Targeting Receptor Tyrosine Kinases in Cancer

摘要: Aberrations in the orderly function of protein families receptor tyrosine kinases (RTK) rank among most frequent oncogenic insults virtually any type cancer. The present chapter delineates how RTKs are perturbed human cancers by multiple mechanisms including mutations, deletions, gene amplification, and genomic rearrangements resulting fusion genes along with molecular underlying transforming tumorigenic potential these aberrations. Moreover, aberrations hardly ever occur alone, but embedded coincidental perturbations that enhance or attenuate RTK signaling. have been made readily detectable routine pathology techniques sequencing, mutation-specific real-time PCR, immunohistochemistry, situ hybridization-based techniques. These technological advances enable individualized therapeutic administration RTK-targeting agents monoclonal antibodies, immunotoxins, decoy receptors, kinase inhibitors, other agents. In patients carefully selected aberration their tumors, demonstrated impressive clinical efficacy. Intrinsic acquired resistance to agents, however, dampens efficacy targeted clinics also reviewed. Finally, we envisage strategies delay overcome