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Fibroblast growth factor (FGF) signal transmission has an essential function in embryonic development and tissue repair, and is dysregulated in the vast majority of malignancies studied. The FGF signaling in the tumor cells is usually increased by autocrine and paracrine mechanisms and gives them a high growth potential, resistance to apoptosis, neoangiogenesis and metastasis, all essential parameters relevant for tumor progression. This makes FGFs, and their tyrosine kinase receptors FGFRs, valuable targets for therapeutic interventions. This book is a collection of 15 recent articles—both original work and reviews—that summarize the current research state effectively. The content covers FGF signaling aspects in gastric, skin, liver, esophageal cancer, melanoma, mesothelioma and glioblastoma, including one article that addresses the role of FGF in the tumor-microenvironment cross-talk. Several reports describe the development of compounds targeting FGFRs, their structure and interaction with the receptor molecules, and their effectivity in preclinical and clinical testing. In summary, the papers demonstrate the complexity of the topic, with various FGF ligands and receptors involved and the need for further research. They also present results that fuel hope that targeting cancer with dysfunctional FGF signaling can become a realistic treatment option.

Medicine --- FGFR4 --- FGF19 --- gene regulation --- cancer signaling --- anticancer --- FRS2 --- FGFR --- NVP-BGJ398 --- LY2874455 --- sarcoma --- cancer-associated fibroblasts --- GPER --- breast cancer --- estrogen --- FGFR1 --- FGF2 --- optogenetics --- ERK --- AKT --- receptor kinase --- neurite outgrowth --- HEK293 --- PC12 --- fibroblast growth factor receptors --- signaling --- receptor cross-talk --- coreceptor --- membrane proteins --- FGFR2 --- ERK1/2 --- phosphorylation --- serine --- negative feedback loop --- cancer --- prognosis --- HCC --- inhibitors --- FGF --- fibroblast growth factor --- autocrine signaling --- skin --- melanoma --- squamous and basal cell carcinoma --- seborrheic keratosis --- targeted therapy --- resistance --- structure --- kinase inhibitor --- gastric cancer --- monoclonal antibody --- small molecule --- FGFR2c --- autophagy --- keratinocyte --- MTOR --- JNK1 --- review --- malignant glioma --- brain cancer --- astrocytoma --- Sprouty proteins --- FGF-mediated signaling --- tumor suppressor --- tumor promoter --- malignant pleural mesothelioma --- overall survival --- immunohistochemistry --- infigratinib sensitivity --- FGF8 --- FGF18 --- adenocarcinoma of the esophagogastric junction --- neoadjuvant therapy --- n/a

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• Reference Manager
• EndNote
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Fibroblast growth factor (FGF) signal transmission has an essential function in embryonic development and tissue repair, and is dysregulated in the vast majority of malignancies studied. The FGF signaling in the tumor cells is usually increased by autocrine and paracrine mechanisms and gives them a high growth potential, resistance to apoptosis, neoangiogenesis and metastasis, all essential parameters relevant for tumor progression. This makes FGFs, and their tyrosine kinase receptors FGFRs, valuable targets for therapeutic interventions. This book is a collection of 15 recent articles—both original work and reviews—that summarize the current research state effectively. The content covers FGF signaling aspects in gastric, skin, liver, esophageal cancer, melanoma, mesothelioma and glioblastoma, including one article that addresses the role of FGF in the tumor-microenvironment cross-talk. Several reports describe the development of compounds targeting FGFRs, their structure and interaction with the receptor molecules, and their effectivity in preclinical and clinical testing. In summary, the papers demonstrate the complexity of the topic, with various FGF ligands and receptors involved and the need for further research. They also present results that fuel hope that targeting cancer with dysfunctional FGF signaling can become a realistic treatment option.

FGFR4 --- FGF19 --- gene regulation --- cancer signaling --- anticancer --- FRS2 --- FGFR --- NVP-BGJ398 --- LY2874455 --- sarcoma --- cancer-associated fibroblasts --- GPER --- breast cancer --- estrogen --- FGFR1 --- FGF2 --- optogenetics --- ERK --- AKT --- receptor kinase --- neurite outgrowth --- HEK293 --- PC12 --- fibroblast growth factor receptors --- signaling --- receptor cross-talk --- coreceptor --- membrane proteins --- FGFR2 --- ERK1/2 --- phosphorylation --- serine --- negative feedback loop --- cancer --- prognosis --- HCC --- inhibitors --- FGF --- fibroblast growth factor --- autocrine signaling --- skin --- melanoma --- squamous and basal cell carcinoma --- seborrheic keratosis --- targeted therapy --- resistance --- structure --- kinase inhibitor --- gastric cancer --- monoclonal antibody --- small molecule --- FGFR2c --- autophagy --- keratinocyte --- MTOR --- JNK1 --- review --- malignant glioma --- brain cancer --- astrocytoma --- Sprouty proteins --- FGF-mediated signaling --- tumor suppressor --- tumor promoter --- malignant pleural mesothelioma --- overall survival --- immunohistochemistry --- infigratinib sensitivity --- FGF8 --- FGF18 --- adenocarcinoma of the esophagogastric junction --- neoadjuvant therapy --- n/a

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For many years, arteriogenesis, also called collateral formation, has been regarded as being a beneficial process to restore blood flow to distal tissues in occluded arteries. Therefore, it is frequently referred to in relation to therapeutic angiogenesis. Despite the big clinical potential and the many promising clinical trials on arteriogenesis and therapeutic angiogenesis, the exact molecular mechanisms involved in the multifactorial processes of arteriogenesis are still not completely understood. A better understanding is needed in order to define successful clinical therapies. In this Special Issue, multiple aspects of arteriogenesis and therapeutic angiogenesis will be addressed, ranging from the role of inflammatory processes and immune cells, to growth factors, microRNAs and environmental factors like hypoxia. Therapeutic angiogenesis will also be discussed in relation to the atherosclerosis and intraplaque angiogenesis in hypoxic lesions, as well as specific forms of arteriogenesis in relation to spinal cord blood supply and aorta surgery. The effects of exercise, a frequently prescribed therapy for PAD patients, on arteriogenesis are also discussed. Overall, the papers in this Special Issue on arteriogenesis and therapeutic angiogenesis provide important new insights in the underlying pathophysiological mechanism of these complex processes and may be helpful to define a successful future intervention directed at therapeutic angiogenesis.

Medicine --- factor VII activating protease --- HABP2 --- VEGF --- matrigel --- neo-vascularization --- hind limb ischemia --- angiogenesis --- arteriogenesis --- ERK --- endothelial cells --- inflammation --- macrophages --- atherosclerosis --- pericyte --- rAAV --- capillary --- microRNA --- isomiRs --- epitranscriptome --- neovascularization --- A-to-I editing --- m6A --- RNA modifications --- RNA methylation --- lower extremity arterial disease --- peripheral arterial disease --- blood flow restriction --- activity-based benefits --- training effects --- effect mechanism --- hyperoxygenation --- vein graft disease --- vascular biology --- spinal cord ischemia --- paraplegia --- aortic disease --- TAAA --- collateral network --- paraspinous compartment --- NO --- NOTCH --- innate immunity --- mast cell --- GH and eNOS --- IGF-I --- oxidative stress and arterial inflammation --- vascular homeostasis --- GHAS trial --- collateral artery growth --- SMC proliferation --- potassium channel --- KV1.3 --- KCa3.1 --- FGFR-1 --- Egr-1 --- PDFG-R --- αSM-actin --- TLR2/6 --- femoral artery ligation --- blood flow recovery --- collateral growth --- VHL loss of function --- microRNA-212/132