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Blood, 1 January 2005, Vol. 105, No. 1, pp. 22-30. Prepublished online as a Blood First Edition Paper on September 9, 2004; DOI 10.1182/blood-2003-11-3896. This Article Full Text (PDF) All Versions of this Article: 2003-11-3896v1 105/1/22    most recent Alert me when this article is cited Alert me if a correction is posted 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 Wadleigh, M. Articles by Stone, R. M Search for Related Content PubMed PubMed Citation Articles by Wadleigh, M. Articles by Stone, R. M Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted November 14, 2003 Accepted August 22, 2004 After chronic myelogenous leukemia: tyrosine kinase inhibitors in other hematologic malignancies Martha Wadleigh, Daniel J Deangelo, James D Griffin, and Richard M Stone* Leukemia Program, Division of Hematologic Malignancy, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA, USA * Corresponding author; email: RStone{at}partners.org. Tyrosine kinases phosphorylate proteins on tyrosine residues, producing a biological signal that influences many aspects of cellular function including cell growth, proliferation, differentiation and death. Constitutive or unregulated activity through mutation or over expression of these enzymes is a common pathologic feature in many acute and chronic leukemias. Inhibition of tyrosine kinases represents a strategy to disrupt signaling pathways that promote neoplastic growth and survival in hematologic malignancies, and likely in other neoplasias as well. This review will focus on tyrosine kinases that have been implicated in the pathogenesis of hematologic diseases other than chronic myelogenous leukemia (CML) and will discuss the evidence for the use of small molecules to target these kinases. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. Trowe, S. Boukouvala, K. Calkins, R. E. Cutler Jr., R. Fong, R. Funke, S. B. Gendreau, Y. D. Kim, N. Miller, J. R. Woolfrey, et al. EXEL-7647 Inhibits Mutant Forms of ErbB2 Associated with Lapatinib Resistance and Neoplastic Transformation Clin. Cancer Res., April 15, 2008; 14(8): 2465 - 2475. [Abstract] [Full Text] [PDF] A. F. Remacha, C. Estivill, M. P. Sarda, J. Mateo, J. C. Souto, C. Canals, J. Nomdedeu, and J. Fontcuberta The V617F mutation of JAK2 is very uncommon in patients with thrombosis Haematologica, February 1, 2007; 92(2): 285 - 286. [Abstract] [Full Text] [PDF] S. Knapper, K. I. Mills, A. F. Gilkes, S. J. Austin, V. Walsh, and A. K. Burnett The effects of lestaurtinib (CEP701) and PKC412 on primary AML blasts: the induction of cytotoxicity varies with dependence on FLT3 signaling in both FLT3-mutated and wild-type cases Blood, November 15, 2006; 108(10): 3494 - 3503. [Abstract] [Full Text] [PDF] S. Schnittger, T. M. Kohl, T. Haferlach, W. Kern, W. Hiddemann, K. Spiekermann, and C. Schoch KIT-D816 mutations in AML1-ETO-positive AML are associated with impaired event-free and overall survival Blood, March 1, 2006; 107(5): 1791 - 1799. [Abstract] [Full Text] [PDF] Q. Xu, J. E. Thompson, and M. Carroll mTOR regulates cell survival after etoposide treatment in primary AML cells Blood, December 15, 2005; 106(13): 4261 - 4268. [Abstract] [Full Text] [PDF] R. Chen and W. Plunkett Sequential Blockade of Oncogenic Kinases Am. Assoc. Cancer Res. Educ. Book, April 1, 2005; 2005(1): 344 - 348. [Full Text] [PDF] J. D. Licht and D. W. Sternberg The Molecular Pathology of Acute Myeloid Leukemia Hematology, January 1, 2005; 2005(1): 137 - 142. [Abstract] [Full Text] [PDF]

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