共 57 条
Mad2 overexpression promotes aneuploidy and tumorigenesis in mice
被引:517
作者:

Sotillo, Rocio
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机构: Mem Sloan Kettering Canc Ctr, Canc Biol & Genet Program, New York, NY 10021 USA

Hernando, Eva
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机构: Mem Sloan Kettering Canc Ctr, Canc Biol & Genet Program, New York, NY 10021 USA

Diaz-Rodriguez, Elena
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机构: Mem Sloan Kettering Canc Ctr, Canc Biol & Genet Program, New York, NY 10021 USA

Teruya-Feldstein, Julie
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机构: Mem Sloan Kettering Canc Ctr, Canc Biol & Genet Program, New York, NY 10021 USA

Cordon-Cardo, Carlos
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机构: Mem Sloan Kettering Canc Ctr, Canc Biol & Genet Program, New York, NY 10021 USA

Lowe, Scott W.
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机构: Mem Sloan Kettering Canc Ctr, Canc Biol & Genet Program, New York, NY 10021 USA

Benezra, Robert
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机构: Mem Sloan Kettering Canc Ctr, Canc Biol & Genet Program, New York, NY 10021 USA
机构:
[1] Mem Sloan Kettering Canc Ctr, Canc Biol & Genet Program, New York, NY 10021 USA
[2] Mem Sloan Kettering Canc Ctr, Dept Pathol, New York, NY 10021 USA
[3] Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA
来源:
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D O I:
10.1016/j.ccr.2006.10.019
中图分类号:
R73 [肿瘤学];
学科分类号:
100214 ;
摘要:
Mad2 is an essential component of the spindle checkpoint that blocks activation of Separase and dissolution of sister chromatids until microtubule attachment to kinetochores is complete. We show here that overexpression of Mad2 in transgenic mice leads to a wide variety of neoplasias, appearance of broken chromosomes, anaphase bridges, and whole-chromosome gains and losses, as well as acceleration of myc-induced lymphomagenesis. Moreover, continued overexpression of Mad2 is not required for tumor maintenance, unlike the majority of oncogenes studied to date. These results demonstrate that transient Mad2 overexpression and chromosome instability can be an important stimulus in the initiation and progression of different cancer subtypes.
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页码:9 / 23
页数:15
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