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Blood, 15 December 2006, Vol. 108, No. 13, pp. 4202-4204. Prepublished online as a Blood First Edition Paper on August 31, 2006; DOI 10.1182/blood-2006-06-026666. This Article Full Text Full Text (PDF) Supplemental Table All Versions of this Article: blood-2006-06-026666v1 108/13/4202    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 Gu, T.-L. Articles by Polakiewicz, R. D. Search for Related Content PubMed PubMed Citation Articles by Gu, T.-L. Articles by Polakiewicz, R. D. Related Collections Neoplasia Oncogenes and Tumor Suppressors Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Brief report Phosphotyrosine profiling identifies the KG-1 cell line as a model for the study of FGFR1 fusions in acute myeloid leukemia Ting-Lei Gu, Valerie L. Goss, Cynthia Reeves, Lana Popova, Julie Nardone, Joan MacNeill, Denise K. Walters, Yi Wang, John Rush, Michael J. Comb, Brian J. Druker, and Roberto D. Polakiewicz Cell Signaling Technology, Danvers, MA; and Department of Hematology and Oncology, Howard Hughes Medical Institute, Oregon Health & Science University Cancer Institute. The 8p11 myeloproliferative syndrome (EMS) is associated with translocations that disrupt the FGFR1 gene. To date, 8 fusion partners of FGFR1 have been identified. However, no primary leukemia cell lines were identified that contain any of these fusions. Here, we screened more than 40 acute myeloid leukemia cell lines for constitutive phosphorylation of STAT5 and applied an immunoaffinity profiling strategy to identify tyrosine-phosphorylated proteins in the KG-1 cell line. Mass spectrometry analysis of KG-1 cells revealed aberrant tyrosine phosphorylation of FGFR1. Subsequent analysis led to the identification of a fusion of the FGFR1OP2 gene to the FGFR1 gene. Small interfering RNA (siRNA) against FGFR1 specifically inhibited the growth and induced apoptosis of KG-1 cells. Thus, the KG-1 cell line provides an in vitro model for the study of FGFR1 fusions associated with leukemia and for the analysis of small molecule inhibitors against FGFR1 fusions. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. W. Tyner, D. K. Walters, S. G. Willis, M. Luttropp, J. Oost, M. Loriaux, H. Erickson, A. S. Corbin, T. O'Hare, M. C. Heinrich, et al. RNAi screening of the tyrosine kinome identifies therapeutic targets in acute myeloid leukemia Blood, February 15, 2008; 111(4): 2238 - 2245. [Abstract] [Full Text] [PDF] A. Chase, F. H. Grand, and N. C. P. Cross Activity of TKI258 against primary cells and cell lines with FGFR1 fusion genes associated with the 8p11 myeloproliferative syndrome Blood, November 15, 2007; 110(10): 3729 - 3734. [Abstract] [Full Text] [PDF] T.-l. Gu, T. Mercher, J. W. Tyner, V. L. Goss, D. K. Walters, M. G. Cornejo, C. Reeves, L. Popova, K. Lee, M. C. Heinrich, et al. A novel fusion of RBM6 to CSF1R in acute megakaryoblastic leukemia Blood, July 1, 2007; 110(1): 323 - 333. [Abstract] [Full Text] [PDF] S. Dong, S. Kang, T.-L. Gu, S. Kardar, H. Fu, S. Lonial, H. J. Khoury, F. Khuri, and J. Chen 14-3-3 integrates prosurvival signals mediated by the AKT and MAPK pathways in ZNF198-FGFR1-transformed hematopoietic cells Blood, July 1, 2007; 110(1): 360 - 369. [Abstract] [Full Text] [PDF]

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