作者: Henry Mead , Mirjana Zeremski , Markus Guba
DOI: 10.1007/978-1-60327-271-1_3
关键词:
摘要: An important feature of tumor blood vessels is that they are in a state constant new vessel growth. In endothelial cells, the PI3K/Akt pathway has been shown to play an role mediating cell survival, proliferation, and migration. The serine/threonine kinase, mammalian target rapamycin (mTOR), downstream mTOR signaling, be involved control growth proliferation. To grow beyond certain size primary metastases dependent on formation or angiogenesis. angiogenesis serves as central regulator. There growing evidence support hypothesis acts critical switch for cellular catabolism anabolism, thus determining whether these cells proliferate. This especially cancer bearing disturbances TOR pathway. several human cancers whereby dysregulated. Gain loss mutations this lead neoplastic transformation. inhibitors downregulate hypoxia-inducible factor 1α (HIF1α)-mediated production pro-angiogenic cytokine, vascular (VEGF), by resulting activation receptors (VEGF-Rs) lymphatic precursor inhibiting survival growth-promoting signals vascularization tumorigenesis. antiangiogenic antilymphangiogenic effects inhibition may well translate into reduced incidence clinically apparent malignancies through metastasis, respectively.