Listing 1 - 4 of 4 |
Sort by
|
Choose an application
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
Choose an application
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
Choose an application
In this Special Issue of Genes entitled “Genetic Conditions Affecting the Skeleton: Congenital, Idiopathic Scoliosis and Arthrogryposis”, evidence is presented that suggests that congenital, idiopathic scoliosis, and arthrogryposis share similar overlapping, but also distinct, etiopathogenic mechanisms, including connective tissue and neuromuscular mechanisms. Congenital scoliosis (CS) is defined by the presence of an abnormal spinal curvature, due to an underlying vertebral bony malformation (VM). Idiopathic scoliosis (IS) is defined by the presence of an abnormal structural spinal curvature of ≥10 degrees in the sagittal plane, in the absence of an underlying VM. Arthrogryposis is defined by the presence of congenital contractures in two or more joints of the appendicular skeleton. All three conditions have complex genetic causes. This Special Issue highlights the complex nature of these conditions and current concepts in our approach to better understand their genetics.
Research & information: general --- Biology, life sciences --- Genetics (non-medical) --- spinal curvatures --- scoliosis --- idiopathic --- DNA methylation --- pyrosequencing --- estrogen receptor 1 --- ESR1 --- scoliosis progression --- adolescent idiopathic scoliosis --- idiopathic scoliosis --- exome sequencing --- spine --- polygenic --- variants --- musculoskeletal disease --- cytoskeleton --- extracellular matrix --- contracture --- arthrogryposis --- congenital --- POC5 --- cilia --- genetics --- spine deformity --- genetic predisposition --- complex trait --- model animal --- genome wide association study --- genetic linkage study --- Amyoplasia --- DECIPHER (DatabasE of genomiC variation and Phenotype in Humans using Ensemble Resources) --- CNV (copy number variant) --- DA (distal arthrogryposis) --- IPA (ingenuity pathway analysis) --- HPO (human phenotype ontology) --- akinesia --- MYOD --- IGF2 --- FGFR1 (Fibroblast growth factor receptor 1) --- genetic variations --- congenital scoliosis --- monozygotic twin --- epigenome-wide association study --- bone --- discordant --- curve severity --- differentially methylated region --- congenital vertebral malformation --- copy number variant --- CNV --- CHRNG --- distal arthrogryposis type 8 --- Escobar --- multiple pterygium syndrome --- MYH3 --- protein tyrosine kinase 7 (PTK7) --- whole exome sequencing --- n/a
Choose an application
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
Listing 1 - 4 of 4 |
Sort by
|