Zwick Esther, Bange Johannes, Ullrich Axel
Dept of Molecular Biology, Max-Planck-Institut of Biochemistry, Am Klopferspitz 18a, 82152, Martinsried, Germany.
Trends Mol Med. 2002 Jan;8(1):17-23. doi: 10.1016/s1471-4914(01)02217-1.
Receptor tyrosine kinases (RTKs) are the primary mediators of the signaling network that transmit extracellular signals into the cell. Gene amplification and/or overexpression of RTK proteins or functional alterations caused by mutations in the corresponding genes or abnormal autocrine-paracrine growth factor loops contribute to constitutive RTK signaling, ultimately resulting in the manifestation of dysregulated cell growth and cancer. The mechanism of uncontrolled RTK signaling that leads to cancer has provided the rationale for anti-RTK drug development. Strategies towards the prevention and interception of RTK signaling include monoclonal antibodies, small-molecule inhibitors, immunotoxins and antisense oligonucleotides.
受体酪氨酸激酶(RTK)是将细胞外信号传递到细胞内的信号网络的主要介导者。RTK蛋白的基因扩增和/或过表达,或由相应基因突变或异常自分泌-旁分泌生长因子环引起的功能改变,会导致RTK信号的组成性激活,最终导致细胞生长失调和癌症的发生。导致癌症的RTK信号失控机制为抗RTK药物的开发提供了理论依据。预防和阻断RTK信号的策略包括单克隆抗体、小分子抑制剂、免疫毒素和反义寡核苷酸。