Mechanisms of receptor tyrosine kinase activation in cancer.

Du Z, Lovly CM
Mol Cancer. 2018 17 (1): 58

PMID: 29455648 · PMCID: PMC5817791 · DOI:10.1186/s12943-018-0782-4

Receptor tyrosine kinases (RTKs) play an important role in a variety of cellular processes including growth, motility, differentiation, and metabolism. As such, dysregulation of RTK signaling leads to an assortment of human diseases, most notably, cancers. Recent large-scale genomic studies have revealed the presence of various alterations in the genes encoding RTKs such as EGFR, HER2/ErbB2, and MET, amongst many others. Abnormal RTK activation in human cancers is mediated by four principal mechanisms: gain-of-function mutations, genomic amplification, chromosomal rearrangements, and / or autocrine activation. In this manuscript, we review the processes whereby RTKs are activated under normal physiological conditions and discuss several mechanisms whereby RTKs can be aberrantly activated in human cancers. Understanding of these mechanisms has important implications for selection of anti-cancer therapies.

MeSH Terms (16)

Animals Cell Transformation, Neoplastic Enzyme Activation Gene Expression Regulation, Neoplastic Humans Ligands Molecular Targeted Therapy Mutation Neoplasms Phosphorylation Protein Binding Protein Interaction Domains and Motifs Protein Kinase Inhibitors Protein Multimerization Receptor Protein-Tyrosine Kinases Signal Transduction

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