ALK signaling and target therapy in anaplastic large cell lymphoma

The discovery by Morris et al. (1994) of the genes contributing to the t(2;5)(p23;q35) translocation has laid the foundation for a molecular based recognition of anaplastic large cell lymphoma and highlighted the need for a further stratification of T-cell neoplasia. Likewise the detection of anapla...

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Published inFrontiers in oncology Vol. 2; p. 41
Main Authors Tabbó, Fabrizio, Barreca, Antonella, Piva, Roberto, Inghirami, Giorgio
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Research Foundation 2012
Frontiers Media S.A
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ISSN2234-943X
2234-943X
DOI10.3389/fonc.2012.00041

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Summary:The discovery by Morris et al. (1994) of the genes contributing to the t(2;5)(p23;q35) translocation has laid the foundation for a molecular based recognition of anaplastic large cell lymphoma and highlighted the need for a further stratification of T-cell neoplasia. Likewise the detection of anaplastic lymphoma kinase (ALK) genetic lesions among many human cancers has defined unique subsets of cancer patients, providing new opportunities for innovative therapeutic interventions. The objective of this review is to appraise the molecular mechanisms driving ALK-mediated transformation, and to maintain the neoplastic phenotype. The understanding of these events will allow the design and implementation of novel tailored strategies for a well-defined subset of cancer patients.
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This article was submitted to Frontiers in Cancer Molecular Targets and Therapeutics, a specialty of Frontiers in Oncology.
Reviewed by: Min Hee Kang, School of Medicine TTUHSC, USA; Lokesh Jain, Food and Drug Administration, USA
Edited by: Yisong Wang, National Cancer Institute at the National Institutes of Health, USA
ISSN:2234-943X
2234-943X
DOI:10.3389/fonc.2012.00041