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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 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 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 Amin, H. M. Articles by Lai, R. Search for Related Content PubMed PubMed Citation Articles by Amin, H. M. Articles by Lai, R. Related Collections Oncogenes and Tumor Suppressors Reviews in Translational Hematology Clinical Trials and Observations Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  REVIEW IN TRANSLATIONAL HEMATOLOGY Pathobiology of ALK+ anaplastic large-cell lymphoma Hesham M. Amin1, and Raymond Lai2 1 Department of Hematopathology, The University of Texas M. D. Anderson Cancer Center, Houston; 2 Department of Laboratory Medicine and Pathology, Cross Cancer Institute and The University of Alberta, Edmonton, Canada Anaplastic large-cell lymphoma (ALCL) was initially recognized on the basis of morphologic features and the consistent expression of CD30. It then became evident that the 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 clinicopathologic 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 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 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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