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 in | Frontiers in oncology Vol. 2; p. 41 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
Frontiers Research Foundation
2012
Frontiers Media S.A |
Subjects | |
Online Access | Get full text |
ISSN | 2234-943X 2234-943X |
DOI | 10.3389/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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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 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 |