Multi-genetic events collaboratively contribute to Pten-null leukaemia stem-cell formation

Wei Guo, Joseph L. Lasky, Chun-Ju Chang, Sherly Mosessian, Xiaoman Lewis, Yun Xiao, Jennifer E. Yeh, James Y. Chen, M. Luisa Iruela-Arispe, Marileila Varella-Garcia and Hong Wu ()
Additional contact information
Wei Guo: Department of Molecular and Medical Pharmacology,
Joseph L. Lasky: Department of Pediatric Hematology/Oncology,
Chun-Ju Chang: Department of Molecular and Medical Pharmacology,
Sherly Mosessian: Department of Molecular and Medical Pharmacology,
Xiaoman Lewis: Department of Molecular and Medical Pharmacology,
Yun Xiao: University of Colorado Cancer Center, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA
Jennifer E. Yeh: Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA
James Y. Chen: Department of Molecular and Medical Pharmacology,
M. Luisa Iruela-Arispe: and
Marileila Varella-Garcia: University of Colorado Cancer Center, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA
Hong Wu: Department of Molecular and Medical Pharmacology,

Nature, 2008, vol. 453, issue 7194, 529-533

Abstract: Cancer model: Pten deletion mimics acute T lymphoblastic leukaemia A new leukaemia model has been established in mice by deleting the Pten tumour suppressor gene in fetal liver haematopoietic stem cells. The mice develop a myeloproliferative disorder that can lead to acute T lymphoblastic leukaemia. Progression of the condition is driven by leukaemia stem cells that require beta-catenin and incorporate a translocation that leads to overexpression of the c-myc oncogene, similar to findings in human acute T lymphoblastic leukaemia. The study illustrates how multiple genetic alterations can dictate hyperproliferative disorders and the progression to cancer.

Date: 2008
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DOI: 10.1038/nature06933

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