作者: Garth L. Nicolson , David G. Menter , John Herrmann , Philip Cavanaugh , Libin Jia
DOI: 10.1615/CRITREVONCOG.V5.I5.20
关键词: Paracrine signalling 、 Immunology 、 Biology 、 Brain metastasis 、 Cancer research 、 Autocrine signalling 、 Tumor progression 、 Growth factor receptor inhibitor 、 Growth factor 、 Neurotrophin 、 Metastasis
摘要: An important clinical endpoint in patients with cancer is formation of metastases the brain. Understanding this phenomenon several types malignancies, including melanoma, lung and breast cancers. Metastatic tumor cells use specific adhesion molecules to home brain, there they must attach microvessel endothelial respond brain cell-derived motility factors invasion invade CNS. Neurotrophins are process, ability into may well depend on metastatic cell responses neurotrophins production base ment membrane-degradative enzymes capable locally destroying blood-brain barrier. Brain-metastatic human melanoma express low-affinity p75 receptor for such as nerve growth factor, but do not high-affinity-type receptors factor encoded by protooncogene trkA. Tumor can proliferate CNS response local paracrine inhibitors, their also depends producing responding autocrine factors. A major organ-derived (paracrine) has been isolated that differentially stimulates Characterization mitogen demonstrated it a transferrin-like glycoprotein; greater numbers transferrin surfaces than poorly or other sites. Transferrin-like expressed fetal could represent stimulate brain-metastatic cells. These probably determining whether successfully invade, colonize, grow