Journal
MOLECULAR CANCER
Volume 17, Issue -, Pages -Publisher
BMC
DOI: 10.1186/s12943-018-0782-4
Keywords
Receptor; Tyrosine kinase; Cancer; Mutation; Chromosomal rearrangement; Targeted therapy; Tyrosine kinase inhibitor (TKI); Oncogene
Categories
Funding
- Damon Runyon Clinical Investigator Award
- LUNGevity Career Development Award
- V Foundation Scholar-in-Training Award
- AACR-Genentech Career Development Award
- LCFA/IASLC Lori Monroe Scholarship
- Vanderbilt Ingram Cancer Center Young Ambassadors Award
- National Institutes of Health (NIH)
- National Cancer Institute (NCI) [R01CA121210, P01CA129243, U10CA180864, P30CA068485-13S5]
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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.
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