Abstract
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.
| Original language | English |
|---|---|
| Article number | Article 41 |
| Journal | Frontiers in Oncology |
| Volume | 2 MAY |
| DOIs | |
| Publication status | Published - 2012 |
| Externally published | Yes |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- Anaplastic large cell lymphoma
- Anaplastic lymphoma kinase
- Chimeric fusion proteins
- Molecular targeted therapy
- Signaling pathways
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