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Correction: Corrigendum: Colorectal carcinomas in mice lacking the catalytic subunit of PI(3)Kγ

The Original Article was published on 24 August 2000

Nature 406, 897–902 (2000).

In this Letter, we reported that mice lacking the catalytic subunit of PI(3)Kγ on 129J backgrounds develop invasive colorectal tumours. We have observed this cancer phenotype in mouse lines derived from two different targeted embryonic stem-cell clones for at least two years. However, after backcrossing these mice onto a C57BL/6 background, we now find that the tumour phenotype has disappeared. Also, when we retargeted the allele in different ES cells using the same targeting construct, no tumours developed. Inactivation of PI(3)Kγ in mice therefore does not in itself cause colon cancer, but may require additional factors—for example, the impaired immunity of p110γ–/– mice may make them susceptible to tumours triggered by environmental and infectious agents1. Our finding that overexpression of p110γ in different human colon-cancer cells results in decreased cell growth still stands, as does the frequent downregulation of p110γ protein in colon-cancer patients (since independently confirmed2).

Some authors (Y.H., A.H., M.R., S.G. and T.W.M.) are not co-signatories to this statement.


  1. 1

    Erdman, S. E. et al. CD4+ CD25+ regulatory T lymphocytes inhibit microbially induced colon cancer in Rag2-deficient mice. Am. J. Pathol. 162, 691–702 (2003)

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  2. 2

    Semba, S. et al. Down-regulation of PIK3CG, a catalytic subunit of phosphatidylinositol 3-OH kinase, by CpG hypermethylation in human colorectal carcinoma. Clin. Cancer Res. 8, 3824–3831 (2002)

    CAS  PubMed  Google Scholar 

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The online version of the original article can be found at 10.1038/35022585

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Sasaki, T., Irie-Sasaki, J., Horie, Y. et al. Correction: Corrigendum: Colorectal carcinomas in mice lacking the catalytic subunit of PI(3)Kγ. Nature 426, 584 (2003).

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