Two examples by which receptor kinase is activated in cancer
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Answer:
Explanation:
Receptor tyrosine kinases (RTKs) are a subclass of tyrosine kinases that are involved in mediating cell-to-cell communication and controlling a wide range of complex biological functions, including cell growth, motility, differentiation, and metabolism. There are 58 known RTKs in humans [1, 2], and all RTKs share a similar protein structure comprised of an extracellular ligand binding domain, a single transmembrane helix, and an intracellular region that contains a juxtamembrane regulatory region, a tyrosine kinase domain (TKD) and a carboxyl (C-) terminal tail [3]. Dysregulation of RTK signaling leads to many human diseases, especially cancer. Given the advent of the genomic era and the implementation of next generation sequencing (NGS) in cancer research as well as routine clinical practice, mutational landscapes have been established in almost all types of human tumors [4]. These genomic studies have revealed the presence of several different types of alterations in the genes encoding RTKs such as EGFR, HER2/ErbB2, MET, amongst many others. The presence of recurrent RTK genomic alterations raises the question about how they function in cancer development and how to best treat cancer patients whose tumors harbor certain RTK mutations. 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, which have important implications for selection of anti-cancer therapies.