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The fibroblast growth factors (FGFs) represent one of the relatively few families of extracellular signalling peptides that have been shown in recent decades to be key regulators of metazoan development. FGFs are required for multiple processes in both protostome and deuterostome groups. Given the wide range of regulatory roles attributed to the FGFs, it is perhaps not surprising that misregulation of this signalling pathway has been implicated in a number of human disease conditions. The focus of the present review is to look at the fundamental components of the FGF pathway and illustrate how this highly conserved regulatory cassette has been deployed to regulate multiple, diverse processes during vertebrate development. This review will explore examples from several vertebrate model organisms and include discussions of the role of FGF signalling in regulating the establishment of the mesoderm, neural patterning, morphogenesis, myogenesis, limb development, and the establishment of right-left asymmetry.

Fibroblast growth factors. --- Vertebrates -- Development. --- Vertebrates -- Growth & development. --- Fibroblast Growth Factors --- Chordata --- Intercellular Signaling Peptides and Proteins --- Animals --- Biological Factors --- Proteins --- Eukaryota --- Peptides --- Amino Acids, Peptides, and Proteins --- Organisms --- Chemicals and Drugs --- Fibroblast Growth Factor 1 --- Vertebrates --- Zoology --- Human Anatomy & Physiology --- Health & Biological Sciences --- Animal Biochemistry --- Animal Anatomy & Embryology --- Growth factors. --- Growth. --- Fibroblast Growth Factors. --- growth & development. --- Fibroblast growth factor --- Mesoderm --- Neurectoderm --- Xenopus --- Organogenesis --- Somites --- Limb --- MyoD --- Somitogenesis --- Morphogenesis --- Left-right asymmetry --- MAPK --- Sprouty --- ERK --- Map kinase phosphatase --- Signal transduction

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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.

Medicine --- 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 --- 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

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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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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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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.

Medicine --- 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 --- 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