Barrett Esophagus

Carlo C Maley, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA
Brian J Reid, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA

Published online: January 2006

DOI: 10.1038/npg.els.0006068

The evolution of neoplastic cell lineages in Barrett esophagus is dominated by mutation, natural selection and genetic drift. The esophageal environment and therapies select for clones with competitive advantages that undergo selective sweeps, driving other cell types to extinction and providing a mechanism for expansion of neutral mutations as hitchhikers on the sweep.

Keywords: Barrett's; esophagus; cancer; evolution; selective sweep; genetic drift; hitchhiker; neoplastic progression

Figure 1. There are multiple genetic routes to cancer in Barrett esophagus (BE). Each node in the diagram represents a cell population observed in our cohort. Clones were defined by loss of heterozygosity (LOH) assays. Nodes labeled 2N represent diploid cells that were ki67 positive, a nuclear antigen expressed by proliferating cells. Nodes labeled 4N represent biopsies with greater than 6% tetraploid cells. Nodes labeled aneuploid represent biopsies that included cells with abnormal complements of chromsomes, being neither diploid nor tetraploid. Each connection between two nodes represents an inferred ancestral relationship between two clones observed in the same individual. However, different branches in the diagram may have been observed in different individuals. The diagram is thus a summary, over the entire cohort, of the variety of different genetic routes to cancer. This stands in contrast to a strict linear ordering of genetic lesions in progression to cancer. (Reproduced with permission from Barrett et al., 1999)
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 Further Reading
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    Rabinovitch PS, Longton G, Blount PL, Levine DS and Reid BJ (2001) Predictors of progression in Barrett's esophagus III: baseline flow cytometric variables. American Journal of Gastroenterology 96: 3071–3083.
    Reid BJ, Prevo LJ, Galipeau PC, et al. (2001) Predictors of progression in Barrett's esophagus II: baseline 17p (p53) loss of heterozygosity identifies a patient subset at increased risk for neoplastic progression. American Journal of Gastroenterology 96: 2839–2848.
 Web Links
    ePath Barrettsinfo.com.Complete, peer-reviewed information on Barrett esophagus, with references http://www.barrettsinfo.com
    ePath Cyclin-dependent kinase inhibitor 2A (melanoma, p16, inhibits CDK4) (CDKN2A); Locus ID: 1029. LocusLink: http://www.ncbi.nlm.nih.gov/LocusLink/LocRpt.cgi?l=1029
    ePath Tumor protein p53 (Li–Fraumeni syndrome) (TP53); Locus ID: 7157. LocusLink: http://www.ncbi.nlm.nih.gov/LocusLink/LocRpt.cgi?l=7157
    ePath Cyclin-dependent kinase inhibitor 2A (melanoma, p16, inhibits CDK4) (CDKN2A); MIM number: 600160. OMIM: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?600160
    ePath Tumor protein p53 (Li–Fraumeni syndrome) (TP53); MIM number: 191170. OMIM: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?191170

Related Sub-Topics:

Evolution: Theories and Ideas | Evolutionary Processes | Selection and Variation | Population Structure and Genetics | Specific Genetic Disorders | Mutational Mechanisms of Genetic Disease | Cancer Genetics
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Article Title: Barrett Esophagus
 
How to Cite close
Maley, Carlo C, and Reid, Brian J(Jan 2006) Barrett Esophagus. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1038/npg.els.0006068]