The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Heterozygous Deletion of Mitotic Arrest–Deficient Protein 1 (MAD1) Increases the Incidence of Tumors in Mice
Abstract
Mitotic arrest–deficient protein 1 (MAD1) is a component of the mitotic spindle assembly checkpoint. We have created a knockout mouse model to examine the physiologic consequence of reduced MAD1 function. Mad1+/− mice were successfully generated, but repeated paired mating of Mad1+/− with Mad1+/− mice failed to produce a single Mad1−/− animal, suggesting that the latter genotype is embryonic lethal. In aging studies conducted for >18 months, Mad1+/− mice compared with control wild-type (wt) littermates showed a 2-fold higher incidence of constitutive tumors. Moreover, 42% of Mad1+/− (P < 0.03), but 0% of wt, mice developed neoplasia after treatment with vincristine, a microtubule depolymerization agent. Mad1+/− mouse embryonic fibroblasts (MEF) were found to be more prone than wt cells to become aneuploid; Mad1+/−, but not wt, MEFs produced fibrosarcomas when explanted into nude mice. Our results indicate an essential MAD1 function in mouse development and correlate Mad1 haploinsufficiency with increased constitutive tumors. [Cancer Res 2007;67(1):160–6]
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Cites
BubR1 insufficiency causes early onset of aging-associated phenotypes and infertility in mice
Baker, D. J., Jeganathan, K. B., Cameron, J. D., Thompson, M., Juneja, S., Kopecka, A., Kumar, R., Jenkins, R. B., de Groen, P. C., Roche, P., et al. (2004) · Nature Genetics · doi:10.1038/ng1382 · Cited by 731
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Matsuoka, M., & Jeang, K.-T. (2007) · Nature Reviews Cancer · doi:10.1038/nrc2111 · Cited by 829
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Kim, H.-S., Vassilopoulos, A., Wang, R.-H., Lahusen, T., Xiao, Z., Xu, X., Li, C., Veenstra, T. D., Li, B., Yu, H., et al. (2011) · Cancer Cell · doi:10.1016/j.ccr.2011.09.004 · Cited by 537
Proliferation of aneuploid human cells is limited by a p53-dependent mechanism
Thompson, S. L., & Compton, D. A. (2010) · Journal of Cell Biology · doi:10.1083/jcb.200905057 · Cited by 494
Bolton, H., Graham, S. J. L., Van der Aa, N., Kumar, P., Theunis, K., Fernandez Gallardo, E., Voet, T., & Zernicka-Goetz, M. (2016) · Nature Communications · doi:10.1038/ncomms11165 · Cited by 451
Metadata
- Authors
- Iwanaga, Y., Chi, Y.-H., Miyazato, A., Sheleg, S., Haller, K., Peloponese, J.-M., Li, Y., Ward, J. M., Benezra, R., & Jeang, K.-T.
- Venue
- Cancer Research
- Published
- 2007-01-01
- Volume
- 67
- Issue
- 1
- Pages
- 160-166
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- OpenAlex
- W2057164389
- Cited by
- 189
- References
- 1
- FWCI
- 6.45
- Type
- journal article
- Language
- en
- Open access
- closed
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- Iwanaga, Y., Chi, Y.-H., Miyazato, A., Sheleg, S., Haller, K., Peloponese, J.-M., Li, Y., Ward, J. M., Benezra, R., & Jeang, K.-T. (2007). Heterozygous Deletion of Mitotic Arrest–Deficient Protein 1 (MAD1) Increases the Incidence of Tumors in Mice. Cancer Research. https://doi.org/10.1158/0008-5472.can-06-3326
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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