Molecular pathways in pancreatic carcinogenesis

Authors

  • Anne M. Macgregor-Das BS,

    1. Pathobiology Program, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins Medical Institutions, Baltimore, Maryland
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  • Christine A. Iacobuzio-Donahue MD, PhD

    Corresponding author
    1. Pathobiology Program, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins Medical Institutions, Baltimore, Maryland
    2. Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins Medical Institutions, Baltimore, Maryland
    • Department of Pathology The Johns Hopkins Hospital, 1550 Orleans Street, CRBII 343, Baltimore, MD 21231. Fax: 410-614-0671.===

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  • The authors have no financial conflicts of interest to disclose related to this work.

Abstract

Pancreatic cancer is a genetic disease. Pancreatic cancers develop from one of three precursor lesions, pancreatic intraepithelial neoplasia (PanIN), intraductal papillary mucinous neoplasms (IPMNs), and mucinous cystic neoplasms (MCNs), and each arises in association with distinct genetic alterations. These alterations not only provide insight into the fundamental origins of pancreatic cancer but provide ample opportunity for improving early diagnosis and management of cystic precursors. J. Surg. Oncol. 2013;107:8–14. © 2012 Wiley Periodicals, Inc.

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