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Premier global open access journal for peer-reviewed science, research, and education regarding the effects of the presence, deficiency, and use of testosterone and other androgens in diverse patient populations and the influence of these hormones on multiple disease states and conditions.

hypogonadism --- testosterone --- andrology --- urology --- sexual and reproductive medicine --- endocrinology --- Androgens --- Androgen Effect --- Androgen Effects --- Androgen Receptor Agonists --- Androgenic Agents --- Androgenic Compounds --- Androgen --- Androgen Receptor Agonist --- Agents, Androgenic --- Agonist, Androgen Receptor --- Agonists, Androgen Receptor --- Compounds, Androgenic --- Effect, Androgen --- Effects, Androgen --- Receptor Agonist, Androgen --- Receptor Agonists, Androgen --- Receptors, Androgen --- agonists --- Periodical

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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact

Medicine --- Oncology --- high risk prostate cancer --- androgen deprivation therapy --- radical prostatecomy --- recurrent prostate cancer --- radiation therapy

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There is extensive evidence from animal models that gonadal steroids, produced in fetal and neonatal life, act on the developing organism to produce sex differences far beyond the reproductive system. That early gonadal steroid exposure also plays an important role in human development is supported by studies of individuals with disorders of sex determination and differentiation. It is much less clear whether normal variation in gonadal steroid exposure predicts sexually dimorphic health outcomes or within-sex variation. This is largely due to challenges related to the assessment of gonadal steroid exposure in the developing fetus and neonate. Regarding the prenatal period, serial measurements of serum hormone levels in the fetus, for use in studies of later development, are not possible for ethical reasons. Researchers have measured hormones in maternal blood, umbilical cord blood, and amniotic fluid; used putative anthropometric indices such as the relative lengths of the 2nd and 4th digits (2D:4D); evaluated common variants in genes related to hormone production, transport, and metabolism; and examined development in opposite sex twins and the offspring of mothers with hyperandrogeny. Each of these approaches has particular strengths and notable weaknesses. Regarding the neonatal period, serial measurements in serum are often impractical for studies of typical development. Salivary hormone assays, frequently used in studies of older children and adults, have not been extensively investigated in neonates. The most appropriate timing for testing is also open to debate. Early work suggested that testosterone levels in males begin to rise after the first postnatal week, peak around the 3rd to 4th months of life, and then drop back to very low levels by 1 year. However a more recent study of 138 infants did not demonstrate this pattern. Testosterone was highest on the day of birth and gradually dropped over the first 6 months. Even less is known about patterns of early estrogen exposure, though highly sensitive bioassays indicated that sex differences are present in early childhood. In addition, the design and interpretation of studies may be impacted by widespread acceptance of conceptual frameworks that are not well-supported empirically. For example, many researchers presume that the free hormone hypothesis, which states that unbound hormone is more readily diffusible into tissues and thus a better measure of actual exposure, is true. However this hypothesis has been challenged on multiple grounds. A second example: it is generally accepted that masculinization of the human brain is primarily mediated by the androgen receptor (in contrast to rodents where the estrogen receptor plays a major role), in part because chromosomal males with complete androgen insensitivity generally espouse a female gender identity. However this is not always the case, and other sexually dimorphic outcomes have not been carefully assessed in CAIS. The aim of this research topic is to gather together experimental and review papers which address the diverse challenges in assessing prenatal and neonatal gonadal steroid exposure for studies of human development with the expectation that this will allow more critical appraisal of existing studies, identify critical research gaps, and improve the design of future studies.

Endocrinology. --- minipuberty --- Testosterone --- androgen receptor --- digit ratio --- prenatal --- sexual differentiation --- umbilical cord blood --- Opposite-sex twins --- Saliva --- Hypogonadism

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Genital Diseases, Male --- Andrology --- Generative organs, Male --- Andrologie --- Organes génitaux mâles --- Periodicals --- Diseases --- Périodiques --- Maladies --- Androgens. --- Endocrinology. --- Genitalia, Male --- Semen. --- Testicular Hormones. --- Andrology. --- physiology. --- Urology --- Endocrinology --- Reproduction --- Chemistry --- Biochemistry --- General and Others --- Genetics --- Zoology --- Health Sciences --- Life Sciences --- Physiology --- Gynaecology. Obstetrics --- Reproduction. --- Chemistry. --- Zoology. --- Health Sciences. --- Life Sciences. --- Organes génitaux mâles --- Périodiques --- MDREPROD --- Hormones, Testicular --- Seminal Plasma --- Plasma, Seminal --- Endocrinology and Metabolism Specialty --- Metabolism and Endocrinology Specialty --- Androgen Effect --- Androgen Effects --- Androgen Receptor Agonists --- Androgenic Agents --- Androgenic Compounds --- Agents, Androgenic --- Agonists, Androgen Receptor --- Compounds, Androgenic --- Effect, Androgen --- Effects, Androgen --- Receptor Agonists, Androgen --- Receptors, Androgen --- agonists --- Human reproduction --- Men --- Endocrine System Diseases --- Endocrine aspects --- Androgens --- Semen --- Testicular Hormones --- Genitals, Male --- Reproductive System, Male --- Accessory Sex Organs, Male --- Genital Organs, Male --- Sex Organs, Accessory, Male --- Genital, Male --- Male Genital --- Male Genital Organs --- Male Genitalia --- Male Genitals --- Male Reproductive System --- Male Reproductive Systems --- Organs, Male Genital --- Reproductive Systems, Male --- System, Male Reproductive --- Systems, Male Reproductive --- physiology --- periodicals --- Androgen --- Androgen Receptor Agonist --- Agonist, Androgen Receptor --- Receptor Agonist, Androgen --- Endocrinology.. --- Andrology - Periodicals --- Genital Diseases, Male - periodicals

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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 --- n/a --- hormone-naïve prostate cancer