Molecular Genetics of Pancreatic Cancer

  • Eric S. Calhoun
  • Scott E. Kern
Part of the M. D. Anderson Solid Tumor Oncology Series book series (MDA)

In cancer, genome stability is compromised. Ductal adenocarcinoma of the pancreas is no exception. Considerable progress in the identification and characterization of somatic and/or germline genetic alterations has provided the mechanistic foundations of this genetically complex disease. Numerous alterations, including chromosomal copy-number gains, amplifications and homozygous deletions, loss of heterozygosity (LOH) with and without copy number reduction, and balanced and unbalanced structural re-arrangements, are commonly observed (1–4). Gross chromosomal changes are often complemented by smaller, more subtle alterations affecting the open reading frames of proto-oncogenes, tumor suppressors, and genome caretaker genes (5–8). Continued evaluation of these and additional yet-unidentified genetic alterations should translate into rational diagnostic and treatment strategies.

This chapter describes the spectrum and frequency of genetic alterations observed in ductal adenocarcinomas of the pancreas, as organized by the underlying presence of two, largely mutually exclusive, types of genome instability: chromosomal instability (CIN) and microsatellite instability (MIN). This distinction is justified, as each tumor type exhibits unique histologic and molecular characteristics ( 9 ).


Pancreatic Cancer Pancreatic Carcinoma Pancreatic Adenocarcinoma Fanconi Anemia Homozygous Deletion 
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© Springer Science + Business Media, LLC 2008

Authors and Affiliations

  • Eric S. Calhoun
    • 1
  • Scott E. Kern
    • 1
  1. 1.The Sidney Kimmel Comprehensive Cancer CenterJohn Hopkins University School of MedicineBaltimoreUSA

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