Molecular pathology of early pancreatic cancer

Issue title: Translational Pathology of Early Cancer

Guest editors: Sudhir Srivastavax and William E. Grizzley

Article type: Research Article

Authors: Remmers, Neeley^a | Bailey, Jennifer M.^b | Mohr, Ashley M.^b | Hollingsworth, Michael A.^{a; b; *}

Affiliations: [a] Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, USA | [b] Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE, USA | [x] Cancer Biomarkers Research Group, Division of Cancer Prevention, National Cancer Institute, Rockville, MD, USA | [y] Department of Pathology, Division of Anatomic Pathology, University of Alabama at Birmingham, Birmingham, AL, USA

Correspondence: [*] Corresponding author: Michael A. Hollingsworth, 986805 Nebraska Medical Center, Omaha, NE 68198, USA. Tel.: +1 402 559 8343; Fax: +1 402 559 3339; E-mail: mahollin@unmc.edu.

Abstract: We describe the pathology of early pancreatic cancer and present an overview of known molecular alterations that occur in these lesions. There are three defined precursor lesions in current models of pancreatic cancer: pancreatic intraepithelial neoplasia (PanIN), mucinous cystic neoplasms (MCN), and intraductal papillary mucinous neoplasms (IPMN). Molecular alterations detected in these lesions include: telomeres, K-ras and downstream targets, p16/CDKN2A, p53, SMAD4/DPC4, microRNAs, mucins and their post-translational processing, inflammatory cytokines, CEACAM, and epigenetic alterations. We summarize previous analyses of these markers as diagnostic markers of disease, and suggest areas of future study.

Keywords: Pancreatic cancer, pancreatic intraepithelial neoplasia (PanIN), mucinous cystic neoplasms (MCN), intraductal papillary mucinous neoplasms (IPMN), mucin, K-ras, p16/CDKN2A, p53, SMAD4/DPC4, microRNA, CEACAM, MIC1, CA19-9

DOI: 10.3233/CBM-2011-0168

Journal: Cancer Biomarkers, vol. 9, no. 1-6, pp. 421-440, 2011