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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: An understanding of these new developments in estrogen signaling and crosstalk pathways may pave the way for innovative combinatorial approaches for treatment of lung cancer and possibly chemoprevention.
Abstract: Lung cancer is the leading cause of death from neoplasia in men and women in the United States. Some studies suggest that women are more susceptible than men to tobaccoinduced carcinogenesis and may show higher risk than men for lung cancer development from smoking. More recently, increasing biochemical and genetic data have supported this male-female difference in response to tobacco. Estrogens may be involved in lung carcinogenesis, and estrogen receptors (ERs), mainly ERâ, are present and functional in normal lung and tumor cell lines and tissues. Estrogen can directly stimulate the transcription of estrogen-responsive genes in the nucleus of lung cells, and it can also transactivate growth factor signaling pathways, in particular the epidermal growth factor pathway. Lung cancer patients currently have few effective therapeutic options. An understanding of these new developments in estrogen signaling and crosstalk pathways may pave the way for innovative combinatorial approaches for treatment of lung cancer and possibly chemoprevention.
97 citations
TL;DR: Preclinical studies have shown that targeting neurotrophins and their receptors induce an inhibition of breast cancer cell survival, proliferation and invasion and this additional effect further strengthens their clinical relevance.
97 citations
TL;DR: It is concluded that activated function of Stat3 is required for the establishment and maintenance of Ros and insulin-like growth factor I receptor PTK-induced cell transformation.
97 citations
TL;DR: The results suggest that there would be an angiogenesis mechanism via VEGF/Flt-1 or VEGf/KDR in HCC, and the V EGF-KDR system would take a more important role.
Abstract: Flt-1 (VEGF receptor-1) and KDR/Flk-1 (VEGF receptor-2) are the high-affinity receptors for the angiogenesis factor, vascular endothelial growth factor (VEGF). VEGF expression has been confirmed in human hepatocellular carcinoma (HCC), and VEGF is thought to be involved in the angiogenesis within HCC tissues. However, expressions of VEGF receptors in HCC have not been reported. We immunohistochemically examined expressions and localizations of Flt-1 and KDR in 28 surgically resected HCC tissues. In non-cancerous area, Flt-1 and KDR were mainly found in macrophages including Kupffer cells; both receptors were found in vascular endothelial cells in the portal veins and arteries within portal tracts; and KDR was also found in some sinusoidal endothelial cells. In cancerous area, Flt-1 and KDR were found in some macrophages, and also in the endothelial cells of intratumoral blood vessels. In 25 moderately and/or poorly differentiated HCCs, KDR expression in the blood space endothelial cells was clear and continuous in 20 cases, and focal in 5 cases. These results suggest that there would be an angiogenesis mechanism via VEGF/Flt-1 or VEGF/KDR in HCC, and the VEGF/KDR system would take a more important role.
97 citations
TL;DR: The importance of the GH/IGF system in diabetic retinopathy and retinal neovascularization has been highlighted by the use of agents that inhibit the system, and approaches may also prove to have benefits for improving vascular patency and vision in patients with diabetic Retinopathy.
Abstract: Growth hormone (GH) and insulin-like growth factor-I (IGF-I) are implicated in the aberrant cell growth and pathological neovascularization that characterises proliferative diabetic retinopathy. While serum levels of IGF-I are reported to be either high or low in diabetic patients, there is evidence that local tissue levels of IGF-I may be more relevant to diabetic retinal pathology. IGF-I and IGF binding proteins (IGFBP) are expressed throughout the retina in vascular, neuronal and glial cells, and are altered in response to hyperglycaemia and hypoxia. Further support for a pathological role for local IGF-I comes from studies showing IGF-I to be increased in the vitreal fluids of patients with proliferative diabetic retinopathy. IGF-I may exert its cell growth promoting properties by stimulating a number of pathways including protein-kinase B (Akt), nuclear factor kB (NF-kappaB)/AP-1 and hypoxic-inducible factor-1alpha (HIF-1alpha). In addition, other growth factors may participate in IGF-I induced cell growth including vascular endothelial growth factor (VEGF), platelet derived growth factor (PDGF) and fibroblast growth factor (FGF). The importance of the GH/IGF system in diabetic retinopathy and retinal neovascularization has been highlighted by the use of agents that inhibit the system. GH receptor antagonists, GH receptor antisense oligonucleotides, somatostatin analogues and receptor neutralising antibodies to IGF-I reduce hypoxic-induced retinal neovascularization. These approaches may also prove to have benefits for improving vascular patency and vision in patients with diabetic retinopathy.
97 citations