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Fibroblast growth factors. --- Receptors, Fibroblast Growth Factor. --- Fibroblast Growth Factor 2. --- Cartilage-Derived Growth Factor --- Class II Heparin-Binding Growth Factor --- FGF-2 --- FGF2 --- Fibroblast Growth Factor-2 --- Heparin-Binding Growth Factor Class II --- Prostate Epithelial Cell Growth Factor --- Prostatropin --- Basic Fibroblast Growth Factor --- Fibroblast Growth Factor, Basic --- HBGF-2 --- Cartilage Derived Growth Factor --- FGF 2 --- FGF Receptor --- Fibroblast Growth Factor Receptor --- Heparin-Binding Growth Factor Receptor --- FGF Receptors --- Fibroblast Growth Factor Receptors --- Receptors, FGF --- Heparin Binding Growth Factor Receptor --- Receptor, FGF --- Fibroblast Growth Factors --- Fibroblast growth factor --- Growth factors --- Mitogens

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Fibroblast growth factors (FGFs) have been recognized primarily as autocrine/paracrine factors that regulate embryonic development and organogenesis. However, recent studies have revealed that some FGFs function as endocrine factors and regulate various metabolic processes in adulthood. Such FGFs, collectively called endocrine FGFs, are comprised of three members (FGF15/19, FGF21, and FGF23: FGF15 is the mouse ortholog of human FGF19). These endocrine FGFs share a common structural feature that enables the endocrine mode of action at the expense of the affinity to FGF receptors. To restore the affinity to FGF receptors in their target organs, the endocrine FGFs have designated the Klotho family of transmembrane proteins as obligate co-receptors. By expressing Klothos in a tissue-specific manner, this unique co-receptor system also enables the endocrine FGFs to specify their target organs among many tissues that express FGF receptors.

Endocrine toxicology. --- Fibroblast growth factors. --- Protein binding. --- Receptors, Growth Factor --- Anatomy --- Glycoside Hydrolases --- Intercellular Signaling Peptides and Proteins --- Metabolic Phenomena --- Peptides --- Proteins --- Receptors, Peptide --- Biological Factors --- Hydrolases --- Phenomena and Processes --- Enzymes --- Amino Acids, Peptides, and Proteins --- Receptors, Cell Surface --- Chemicals and Drugs --- Membrane Proteins --- Enzymes and Coenzymes --- Metabolism --- Receptors, Fibroblast Growth Factor --- Fibroblast Growth Factors --- Endocrine System --- Glucuronidase --- Biology --- Human Anatomy & Physiology --- Health & Biological Sciences --- Cytology --- Animal Biochemistry --- Fibroblast growth factors --- Endocrinology. --- Endocrine aspects. --- Metabolism. --- Fibroblast growth factor --- Life sciences. --- Gene expression. --- Cell biology. --- Life Sciences. --- Cell Biology. --- Gene Expression. --- Cell biology --- Cellular biology --- Cells --- Cytologists --- Genes --- Genetic regulation --- Biosciences --- Sciences, Life --- Science --- Expression --- Growth factors --- Mitogens --- Internal medicine --- Hormones --- Cytology.

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The number of males diagnosed with prostate cancer (PCa) is increasing all over the world. Most patients with early-stage PCa can be treated with appropriate therapy, such as radical prostatectomy or irradiation. On the other hand, androgen deprivation therapy (ADT) is the standard systemic therapy given to patients with advanced PCa. ADT induces temporary remission, but the majority of patients (approximately 60%) eventually progress to castration-resistant prostate cancer (CRPC), which is associated with a high mortality rate. Generally, well-differentiated PCa cells are androgen dependent, i.e., androgen receptor (AR) signalling regulates cell cycle and differentiation. The loss of AR signalling after ADT triggers androgen-independent outgrowth, generating poorly differentiated, uncontrollable PCa cells. Once PCa cells lose their sensitivity to ADT, effective therapies are limited. In the last few years, however, several new options for the treatment of CRPC have been approved, e.g., the CYP17 inhibitor, the AR antagonist, and the taxane. Despite this progress in the development of new drugs, there is a high medical need for optimizing the sequence and combination of approved drugs. Thus, the identification of predictive biomarkers may help in the context of personalized medicine to guide treatment decisions, improve clinical outcomes, and prevent unnecessary side effects. In this Special Issue Book, we focused on the cytobiology of human PCa cells and its clinical applications to develop a major step towards personalized medicine matched to the individual needs of patients with early-stage and advanced PCa and CRPC. We hope that this Special Issue Book attracts the attention of readers with expertise and interest in the cytobiology of PCa cells.

androgen receptor --- docetaxel --- cabazitaxel --- castration-resistant prostate cancer --- chemotherapy --- P-glycoprotein --- EPI-002 --- splice variant --- prostate-specific antigen --- androgen deprivation therapy --- time to PSA nadir --- fibroblasts --- prostate cancer --- androgen sensitivity --- pirfenidone --- TGFβ1 --- G1 cell cycle arrest --- fibroblast growth factor --- fibroblast growth factor receptor --- obesity --- inflammation --- immune cells --- cytokine --- high-fat diet --- KIFC1 --- docetaxel resistance --- apoptosis --- CW069 --- Caveolin-1 --- TP53-regulated inhibitor of apoptosis 1 --- tumour stroma --- tumour microenvironment --- fibroblast --- CAF --- resistance --- radiotherapy --- CCL2 --- CCL22 --- CCL5 --- migration --- LSD1 --- epigenetics --- autophagy --- abiraterone --- enzalutamide --- testosterone --- castration resistant prostate cancer --- animal model --- diet --- fat --- in vitro --- in vivo --- mouse --- AKR1C3 --- hormone-naïve prostate cancer --- immunohistochemistry --- tissue microarray --- androgen receptor dependency --- fibroblast-dependent androgen receptor activation --- n/a --- hormone-naïve prostate cancer

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Nephropathic cystinosis (MIM # 219800) is a rare autosomal recessive disorder caused by mutations in the lysosomal cystine transporter cystinosin, encoded by the CTNS gene (17p13.2). This devastating condition initially affects kidneys and subsequently many other organs including eyes, thyroid, pancreas, muscles, and brain. While lysosomal cystine storage is a key feature of the disease and the main target of current therapy, recent groundbreaking research has revealed that cystinosin has diverse functions in cells, being involved in vesicle trafficking, energy homeostasis, and cell death mechanisms. These discoveries deepen our insights into the mechanisms of cystinosis and of lysosomal biology in general. In this Special Issue dedicated to the pioneer of cystinosis research Dr. Jerry Schneider, we highlight the state-of-the-art understanding of cellular and molecular mechanisms of various disease features, opening new horizons for innovative treatment strategies for cystinosis and potentially other lysosomal storage diseases.

cystinosis --- cysteamine --- bone --- osteoclast --- genotype --- CD34+ hematopoietic stem and progenitor cells --- gene therapy --- pre-clinical studies --- investigational new drug application --- clinical trial --- disulfiram --- mice --- zebrafish --- fertility --- azoospermia --- hypogonadism --- histopathology --- mouse model --- lysosomal storage disease --- cell and animal models --- infantile nephropathic cystinosis --- bone-muscle wasting --- fibroblast growth factor 23 --- osteoclasts --- sclerostin --- leptin --- fractures --- nephropathic cystinosis --- hollow fiber membrane --- 3-dimensional models --- autophagy --- macrophages --- inflammasome --- proximal tubular cells --- endocytosis --- apoptosis --- chitotriosidase --- interleukins --- galectin-3 --- novel therapies --- endolysosome --- epithelial cell differentiation --- homeostasis --- lysosomal storage diseases --- mitochondrial distress --- kidney proximal tubule --- programmed cell death --- central nervous system --- cortical atrophy --- arterial spin labelling --- cystine blood level --- lysosomal storage disorder --- history --- treatment strategies for cystinosis --- newborn screening --- clinical course --- CTNS-pathogenic variants --- newborn screening for cystinosis --- kidney progenitors --- cell model --- biomarkers --- cystine --- kidney --- therapeutic monitoring

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The regenerative and immunomodulatory properties of mesenchymal stem cells (MSCs) have made these cells the focus of multiple pre-clinical studies and clinical trials. While the results from these clinical studies have established that MSCs are safe, the efficacy of these cells is not as well-established. In this regard, there have been increased efforts towards generating potentiated/activated MSCs with enhanced therapeutic efficacy. Research on the mechanisms for enhancing MSC potency and efficacy is an area of active study with great potential for translation into clinical settings. The purpose of this book is to bring together recent research from a broad range of topics relating to potentiation strategies for enhancing MSC therapeutic efficacy, including growth factor pre-conditioning, hypoxia, and 3D culture. The research compiled in this book increases the basic understanding of MSC culture techniques and describes some MSC preparations for potential novel therapeutic applications.

cell therapy --- immunomodulation --- polyunsaturated fatty acid --- CD206 --- phagocytosis --- mesenchymal stem cells --- Vadadustat --- AKB-6548 --- preconditioning --- priming --- secretome --- chemotaxis --- Wharton’s jelly mesenchymal stem cells --- umbilical cord --- oxygen conditions --- secretory profile --- neuroprotection --- mesenchymal stromal cells --- 3D culture --- neurospheres --- spheroids --- pluripotency --- neural --- quiescence --- mesothelioma --- malignant pleural mesothelioma (MPM) --- liver cirrhosis --- placenta-derived mesenchymal stem cells --- WKYMVm --- combination therapy --- iPSC-derived MSCs --- iMSC secretome --- pre-conditioning --- angiogenesis --- IFN-γ --- hypoxia --- potentiation of iMSC efficacy --- nanofiber-hydrogel composite --- spinal cord injury --- inflammation --- macrophages --- secondary injury --- astrocytes --- axon growth --- adipose tissue-derived stem cells (ASCs) --- autophagy --- rapamycin --- 3-methyladenine --- immunosuppression --- exosome --- engineered cardiac patches --- adipose-derived stem cell --- paracrine potential --- osteogenic differentiation --- hepatocyte growth factor --- fibroblast growth factor 2