Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Correspondence
  • Published:

Constitutive activation of PI3K is involved in the spontaneous proliferation of primary acute myeloid leukemia cells: direct evidence of PI3K activation

Leukemia volume 18, pages 1438–1440 (2004)Cite this article

TO THE EDITOR

The phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway plays an important role in the proliferation, differentiation and survival of hematopoietic cells.1 Recently, it was found that Akt was phosphorylated and activated in the majority of primary acute myeloid leukemia (AML) cells, and that constitutive activation of the PI3K/Akt pathway is necessary for the survival of AML cells.2, 3 In addition, constitutive phosphorylation of Akt was associated with poor prognosis of AML.3 Although phosphorylation and activation of Akt is used as an indicator of PI3K activation, a recent study demonstrated that Akt was activated by a PI3K-independent mechanism.4 Since PI3K activity in primary AML cells has not yet been analyzed in previous studies,2, 3 we examined PI3K activity and phosphorylation of Akt in primary AML cells and the function of PI3K in the proliferation of leukemia cells.

This is a preview of subscription content, access via your institution

Relevant articles

Open Access articles citing this article.

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

Figure 1

References

  1. Steelman LS, Pohnert SC, Shelton JG, Franklin RA, Bertrand FE, McCubrey JA . JAK/STAT, Raf/MEK/ERK, PI3K/Akt and BCR-ABL in cell cycle progression and leukemogenesis. Leukemia 2004; 18: 189–218.

    Article  CAS  Google Scholar 

  2. Xu Q, Simpson SE, Scialla TJ, Bagg A, Carroll M . Survival of acute myeloid leukemia cells requires PI3 kinase activation. Blood 2003; 102: 972–980.

    Article  CAS  Google Scholar 

  3. Min YH, Eom JI, Cheong JW, Maeng HO, Kim JY, Jeung HK et al. Constitutive phosphorylation of Akt/PKB protein in acute myeloid leukemia: its significance as a prognostic variable. Leukemia 2003; 17: 995–997.

    Article  CAS  Google Scholar 

  4. Woods Ignatoski KM, Livant DL, Markwart S, Grewal NK, Ethier SP . The role of phosphatidylinositol 3'-kinase and its downstream signals in erbB-2-mediated transformation. Mol Cancer Res 2003; 1: 551–560.

    CAS  PubMed  Google Scholar 

  5. Kubota Y, Tanaka T, Kitanaka A, Ohnishi H, Okutani Y, Waki M et al. Src transduces erythropoietin-induced differentiation signals through phosphatidylinositol 3-kinase. EMBO J 2001; 20: 5666–5677.

    Article  CAS  Google Scholar 

  6. Ohnishi H, Ledbetter JA, Kanner SB, Linsley PS, Tanaka T, Geller AM et al. CD28 cross-linking augments TCR-mediated signals and costimulates superantigen responses. J Immunol 1995; 154: 3180–3193.

    CAS  PubMed  Google Scholar 

  7. Kiyoi H, Towatari M, Yokota S, Hamaguchi M, Ohno R, Saito H et al. Internal tandem duplication of the FLT3 gene is a novel modality of elongation mutation which causes constitutive activation of the product. Leukemia 1998; 12: 1333–1337.

    Article  CAS  Google Scholar 

  8. Lee Jr JT, McCubrey JA . The Raf/MEK/ERK signal transduction cascade as a target for chemotherapeutic intervention in leukemia. Leukemia 2002; 16: 486–507.

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Department of Transfusion Medicine, Kagawa University, Kagawa, Japan

    Y Kubota

  2. First Department of Internal Medicine, Kagawa University, Kagawa, Japan

    H Ohnishi & T Ishida

  3. Department of Laboratory Medicine, Faculty of Medicine, Kagawa University, Kagawa, Japan

    A Kitanaka

  4. Environmental Health Sciences, Kagawa University, Kagawa, Japan

    T Tanaka

Authors
  1. Y Kubota
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. H Ohnishi
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. A Kitanaka
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. T Ishida
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. T Tanaka
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Y Kubota.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Kubota, Y., Ohnishi, H., Kitanaka, A. et al. Constitutive activation of PI3K is involved in the spontaneous proliferation of primary acute myeloid leukemia cells: direct evidence of PI3K activation. Leukemia 18, 1438–1440 (2004). https://doi.org/10.1038/sj.leu.2403402

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/sj.leu.2403402

This article is cited by

Search

Advanced search

Quick links