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About Pancreatic Cancer

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About Pancreatic Cancer PowerPoint Presentation

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Published 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)