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PKR is activated in MDS patients and its subcellular localization depends on disease severity

Leukemia volume 22, pages 2267–2269 (2008)Cite this article

Myelodysplastic syndromes (MDS) are a group of hematological disorders characterized by progressive cytopenia and increased tendency of acute myeloid leukemia (AML) transformation.1 While the majority of patients are diagnosed with low-grade disease, approximately two-thirds will succumb to complications of peripheral blood cytopenia or progression into AML. That is why the phenotype of high risk MDS has often been associated with some AML features. However, a unique aspect of MDS is the notion that both bone marrow failure and the propensity towards development of AML coexist. As both properties contribute to peripheral blood cytopenia and the natural history of the disease, it is thought that proliferative advantages lend themselves more to leukemic transformation, while initially accelerated apoptosis is responsible for the cytopenia.1

It is likely that aberrant regulation of intracellular signaling pathways is involved in the pathogenesis of MDS.

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References

  1. Corey SJ, Minden MD, Barber DL, Kantarjian H, Wang JC, Schimmer AD . Myelodysplastic syndromes: the complexity of stem-cell diseases. Nature Rev Cancer 2007; 7: 118–129.

    Article  CAS  Google Scholar 

  2. Martelli AM, Nyakern M, Tabellini G, Bortul R, Tazzari PL, Evangelisti C et al. Phosphoinositide 3-kinase/Akt signaling pathway and its therapeutical implications for human acute myeloid leukemia. Leukemia 2006; 20: 911–928.

    Article  CAS  PubMed  Google Scholar 

  3. Doepfner KT, Spertini O, Arcaro A . Autocrine insulin-like growth factor-I signaling promotes growth and survival of human acute myeloid leukemia cells via the phosphoinositide 3-kinase/Akt pathway. Leukemia 2007; 21: 1921–1930.

    Article  CAS  PubMed  Google Scholar 

  4. Nyakern M, Tazzari PL, Finelli C, Bosi C, Follo MY, Grafone T et al. Frequent elevation of Akt kinase phosphorylation in blood marrow and peripheral blood mononuclear cells from high-risk myelodysplastic syndrome patients. Leukemia 2006; 20: 230–238.

    Article  CAS  PubMed  Google Scholar 

  5. Follo MY, Mongiorgi S, Bosi C, Cappellini A, Finelli C, Chiarini F et al. The Akt/mammalian target of rapamycin signal transduction pathway is activated in high-risk myelodysplastic syndromes and influences cell survival and proliferation. Cancer Res 2007; 67: 4287–4294.

    Article  CAS  PubMed  Google Scholar 

  6. Follo MY, Finelli C, Bosi C, Martinelli G, Mongiorgi S, Baccarani M et al. PI-PLCbeta-1 and activated Akt levels are linked to azacitidine responsiveness in high-risk myelodysplastic syndromes. Leukemia 2008; 22: 198–200.

    Article  CAS  PubMed  Google Scholar 

  7. Garcia MA, Gil J, Ventoso I, Guerra S, Domingo E, Rivas C et al. Impact of protein kinase PKR in cell biology: from antiviral to antiproliferative action. Microbiol Mol Biol Rev 2006; 70: 1032–1060.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  8. Lim MA, Kikani CK, Wick MJ, Dong LQ . Nuclear translocation of 3′-phosphoinositide-dependent protein kinase 1 (PDK-1): a potential regulatory mechanism for PDK-1 function. Proc Natl Acad Sci USA 2003; 100: 14006–14011.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

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Acknowledgements

This work was supported by grants from: CARISBO Foundation, Progetti Strategici Università di Bologna EF2006.

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Authors and Affiliations

  1. Dipartimento di Scienze Anatomiche Umane e Fisiopatologia dell’Apparato Locomotore, Sezione di Anatomia, Cell Signaling Laboratory, Università di Bologna, Bologna, Italy

    M Y Follo, S Mongiorgi, W L Blalock, L Cocco & A M Martelli

  2. Dipartimento di Ematologia e Scienze Oncologiche ‘L e A Seràgnoli’, Università di Bologna, Bologna, Italy

    C Finelli, C Clissa, C Bosi & G Martinelli

  3. Hematology Unit, Ospedale Civile di Piacenza, Piacenza, Italy

    C Bosi

  4. Istituto di Genetica Molecolare del CNR, c/o IOR, Bologna, Italy

    A M Martelli

Authors
  1. M Y Follo
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  2. C Finelli
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  3. S Mongiorgi
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  4. C Clissa
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  6. G Martinelli
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  7. W L Blalock
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  8. L Cocco
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  9. A M Martelli
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Corresponding author

Correspondence to A M Martelli.

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Supplementary Information accompanies the paper on the Leukemia website (http://www.nature.com/leu)

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Follo, M., Finelli, C., Mongiorgi, S. et al. PKR is activated in MDS patients and its subcellular localization depends on disease severity. Leukemia 22, 2267–2269 (2008). https://doi.org/10.1038/leu.2008.122

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