Anaplastic lymphoma kinase in human cancer
- Antonella Barreca1,
- Elena Lasorsa1,
- Ludovica Riera1,
- Rodolfo Machiorlatti1,
- Roberto Piva1,2,
- Maurilio Ponzoni3,
- Ivo Kwee4,
- Francesco Bertoni4,
- Pier Paolo Piccaluga5,
- Stefano A Pileri5,
- Giorgio Inghirami1,2 and
- The European T-Cell Lymphoma Study Group†
- 1Department of Pathology and Center for Experimental Research and Medical Studies (CeRMS), University of Torino, Via Santena 7, Torino 10126, Italy
2Department of Pathology, NYU Cancer Center, New York University School of Medicine, New York, New York 10016, USA
3Unit of Lymphoid Malignancies, San Raffaele H Scientific Institute, Milan 20132, Italy
4Laboratory of Experimental Oncology and Lymphoma Unit, Oncology Institute of Southern Switzerland (IOSI), Bellinzona 6900, Switzerland
5Hematopathology Section, Department of Hematology and Oncological Sciences ‘L. and A. Seràgnoli’, S. Orsola-Malpighi Hospital, University of Bologna, Bologna 40138, Italy
- (Correspondence should be addressed to G Inghirami at Department of Pathology and Center for Experimental Research and Medical Studies (CeRMS), University of Torino; Email: giorgio.inghirami{at}unito.it)
Abstract
The receptor tyrosine kinases (RTKs) play a critical role, controlling cell proliferation, survival, and differentiation of normal cells. Their pivotal function has been firmly established in the pathogenesis of many cancers as well. The anaplastic lymphoma kinase (ALK), a transmembrane RTK, originally identified in the nucleophosmin (NPM)–ALK chimera of anaplastic large cell lymphoma, has emerged as a novel tumorigenic player in several human cancers. In this review, we describe the expression of the ALK–RTK, its related fusion proteins, and their molecular mechanisms of activation. Novel tailored strategies are briefly illustrated for the treatment of ALK-positive neoplasms.
- Revision received 28 March 2011
- Accepted 18 April 2011
- © 2011 Society for Endocrinology
