Abstract
Oncogenic conversion of receptor protein tyrosine kinases (RTK) is a frequent feature of malignant cells. This knowledge has fostered efforts to develop target-specific low molecular weight therapeutics able to obstruct RTK signalling. The clinical efficacy of the ABL- and KIT-inhibitors are paradigmatic of the power of this approach. Here, we focus on small-molecule inhibitors for RTKs involved in human cancer. In particular, we examine the KIT, MET and RET receptors that are targeted by genetic alterations in both sporadic and familial human tumours.
Keywords: kinase, tyrosine, oncogene, germline, thyroid, kit, met, ret
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