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About Pancreatic Cancer PowerPoint Presentation

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On : Feb 24, 2014

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  • Slide 1 - Pancreatic cancer Ayman Hasan Linjawi, MD, FRCSC, Consultant general and oncology surgery
  • Slide 2 - Pancreatic cancer Rare tumor, round 200 cases per year newly diagnosed patient in Saudi Arabia Risk factors:
  • Slide 3 - Molecular genetics Tumor suppressor genes: function to control cellular proliferation. When they are mutated, abnormal growth to the cell will happen. Examples, p53, p16, BRACA2….. Oncogenes: derived from protooncogenes. Activation of these proteins will lead to abnormal cell growth, example I K-ras Mismatch-repair genes: function to insure the accuracy of DNA replication (maintenance) therefore when mutated abnormal growth will happen. Example, bMSH2, bMLH1.
  • Slide 4 - Pathology Tumor of the pancreas are endocrine and exocrine. The most common neoplasm of the exocrine pancreas (our topic) is adenocarcinomas. 60% arise from the head, 15% body or tail and 20% diffusely involve the whole gland They are either solid or cystic.
  • Slide 5 - Solid epithelial tumors Ductal adenocarcinomas: 75% of all nonedocrine pancreatic cancer, aggressive tumor metastasis to liver, peritoneum and lung in 80%, the precursor lesions are referred to pancreatic intra epithelial neoplasm (pan IN) or carcinoma in situ. Adenosquamous carcinomas: rare, contains both glandular and squamous differentiation, more common in patient received chemoradiation therapy. Acinar cell carcinomas: rare, common in male, larger size, slightly better prognosis.
  • Slide 6 - Solid epithelial tumors Giant cell carcinoma: large size, more than 15cm, poorer prognosis. Pancreatoblastoma: occur primarily in children age 1 to 15 years.
  • Slide 7 - Cystic epithelial tumors Serous cystic neoplasm: more in female, vary in size, 30% asymptomatic, symptoms include epigastric pain and nausia, located anywhere in pancreas and do no communicate with pancreatic ducts, CT shows honeycomb pattern, rarely malignant (known by metastasis). Mucinous cystic neoplasm: common in female (9:1 ratio ), do not communicate with pancreatic duct, associated with ovarian type of stroma, 33% associated with invasive carcinoma, 70% arise from body and tail, therefore it is considered premalignant and should be resected.
  • Slide 8 - Cystic epithelial tumors Intraductal papillary mucinous neoplasm: intraductal mucin producing neoplasm, involve the main pancreatic duct or major side branches (communicate with the duct), more common in head and neck and uncinate process, male=female, mucin can be seen oozing from the ampulla of Vater in ERCP, has malignant potential and should be resected. Solid and cystic papillary neoplasm: primarily in woman (Hamoudi tumor), treated by resection and rarely metastasis.
  • Slide 9 - Diagnosis Symptoms and signs: Virchow node: left supraclavicular adenopathy. Sister Mary Joseph node: periumblical adenopathy. Blumers shelf: pelvic drop metastasis
  • Slide 10 - Diagnosis Lab test: increase lft, bilirubin, INR (decrease hepatic production of vitamin K-dependent clotting factor). Increase CA 19-9. Radiological test: trans abdominal ultrasound (TAUS) for assessment and biopsy, CT scan for assessment and metastasis, MRCP for assessment of biliary duct, ERCP for assessment of biliary duct and brush biopsy
  • Slide 11 - Signs of irresectability Metastasis to any organ Involvement of superior mesenteric vein or artery Portal vein involvement Celiac axis involvement Splenic vein involvement
  • Slide 12 - Treatment Surgical excision is the only hope for cure Total or subtotal pancreatectomy for body and tail. Pancreaticoduodenectomy for head and uncinate process (whipple). 5 year survival rate is only 10% with successful surgery
  • Slide 13 - Surgical treatment
  • Slide 14 - Treatment Adjuvant chemotherapy and radiotherapy: did not show significant improvement of DFS and OS. Neoadjuvant chemotherapy: also failed to show any benefit , used reduce tumor size (down stage the tumor)

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