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Correspondence re: T. Zhang et al., Evidence That APC Regulates Survivin Expression: A Possible Mechanism Contributing to the Stem Cell Origin of Colon Cancer. Cancer Res., 61: 8664–8667, 2001.

Maria Grazia Daidone, Aurora Costa, Milo Frattini, Debora Balestra, Lucio Bertario and Marco A. Pierotti
Maria Grazia Daidone
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Aurora Costa
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Milo Frattini
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Debora Balestra
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Lucio Bertario
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Marco A. Pierotti
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DOI:  Published January 2004
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    Scheme. 1.

    This scheme is a diagram of the β-catenin/TCF-4/survivin pathway and its possible role in promoting colon tumorigenesis. The left side of the scheme shows the effect of APC on β-catenin when both proteins are wild type. The right side shows the consequences of homozygous mutations in APC or an activating mutation in β-catenin. These two conditions, which are depicted on the left and right side of the scheme, portray mechanisms linked to normal colonic epithelial homeostasis and enhanced colon tumorigenesis, respectively. aThe APC:β-Catenin protein complex also contains the proteins axin and GSK3β. bThe Survivin:Aurora B Kinase protein complex also contains the INCENP protein.

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    Biological features associated with proliferation and apoptosis in colon cancers characterized for dysregulation in the APC/β-catenin/T-cell factor pathway

    Total casesSurvivin expressionaApoptotic indexb median value (range)Proliferation indexc median value (range)
    Median value (range)% of positive cases
    β-Catenin negatived (microsatellite instability positive)1070 (0–100)80%0.6 (0–1.2)72.5 (50–100)
    β-Catenin positive (microsatellite instability negative)6150 (0–90)74%0.4 (0–18.7)85.0 (50–100)
    • a Percentage of tumor cells with cytoplasmic immunostaining. Cut-off value for positive cases = 25% of positive cells.

    • b Percentage of tumor cells with cytoplasmic immunostaining for M30.

    • c Percentage of tumor cells with nuclear immunostaining for MIB-1.

    • d β-Catenin protein expression was evaluated on formalin-fixed, paraffin-embedded samples by immunohistochemistry (mouse monoclonal anti-β-catenin antibody; Transduction Laboratories, Lexington, KY) for the presence of nuclear, cytoplasmic, and membranous accumulation in both tumor and normal surrounding tissues.

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Cancer Research: 64 (2)
January 2004
Volume 64, Issue 2
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Correspondence re: T. Zhang et al., Evidence That APC Regulates Survivin Expression: A Possible Mechanism Contributing to the Stem Cell Origin of Colon Cancer. Cancer Res., 61: 8664–8667, 2001.
Maria Grazia Daidone, Aurora Costa, Milo Frattini, Debora Balestra, Lucio Bertario and Marco A. Pierotti
Cancer Res January 15 2004 (64) (2) 776-779;

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Correspondence re: T. Zhang et al., Evidence That APC Regulates Survivin Expression: A Possible Mechanism Contributing to the Stem Cell Origin of Colon Cancer. Cancer Res., 61: 8664–8667, 2001.
Maria Grazia Daidone, Aurora Costa, Milo Frattini, Debora Balestra, Lucio Bertario and Marco A. Pierotti
Cancer Res January 15 2004 (64) (2) 776-779;
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