < 2 cm

pT2 > 2 cm pT3: into peripancreatic tissue pT2 > 2 cm pT4: into

Figure 3.6. Pancreatic carcinoma.

pT4: into pT4: into coeliac axis or superior mesenteric artery

Figure 3.6. Pancreatic carcinoma.

lesions, ±CDX-2. Prognosis

Prognosis in pancreatic ductal carcinoma is poor with most patients dead within several months. It relates to tumour site (body and tail are worse than head, as the latter may present early with obstructive jaundice), size (>4.5 cm is adverse), histological grade and stage. Overall 5-year survival is 2%, even disease confined to the pancreas only reaching 15%. There is limited suitability for resection (5-10% of cases), namely, node-negative tumours of the pancreatic head <3 cm diameter with no major (superior mesenteric or portal) vessel invasion. The majority present with advanced disease into lymph node and retroperitoneal tissues. Treatment is palliative with relief of ductal biliary obstruction by open or laparoscopic bypass or endoscopic stent insertion. Mucinous cystic tumours are less frequent but potentially resectable. Pancreatic endocrine tumours may present with their associated metabolic or gastrointestinal syndrome and have an indolent time course being of low- to intermediate-grade malignancy. Ampullary carcinoma is more favourable than pancreatic or bile duct carcinoma with a 5-year survival of 25-50%. This can improve to 80-85% if the tumour is at an early stage and confined to the sphincter of Oddi (pT1). Transduodenal wide local excision may be adequate for carefully selected ampullary tumours, e.g. adenoma, but only after careful staging and exclusion of an underlying mass lesion requiring radical surgery.

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