Tumors of the Nervous System
Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw in Hankey's Clinical Neurology, 2020
Growth factor and growth factor receptor overexpression are common in malignant gliomas and may accelerate tumorigenesis and tumor progression. Most of these are found predominantly in diffuse, high-grade, astrocytic tumors and include the following: EGFR.Platelet-derived growth factor (PDGF).Vascular endothelial growth factor (VEGF).Insulin-like growth factor (IGF-1).Basic fibroblast growth factor (bFGF, FGF-2).Transforming growth factor (TGF)-alpha.
Age-Related Macular Degeneration Drug Delivery
Glenn J. Jaffe, Paul Ashton, P. Andrew Pearson in Intraocular Drug Delivery, 2006
Vascular endothelial growth factor (VEGF) is an important molecule in angiogenesis development. Thus, anti-VEGF therapy is an attractive approach to treat AMD (64–66). In human studies, high VEGF concentrations are present in the vitreous in angiogenic retinal disorders but not in inactive or non-neovascularization-associated disease states (65,66). Further, VEGF is preferably localized within the cytoplasm of retinal pigment epithelial cells in the highly vascularized regions of surgically excised CNV membranes in humans and in animal models (64,67). Recent preclinical and clinical studies have demonstrated that blocking VEGF may have potential importance in the treatment of CNV secondary to AMD (68,69). In addition, anti-VEGF therapy may address the destructive effects caused by leakage secondary to CNV. VEGF, also known as vascular permeability factor, increases vascular leakage 50,000 times more potently than does histamine (70). Recent laboratory work suggested that anti-VEGF therapy may inhibit diabetes-induced blood–retinal barrier breakdown in animals (71).
Radiolabeled Agents for Molecular Imaging and/or Therapy
George C. Kagadis, Nancy L. Ford, Dimitrios N. Karnabatidis, George K. Loudos in Handbook of Small Animal Imaging, 2018
Vascular endothelial growth factor-A (VEGF-A) plays a central role in inducing the formation of new blood vessels during physiological and pathological angiogenesis. Bevacizumab and ranibi-zumab are antibodies directed against VEGF-A. The visualization of tumor VEGF expression using molecular imaging techniques was the aim of many research studies. 111In-bevacizumab (SPECT) can image VEGF expression in various malignancies (Nagengast et al. 2011). There was, however, no direct correlation between radiolabeled bevacizumab uptake and VEGF-A expression in tumor as determined by conventional methods suggesting that other factors may play a role in bevacizumab targeting (e.g., vascular volume and permeability). Nevertheless, there is an ongoing effort for noninvasive measurement of VEGF levels in tumors.
Astragaloside IV alleviates heart failure by promoting angiogenesis through the JAK-STAT3 pathway
Published in Pharmaceutical Biology, 2019
Yan-Bo Sui, Yu Wang, Li Liu, Feng Liu, Yi-Qing Zhang
Recent research found that angiogenesis-mediated recovery of the microvasculature is stimulated by pharmacological or genetic intervention that may have a greater potential in the therapy of HF (Ylä-herttuala and Alitalo 2003; van der Laan et al. 2009). Angiogenesis is the physiological process through which new blood vessels form from preexisting vessels (Carmeliet 2005). Vascular endothelial growth factor (VEGF) is a crucial regulator of angiogenesis, which is produced by cells and can stimulate the formation of blood vessels (Ferrara et al. 2003; Olsson et al. 2006). Signal transducer and activator of transcription 3 (STAT3) is an extensively investigated nuclear factor which is activated by cytokine receptors via Janus kinase (JAK) (Levy and Darnell 2002). STAT3 exerts crucial effects on angiogenesis in heart pathogenesis, and is a potential molecular target of angiogenesis-mediated therapy (Osugi et al. 2002; Hilfiker-kleiner et al. 2004).
Isotretinoin does not alter VEGF-A and VEGF-C levels: do retinoids behave differently in dose-dependent and/or in vivo/in vitro conditions?
Published in Cutaneous and Ocular Toxicology, 2020
Erhan Ayhan, Eşref Araç, Özgür Aslan
Vascular endothelial growth factor (VEGF) family consists of VEGF-A (known as VEGF), VEGF-B, VEGF-C, VEGF-D and placental growth factor (PlGF). VEGF-A is an important regulator involved in the developmental vasculogenesis, angiogenesis and differentiation of progenitor endothelial cells. VEGF-B and PlGF induce angiogenesis in normal tissues, but their activity is much weaker than that of VEGF-A1,2. VEGF-C and VEGF-D are produced from their precursors and regulate lymphangiogenesis3,4. There are publications reporting that retinoids including isotretinoin (13-cis-retinoic acid) are successful in lymphangioma circumscriptum, angiolymphoid hyperplasia with eosinophilia, diffuse dermal angiomatosis, and Kaposi’s sarcoma5–12. In some publications, the effect of success is claimed to be the inhibitory effect on VEGF5,6. However, in the literature, it is seen that various forms of retinoids have different results on VEGF-A and VEGF-C levels when tested at different dosages, in different diseases and under different conditions such as in vivo or in vitro.13–18 However, there is no study on using only isotretinoin and its effect on VEGF-A and VEGF C in humans. Therefore, we aimed to investigate whether isotretinoin commonly used in dermatology has an effect on VEGF-A and VEGF-C.
The role of tumor angiogenesis as a therapeutic target in colorectal cancer
Published in Expert Review of Anticancer Therapy, 2018
Francesca Battaglin, Alberto Puccini, Rossana Intini, Marta Schirripa, Alessandra Ferro, Francesca Bergamo, Sara Lonardi, Vittorina Zagonel, Heinz-Josef Lenz, Fotios Loupakis
Angiogenesis is a complex process regulated by various pro- and anti-angiogenic factors, which is crucial for tissue growth and development. The loss of its fine equilibrium is one of the hallmarks of cancer [1]. Vascular endothelial growth factor (VEGF) is a key regulator of angiogenesis both in physiological processes and pathological events, such as cancer development. The VEGF family comprises five members: VEGF-A, -B, -C, -D, and placental growth factor (PlGF) [2]. VEGF-A is the most widely recognized and major player in tumor angiogenesis. It undergoes alternative splicing, which leads to several isoforms that differ in terms of distribution and function [3]. Although many elements may influence the VEGF pathway, hypoxia remains the main factor that regulates angiogenesis. Hypoxia induces VEGF expression through transcription factor hypoxia inducible factor-1 (HIF-1) and HIF-2. Moreover, low oxygen tension promotes VEGF upregulation by an increase in the stability of its mRNA51 [4]. Three different receptor tyrosine kinases (RTKs) are involved in VEGF signaling: VEGFR-1, -2, and -3. VEGF-A interacts mainly with VEGFR-2, which is normally expressed by endothelial cells, but it can also bind to VEGFR-1. VEGF-B and PlGF bind to VEGFR-1, while VEGF-C and -D bind to VEGF-2 and VEGFR-3, although with a higher affinity for the latter [5].
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