Genomic Instability in Sporadic Colorectal Cancer

A Destabilized Genome Producing Accelerated Cellular Evolution as the Fundamental Nature of Cancer
  • Garth R. Anderson
  • Daniel L. Stoler
  • Morton S. Kahlenberg
  • Nicholas J. Petrelli
Part of the Pezcoller Foundation Symposia book series (PFSO, volume 9)


Two major forms of genomic alterations are seen abundantly in solid tumors (1). The predominant form is intrachromosomal genomic instability, which manifests itself as deletions, insertions, amplifications and translocations (2). The molecular basis of this form of instability has not been established, and recent evidence indicates p53 is unlikely to be involved here (3). A common feature of this major type of instability is an early role for DNA breakage, suggesting nuclease involvement. Aneuploidy produces gains or losses of entire chromosomes, in a process involving p53 and inappropriate meiotic-like segregation (5). Microsatellite instability represents a less common third type of genomic instability which produces oligonucleotide insertions or deletions within repetitive sequences; this is most often seen in hereditary cancer syndromes (e.g. HNPCC), where it somehow tends to preclude the appearance of the other types of instability (6).


Genomic Instability Primer Binding Site Genomic Event Sporadic Colorectal Cancer Hereditary Cancer Syndrome 
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Copyright information

© Springer Science+Business Media New York 1998

Authors and Affiliations

  • Garth R. Anderson
    • 1
    • 2
  • Daniel L. Stoler
    • 1
  • Morton S. Kahlenberg
    • 2
  • Nicholas J. Petrelli
    • 2
  1. 1.Department of Molecular and Cellular BiologyRoswell Park Cancer InstituteBuffaloUSA
  2. 2.Department of Surgical OncologyRoswell Park Cancer InstituteBuffaloUSA

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