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Anaplastic lymphoma kinase in human cancer
Antonella Barreca1, Elena Lasorsa, Ludovica Riera
1Department of Pathology and Center for Experimental Research and Medical Studies (CeRMS), University of Torino, Via Santena 7, Torino 10126, Italy.
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.
Insights
Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase crucial in normal cell functions and cancer development. This review details ALK expression, fusion proteins, activation mechanisms, and targeted therapies for ALK-positive cancers.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Receptor tyrosine kinases (RTKs) regulate vital cellular processes like proliferation, survival, and differentiation.
- Dysregulation of RTKs is implicated in the pathogenesis of numerous human cancers.
- The anaplastic lymphoma kinase (ALK) is a transmembrane RTK identified as a key player in various cancers.
Purpose of the Study:
- To review the expression patterns of ALK-RTK and its associated fusion proteins.
- To elucidate the molecular mechanisms underlying ALK activation in tumorigenesis.
- To briefly discuss emerging therapeutic strategies for ALK-driven neoplasms.
Main Methods:
- Literature review of ALK expression, function, and therapeutic targeting.
- Analysis of molecular mechanisms of ALK activation and fusion protein formation.
- Synthesis of current knowledge on ALK-positive cancer pathogenesis.
Main Results:
- ALK expression and aberrant activation through fusion proteins are critical in several human cancers.
- Understanding ALK's molecular mechanisms provides insights into its oncogenic potential.
- Targeted therapies show promise for ALK-positive malignancies.
Conclusions:
- ALK is a significant oncogenic driver in various cancers.
- Targeted inhibition of ALK represents a promising therapeutic avenue.
- Further research into ALK biology and treatment is warranted.
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