The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
17p (p53) allelic losses, 4N (G2/tetraploid) populations, and progression to aneuploidy in Barrett's esophagus.
Open accessAbstract
Increased 4N (G2/tetraploid) cell populations have been postulated to be genetically unstable intermediates in the progression to many cancers, but the mechanism by which they develop and their relationship to instability have been difficult to investigate in humans in vivo. Barrett's esophagus is an excellent model system in which to investigate the order in which genetic and cell cycle abnormalities develop relative to each other during human neoplastic progression. Neoplastic progression in Barrett's esophagus is characterized by inactivation of the p53 gene, the development of increased 4N (G2/tetraploid) cell fractions, and the appearance of aneuploid cell populations. We investigated the hypothesis that patients whose biopsies have increased 4N (G2/tetraploid) cell fractions are predisposed to progression to aneuploidy and determined the relationship between inactivation of p53 and the development of 4N abnormalities in Barrett's epithelium. Our results indicate that increased 4N (G2/tetraploid) populations predict progression to aneuploidy and that the development of 4N abnormalities is interdependent with inactivation of the p53 gene in Barrett's esophagus in vivo.
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Cites
p53 Mutations in Human Cancers
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Mice Lacking p21CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control
Deng, C., Zhang, P., Wade Harper, J., Elledge, S. J., & Leder, P. (1995) · Cell · doi:10.1016/0092-8674(95)90039-x · Cited by 2,113
Cited by
The causes and consequences of genetic heterogeneity in cancer evolution
Burrell, R. A., McGranahan, N., Bartek, J., & Swanton, C. (2013) · Nature · doi:10.1038/nature12625 · Cited by 2,262
How Proteolysis Drives the Cell Cycle
King, R. W., Deshaies, R. J., Peters, J.-M., & Kirschner, M. W. (1996) · Science · doi:10.1126/science.274.5293.1652 · Cited by 1,273
Cytokinesis failure generating tetraploids promotes tumorigenesis in p53-null cells
Fujiwara, T., Bandi, M., Nitta, M., Ivanova, E. V., Bronson, R. T., & Pellman, D. (2005) · Nature · doi:10.1038/nature04217 · Cited by 1,067
Boveri revisited: chromosomal instability, aneuploidy and tumorigenesis
Holland, A. J., & Cleveland, D. W. (2009) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2718 · Cited by 859
Telomeres in cancer: tumour suppression and genome instability
Maciejowski, J., & de Lange, T. (2017) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm.2016.171 · Cited by 745
Metadata
- Authors
- Galipeau, P. C., Cowan, D. S., Sanchez, C. A., Barrett, M. T., Emond, M. J., Levine, D. S., Rabinovitch, P. S., & Reid, B. J.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1996-07-09
- Volume
- 93
- Issue
- 14
- Pages
- 7081-7084
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2141513637
- Cited by
- 360
- References
- 4
- FWCI
- 8.33
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: 17p (p53) allelic losses, 4N (G2/tetraploid) populations, and progression to aneuploidy in Barrett's esophagus. https://app.cochat.ai/papers/10.1073/pnas.93.14.7081
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- Galipeau, P. C., Cowan, D. S., Sanchez, C. A., Barrett, M. T., Emond, M. J., Levine, D. S., Rabinovitch, P. S., & Reid, B. J. (1996). 17p (p53) allelic losses, 4N (G2/tetraploid) populations, and progression to aneuploidy in Barrett's esophagus. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.93.14.7081
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
