Genetic clonal diversity predicts progression to esophageal adenocarcinoma

Nature Genetics

Volumn 38, Issue 4, 2006, Pages 468-473

  Maley, Carlo C ^a   Galipeau, Patricia C ^b   Finley, Jennifer C ^c   Wongsurawat, V Jon ^c   Li, Xiaohong ^b   Sanchez, Carissa A ^b   Paulson, Thomas G ^b   Blount, Patricia L ^b,c   Risques, Rosa Ana ^c   Rabinovitch, Peter S ^b,c   Reid, Brian J ^b,c  

^a WISTAR INSTITUTE   (United States)

^b Fred Hutchinson Cancer Research Center   (United States)

^c UNIVERSITY OF WASHINGTON   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

PROTEIN P53;

ADULT; AGED; ARTICLE; BARRETT ESOPHAGUS; CANCER GENETICS; CARCINOGENESIS; CONTROLLED STUDY; ECOLOGY; ESOPHAGEAL ADENOCARCINOMA; EVOLUTION; FEMALE; GENETIC RISK; GENETIC VARIABILITY; HUMAN; HUMAN TISSUE; MAJOR CLINICAL STUDY; MALE; MOLECULAR CLONING; PLOIDY; PREDICTION; PRIORITY JOURNAL; PROSPECTIVE STUDY; RISK FACTOR;

ADENOCARCINOMA; DISEASE PROGRESSION; ESOPHAGEAL NEOPLASMS; GENES, P16; GENES, P53; HUMANS; IN SITU HYBRIDIZATION, FLUORESCENCE; LOSS OF HETEROZYGOSITY;

EID: 33645396945     PISSN: 10614036     EISSN: 15461718     Source Type: Journal    
DOI: 10.1038/ng1768     Document Type: Article

References (30)

1. Gonzalez-Garcia, I., Sole, R.V. & Costa, J. Metapopulation dynamics and spatial heterogeneity in cancer. Proc. Natl. Acad. Sci. USA 99, 13085-13089 (2002).
2. Rajagopalan, H., Nowak, M.A., Vogelstein, B. & Lengauer, C. The significance of unstable chromosomes in colorectal cancer. Nat. Rev. Cancer 3, 695-701 (2003).
3. Nowell, P.C. The clonal evolution of tumor cell populations. Science 194, 23-28 (1976).
4. Sieber, O.M., Heininmann, K. & Tomlinson, I.P. Genomic instability - the engine of tumorigenesis? Nat. Rev. Cancer 3, 701-708 (2003).
5. Hanahan, D. & Weinberg, R.A. The hallmarks of cancer. Cell 100, 57-70 (2000).
6. Reid, B.J. et al. Predictors of progression in Barrett's esophagus II: baseline 17p (p53) loss of heterozygosity identifies a patient subset at increased risk for neoplastic progression. Am. J. Gastroenterol. 96, 2839-2848 (2001).
7. Rabinovitch, P.S., Longton, G., Blount, P.L., Levine, D.S. & Reid, B.J. Predictors of progression in Barrett's esophagus III: baseline flow cytometric variables. Am. J. Gastroenterol. 96, 3071-3083 (2001).
8. Breivik, J. The evolutionary origin of genetic instability in cancer development. Semin. Cancer Biol. 15, 51-60 (2005).
9. Tsao, J.L. et al. Genetic reconstruction of individual colorectal tumor histories. Proc. Natl. Acad. Sci. USA 97, 1236-1241 (2000).
10. Maley, C.C. et al. Selectively advantageous mutations and hitchhikers in neoplasms: p16 lesions are selected in Barrett's esophagus. Cancer Res. 64, 3414-3427 (2004).
11. Boland, C.R. et al. A National Cancer Institute workshop on microsatellite instability for cancer detection and familial predisposition: development of international criteria for the determination of microsatellite instability in colorectal cancer. Cancer Res. 58, 5248-5257 (1998).
12. Barrett, M.T. et al. Evolution of neoplastic cell lineages in Barrett oesophagus. Nat Genet. 22, 106-109 (1999).
13. Wong, D.J. et al. p16 INK4a lesions are common, early abnormalities that undergo clonal expansion in Barrett's metaplastic epithelium. Cancer Res. 61, 8284-8289 (2001).
14. Haggitt, R.C. Barrett's esophagus, dysplasia, and adenocarcinoma. Hum. Pathol. 25, 982-993 (1994).
15. Rudolph, R.E. et al. The effect of segment length on the risk of neoplastic progression in patients with Barrett's esophagus. Ann. Intern. Med. 132, 612-620 (2000).
16. Doak, S.H. et al. Chromosome 4 hyperploidy represents an early genetic aberration in premalignant Barrett's oesophagus. Gut 52, 623-628 (2003).
17. Conio, M. et al. Long-term endoscopic surveillance of patients with Barrett's esophagus. Incidence of dysplasia and adenocarcinoma: a prospective study. Am. J. Gastroenterol. 98, 1931-1939 (2003).
18. Macdonald, C.E., Wicks, A.C. & Playford, R.J. Final results from 10 year cohort of patients undergoing surveillance for Barrett's oesophagus: observational study. Br. Med. J. 321, 1252-1255 (2000).
19. Shackney, S.E. & Shackney, T.V. Common patterns of genetic evolution in human solid tumors. Cytometry 29, 1-27 (1997).
20. Rocco, J.W. & Sidransky, D. p16(MTS-1/CDKN2/INK4a) in cancer progression. Exp. Cell Res. 264, 42-55 (2001).
21. Sherr, C.J. Tumor surveillance via the ARF-p53 pathway. Genes Dev. 12, 2984-2991 (1998).
22. Sampliner, R.E. Updated guidelines for the diagnosis, surveillance, and therapy of Barrett's esophagus. Am. J. Gastroenterol. 97, 1888-1895 (2002).
23. Magurran, A.E. Measuring Biological Diversity (Blackwell, Malden, Massachusetts, 2004).
24. Clarke, K.R. & Warwick, R.M. A taxonomic distinctness index and its statistical properties. J. Appl. Ecol. 35, 523-531 (1998).
25. Nei, M. Molecular Evolutionary Genetics (Columbia Univ. Press, New York, 1987).
26. Rabinovitch, P.S., Reid, B.J., Haggitt, R.C., Norwood, T.H. & Rubin, C.E. Progression to cancer in Barrett's esophagus is associated with genomic instability. Lab. Invest. 60, 65-71 (1989).
27. Palanca-Wessels, M.C. et al. Extended lifespan of Barrett's esophagus epithelium transduced with the human telomerase catalytic subunit: a useful in vitro model. Carcinogenesis 24, 1183-1190 (2003).
28. Maley, C.C. et al. The combination of genetic instability and clonal expansion predicts progression to esophageal adenocarcinoma. Cancer Res. 64, 7629-7633 (2004).
29. Levine, D.S., Blount, P.L., Rudolph, R.E. & Reid, B.J. Safety of a systematic endoscopic biopsy protocol in patients with Barrett's esophagus. Am. J. Gastroenterol. 95, 1152-1157 (2000).
30. O'Sullivan, J.N. et al. Chromosomal instability in ulcerative colitis is related to telomere shortening. Nat. Genet. 32, 280-284 (2002).