Journal home
Advance online publication
Current issue
Archive
Press releases
Free Association (blog)
Supplements
Focuses
Guide to authors
Online submissionOnline submission
For referees
Free online issue
Contact the journal
Subscribe
Advertising
work@npg
Reprints and permissions
About this site
For librarians
 
NPG Resources
Nature
Nature Biotechnology
Nature Cell Biology
Nature Medicine
Nature Methods
Nature Reviews Cancer
Nature Reviews Genetics
Nature Reviews Molecular Cell Biology
news@nature.com
Nature Conferences
RNAi Gateway
NPG Subject areas
Biotechnology
Cancer
Chemistry
Clinical Medicine
Dentistry
Development
Drug Discovery
Earth Sciences
Evolution & Ecology
Genetics
Immunology
Materials Science
Medical Research
Microbiology
Molecular Cell Biology
Neuroscience
Pharmacology
Physics
Browse all publications
Letter
Nature Genetics 38, 468 - 473 (2006)
Published online: 26 March 2006; | doi:10.1038/ng1768

Genetic clonal diversity predicts progression to esophageal adenocarcinoma

Carlo C Maley1, Patricia C Galipeau2, 3, Jennifer C Finley4, V Jon Wongsurawat5, Xiaohong Li2, 3, Carissa A Sanchez2, 3, Thomas G Paulson2, 3, Patricia L Blount2, 3, 5, Rosa-Ana Risques4, Peter S Rabinovitch2, 3, 4 & Brian J Reid2, 3, 5, 6

1  The Wistar Institute, 3601 Spruce St., Philadelphia, Pennsylvania 19104, USA.

2  Division of Human Biology, Fred Hutchinson Cancer Research Center, P.O. Box 19024, Seattle, Washington 98109, USA.

3  Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, P.O. Box 19024, Seattle, Washington 98109, USA.

4  Department of Pathology, University of Washington, Seattle, Washington 98195, USA.

5  Department of Medicine, University of Washington, Seattle, Washington 98195, USA.

6  Department of Genome Sciences, University of Washington, Seattle, Washington 98195, USA.

Correspondence should be addressed to Carlo C Maley cmaley@alum.mit.edu

Neoplasms are thought to progress to cancer through genetic instability generating cellular diversity1, 2 and clonal expansions driven by selection for mutations in cancer genes3, 4. Despite advances in the study of molecular biology of cancer genes5, relatively little is known about evolutionary mechanisms that drive neoplastic progression. It is unknown, for example, which may be more predictive of future progression of a neoplasm: genetic homogenization of the neoplasm, possibly caused by a clonal expansion, or the accumulation of clonal diversity. Here, in a prospective study, we show that clonal diversity measures adapted from ecology and evolution can predict progression to adenocarcinoma in the premalignant condition known as Barrett's esophagus, even when controlling for established genetic risk factors, including lesions in TP53 (p53; ref. 6) and ploidy abnormalities7. Progression to cancer through accumulation of clonal diversity, on which natural selection acts, may be a fundamental principle of neoplasia with important clinical implications.


MORE ARTICLES LIKE THIS

These links to content published by NPG are automatically generated.

NEWS AND VIEWS

Clonal diversity in tumor progression

Nature Genetics News and Views (01 Apr 2006)

Chromosome instability leaves its mark

Nature Genetics News and Views (01 Sep 2006)

 Top
Abstract
Previous | Next
Table of contents
Full textFull text
Download PDFDownload PDF
Send to a friendSend to a friend
rights and permissionsRights and permissions
CrossRef lists 290 articles citing this articleCrossRef lists 290 articles citing this article
Save this linkSave this link
Figures & Tables
Supplementary info
See also: News and Views by Shibata
Export citation

natureevents

natureproducts

Search buyers guide:

 
Nature Genetics
ISSN: 1061-4036
EISSN: 1546-1718
Journal home | Advance online publication | Current issue | Archive | Press releases | Supplements | Focuses | For authors | Online submission | Permissions | For referees | Free online issue | About the journal | Contact the journal | Subscribe | Advertising | work@npg | naturereprints | About this site | For librarians
Nature Publishing Group, publisher of Nature, and other science journals and reference works©2006 Nature Publishing Group | Privacy policy