作者: Ilana Stancovski , Michael Sela , Yosef Yarden
DOI: 10.1007/978-1-4615-2592-9_9
关键词: Epidermal growth factor receptor 、 Cancer research 、 Biology 、 Receptor tyrosine kinase 、 Epidermal growth factor 、 Cell surface receptor 、 Growth factor receptor 、 Signal transduction 、 ErbB 、 Platelet-derived growth factor receptor
摘要: Tumorigenesis in model experimental systems involves multiple steps that include activation of cell growth and inactivation inhibitory processes [1,2]. Tumor development humans is thought to reflect the multiplicity events accumulation independent mutations affect clonal cancerous [3]. The identity group genes confer malignancy vitro appears be similar set are mutated animal human tumors [4]. All whose products undergo mutational (oncogenes) encode key regulatory elements signal transduction pathways lead [5]. Thus, oncogenic proteins may factors, their membrane receptors, cytoplasmic effector proteins, or nuclear factors control gene expression. In systems, altered forms receptors for can induce tumorigenesis. Examples fms erbB retroviral portions colony stimulating factor 1 (CSF-1) [6] epidermal (EGF) [7], respectively. However, possibility modifications one molecular crucial tumor remains open.