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Growth factor receptor inhibitor
About: Growth factor receptor inhibitor is a research topic. Over the lifetime, 4730 publications have been published within this topic receiving 297500 citations.
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TL;DR: Of the various VEGF species, the best characterized is the 165 amino acid long form (VEGF165), which is a heparin binding growth factor, and its interaction with V EGF receptors on the cell surface of vascular endothelial cells depends on the presence ofHeparin-like molecules.
204 citations
TL;DR: Results suggest that IL‐18 may participate in the regulation of a switch of tumor angiogenesis and tumor suppressor, and suggest thatIL‐18 is a novel antiangiogenic and antitumor cytokine.
Abstract: Interleukin-18 (IL-18), also called interferon-γ (IFN-γ)-inducing factor, has recently been characterized as a potent IFN-γ-inducing cytokine We now report that IL-18 is a novel antiangiogenic and antitumor cytokine In vitro, IL-18 specifically inhibits fibroblast growth factor-2-stimulated proliferation of capillary endothelial cells In vivo, IL-18 is sufficiently potent to suppress the fibroblast growth factor-induced corneal neovascularization by systemic administration in mice This cytokine also inhibits embryonic angiogenesis in the chick chorioallantoic membrane assay Systemic and intralesional administrations of IL-18 produce a significant suppression of the growth of murine T241 fibrosarcoma in syngeneic C57Bl6/J and immunodeficient SCID mice The antitumor effect appears to be potent because an average of >75% inhibition of primary tumor growth was observed at a dose of 50 μg/kg/day In cell culture, murine T241 fibrosarcoma cells are insensitive to recombinant IL-18 at concentrations that s
204 citations
TL;DR: D disruption of the 5‐LO signaling pathway mediates growth arrest and apoptosis in breast cancer cells, and additional experiments suggest that this involves the interplay of several factors, including the loss of growth stimulation by 5‐ LO products, the induction of PPARγ, and the potential activation of PParγ by interactions with shunted endoperoxides.
Abstract: SPECIFIC AIMSIn recent studies we have described the function of various arachidonic acid (AA) metabolites in the growth regulation of aerodigestive cancers demonstrating overexpression of IGF-R and its ligand as conserved features of lung cancer and breast cancer. In lung cancer, IGF-1-dependent growth stimulation and a survival effect can be neutralized by blocking five-lipoxygenase (5-LO). We now address the hypothesis that products of 5-LO activity participate in the growth stimulation of breast cancer cells and reciprocally how other specific AA metabolites arising as a consequence of blockage of 5-LO activity may be relevant in the inhibition of breast cancer growth.PRINCIPAL FINDINGS1. Production of the 5-LO metabolite 5-HETE occurs in vitro and mediates growth stimulationInsulin-like growth factor 1 (IGF-1) stimulation of breast cancer cells induces the activity of the 5-LO enzyme as demonstrated by a specific RIA for 5-HETE. Four breast cancer cell lines were exposed to IGF-1 or transferrin, resu...
203 citations
TL;DR: Analysis of the signal transduction mechanisms underlying the up-regulating effect of TGF-β1 on collagenase-3 expression demonstrated that this growth factor acts through a signaling pathway involving protein kinase C and tyrosine kinase activities.
202 citations