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Blood, 1 October 2006, Vol. 108, No. 7, pp. 2349-2357. Prepublished online as a Blood First Edition Paper on June 8, 2006; DOI 10.1182/blood-2004-08-009498. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2004-08-009498v1 108/7/2349    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Parikh, C. Articles by Ren, R. Search for Related Content PubMed PubMed Citation Articles by Parikh, C. Articles by Ren, R. Related Collections Oncogenes and Tumor Suppressors Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Oncogenic NRAS rapidly and efficiently induces CMML- and AML-like diseases in mice Chaitali Parikh, Ramesh Subrahmanyam, and Ruibao Ren From the Rosenstiel Basic Medical Sciences Research Center, Department of Biology; and the Graduate Program in Biophysics and Structural Biology, Department of Biochemistry, Brandeis University, Waltham, MA. Activating mutations in RAS, predominantly NRAS, are common in myeloid malignancies. Previous studies in animal models have shown that oncogenic NRAS is unable to induce myeloid malignancies effectively, and it was suggested that oncogenic NRAS might only act as a secondary mutation in leukemogenesis. In this study, we examined the leukemogenicity of NRAS using an improved mouse bone marrow transduction and transplantation model. We found that oncogenic NRAS rapidly and efficiently induced chronic myelomonocytic leukemia (CMML)– or acute myeloid leukemia (AML)– like disease in mice, indicating that mutated NRAS can function as an initiating oncogene in the induction of myeloid malignancies. In addition to CMML and AML, we found that NRAS induced mastocytosis in mice. This result indicates that activation of the RAS pathway also plays an important role in the pathogenesis of mastocytosis. The mouse model for NRAS leukemogenesis established here provides a system for further studying the molecular mechanisms in the pathogenesis of myeloid malignancies and for testing relevant therapies. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. P. Quinlan, S. E. Quatela, M. R. Philips, and J. Settleman Activated Kras, but Not Hras or Nras, May Initiate Tumors of Endodermal Origin via Stem Cell Expansion Mol. Cell. Biol., April 15, 2008; 28(8): 2659 - 2674. [Abstract] [Full Text] [PDF] S.-J. Zhang, L.-Y. Ma, Q.-H. Huang, G. Li, B.-W. Gu, X.-D. Gao, J.-Y. Shi, Y.-Y. Wang, L. Gao, X. Cai, et al. Gain-of-function mutation of GATA-2 in acute myeloid transformation of chronic myeloid leukemia PNAS, February 12, 2008; 105(6): 2076 - 2081. [Abstract] [Full Text] [PDF] L. Motoda, M. Osato, N. Yamashita, B. Jacob, L. Q. Chen, M. Yanagida, H. Ida, H.-J. Wee, A. X. Sun, I. Taniuchi, et al. Runx1 Protects Hematopoietic Stem/Progenitor Cells from Oncogenic Insult Stem Cells, December 1, 2007; 25(12): 2976 - 2986. [Abstract] [Full Text] [PDF] C. Parikh, R. Subrahmanyam, and R. Ren Oncogenic NRAS, KRAS, and HRAS Exhibit Different Leukemogenic Potentials in Mice Cancer Res., August 1, 2007; 67(15): 7139 - 7146. [Abstract] [Full Text] [PDF]

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