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Mad2 overexpression promotes aneuploidy and tumorigenesis in mice.

Mad2 overexpression promotes aneuploidy and tumorigenesis in mice. Research Abstract Details 

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  • Mad2 overexpression promotes aneuploidy and tumorigenesis in mice. Abstract Text:

    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.

    Mad2 overexpression promotes aneuploidy and tumorigenesis in mice. Publishing Authors By Initials

    For similar neoplasms research abstracts see: neoplasms research

    PUBMED ID PMID:

    MEDLINE DATE:

    Mad2 overexpression promotes aneuploidy and tumorigenesis in mice. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Cancer cell

    VOLUME: 11

    Page Numbers: 9-23

    Journal Abbreviation: Cancer Cell

    ISSN: 1535-6108

    DAY: 28

    MONTH: 12

    YEAR: 2006

    Mad2 overexpression promotes aneuploidy and tumorigenesis in mice. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 101130617

    Mad2 overexpression promotes aneuploidy and tumorigenesis in mice. Keywords Mesh Terms:

    KEYWORDS: Neoplasms

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Mad2 overexpression promotes aneuploidy and tumorigenesis in mice. Information

    Substance Name: MAD2 protein, mouse

    Registry Number: 0

    Grant and Affiliation Information for Mad2 overexpression promotes aneuploidy and tumorigenesis in mice.

    AFFILIATION: Cancer Biology and Genetics Program, Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NCI

    GRANT: R01 CA124378-08A1

    ACRONYM: CA

    MEDLINETA: Cancer Cell

    REFSOURCE: Cancer Cell. 2007 Jan;11(1):1-3

    DATABASENAME:

    ACCESSION NUMBER:

    Number Hits: 0

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