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Blood, 1 October 2007, Vol. 110, No. 7, pp. 2259-2267. Prepublished online as a Blood First Edition Paper on May 22, 2007; DOI 10.1182/blood-2007-04-060715. This Article Full Text (PDF) All Versions of this Article: blood-2007-04-060715v1 110/7/2259    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 Amin, H. M. Articles by Lai, R. Search for Related Content PubMed PubMed Citation Articles by Amin, H. M. Articles by Lai, R. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted April 2, 2007 Accepted May 19, 2007 Pathobiology of ALK+ anaplastic large-cell lymphoma Hesham M. Amin* and Raymond Lai Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, United States Department of Laboratory Medicine and Pathology, Cross Cancer Institute and The University of Alberta, Edmonton, Alberta, Canada * Corresponding author; email: hamin{at}mdanderson.org. Anaplastic large-cell lymphoma (ALCL) was initially recognized on the basis of morphological features and the consistent expression of CD30. It then became evident that the vast majority of these tumors are derived from lymphoid cells of T or null immunophenotype. The subsequent finding that t(2;5)(p23;q35) occurs in 40% to 60% of ALCL patients established a distinct clinicopathological entity. This chromosomal translocation induces the formation of the chimeric protein nucleophosmin-anaplastic lymphoma kinase (NPM-ALK), which possesses significant oncogenic potential resulting from the constitutive activation of the tyrosine kinase ALK. In addition to its specific pathophysiologic events, NPM-ALK-expressing lymphoma presents with consistent clinical manifestations. Only 13 years after the identification of NPM-ALK, tremendous progress has been made in our understanding of this molecule because of the relentless efforts of multiple investigators who have dissected its biologic roles by using in vitro and in vivo experimental models. Several upstream modulators, cross-reacting oncogenes, and downstream effectors of NPM-ALK have been identified and characterized. Understanding of these interacting oncogenic systems is expected to facilitate the design of new therapeutic strategies and agents. In this review, we briefly discuss ALCL and focus on NPM-ALK. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. P. Koivunen, C. Mermel, K. Zejnullahu, C. Murphy, E. Lifshits, A. J. Holmes, H. G. Choi, J. Kim, D. Chiang, R. Thomas, et al. EML4-ALK Fusion Gene and Efficacy of an ALK Kinase Inhibitor in Lung Cancer Clin. Cancer Res., July 1, 2008; 14(13): 4275 - 4283. [Abstract] [Full Text] [PDF]

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