Literature DB >> 10454945

Early diagnosis and treatment of pancreatic dysplasia in patients with a family history of pancreatic cancer.

T A Brentnall1, M P Bronner, D R Byrd, R C Haggitt, M B Kimmey.   

Abstract

BACKGROUND: Pancreatic cancer, the fourth most common cause of cancer death in the United States, is hereditary in an estimated 10% of cases. Surveillance of patients with a familial predisposition for pancreatic cancer has not been systematically evaluated.
OBJECTIVE: To develop a surveillance program that can identify and treat patients who have precancerous conditions of the pancreas and a family history of pancreatic cancer.
DESIGN: Prospective cohort study.
SETTING: University medical center. PATIENTS: 14 patients from three kindreds with a history of pancreatic cancer.
INTERVENTIONS: Endoscopic ultrasonography, endoscopic retrograde cholangiopancreatography (ERCP), spiral computed tomography, and serum carcinoembryonic antigen and CA19-9 analysis were performed in all patients. Four affected patients were tested for the K-ras mutation. MAIN OUTCOME MEASUREMENT: Pancreatic dysplasia was determined by histologic evaluation.
RESULTS: Seven of the 14 patients were believed to have dysplasia on the basis of clinical history and abnormalities on endoscopic ultrasonography and ERCP and were referred for pancreatectomy. All 7 patients had histologic evidence of dysplasia in pancreatectomy specimens. Findings on endoscopic ultrasonography were subtle, nonspecific, and similar to those seen in patients with chronic pancreatitis. Findings on ERCP ranged from mild and focal side-branch duct irregularities and small sacculations to main-duct strictures and grapelike clusters of saccules. Some of these changes are typical of chronic pancreatitis, but others are more distinctive. Spiral computed tomography and serum tumor markers had low sensitivity in the detection of pancreatic dysplasia. Analysis for the K-ras mutation yielded positive results in 3 of 4 patients with dysplasia.
CONCLUSIONS: Thorough screening of patients with a family history of pancreatic cancer is feasible. Clinical data combined with imaging studies (endoscopic ultrasonography and ERCP) can be used to identify high-risk patients who have dysplasia. The role of molecular genetic testing is uncertain at this time.

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Year:  1999        PMID: 10454945     DOI: 10.7326/0003-4819-131-4-199908170-00003

Source DB:  PubMed          Journal:  Ann Intern Med        ISSN: 0003-4819            Impact factor:   25.391


  129 in total

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Review 3.  Familial pancreatic cancer--current knowledge.

Authors:  Detlef K Bartsch; Thomas M Gress; Peter Langer
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4.  Targeted screening of individuals at high risk for pancreatic cancer: results of a simulation model.

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5.  Genetic susceptibility to pancreatic cancer.

Authors:  Alison P Klein
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Review 6.  Update on familial pancreatic cancer.

Authors:  H T Lynch; R E Brand; C A Deters; R M Fusaro
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7.  Periampullary and pancreatic incidentaloma: a single institution's experience with an increasingly common diagnosis.

Authors:  Jordan M Winter; John L Cameron; Keith D Lillemoe; Kurtis A Campbell; David Chang; Taylor S Riall; Joann Coleman; Patricia K Sauter; Marcia Canto; Ralph H Hruban; Richard D Schulick; Michael A Choti; Charles J Yeo
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8.  KrasG12D-induced IKK2/β/NF-κB activation by IL-1α and p62 feedforward loops is required for development of pancreatic ductal adenocarcinoma.

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Review 9.  Precursors to pancreatic cancer.

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