ALK signaling and target therapy in anaplastic large cell lymphoma

被引：38

作者：

Tabbo, Fabrizio ^{[1
]}

Barreca, Antonella ^{[1
]}

Piva, Roberto ^{[1
,2
]}

Inghirami, Giorgio ^{[1
,2
]}

机构：

[1] Univ Torino, Ctr Expt Res & Med Studies, Dept Pathol, Via Santena 7, I-10126 Turin, Italy

[2] NYU, Sch Med, Dept Pathol, Canc Ctr, New York, NY USA

来源：

FRONTIERS IN ONCOLOGY | 2012年 / 2卷

关键词：

anaplastic large cell lymphoma; chimeric fusion proteins; signaling pathways; molecular targeted therapy; anaplastic lymphoma kinase;

D O I：

10.3389/fonc.2012.00041

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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 fora 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.

引用

页数：12

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