The Prostate. Supplement最新文献

{"title":"Cell kinetics of prostate exocrine and neuroendocrine epithelium and their differential interrelationship: new perspectives.","authors":"Y Xue,&nbsp;F Smedts,&nbsp;A Verhofstad,&nbsp;F Debruyne,&nbsp;J de la Rosette,&nbsp;J Schalken","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The prostate gland consists of a complex ductal system lined with exocrine basal and luminal cells, and neuroendocrine epithelial cells. This paper reviews the histologic and molecular cell biologic characteristics of these cells, in normal adult tissue, during prostate morphogenesis, and in the development of benign and malignant neoplastic conditions. Expression of differentiation markers, as well as proliferation and apoptosis markers, growth factors and associated receptors, and abnormalities in genes and chromosomes are reviewed. Accumulating data indicate that (1) pluripotent immortal stem cells are located in the basal cell compartment of the prostate; (2) there is a subpopulation of epithelial cells in the prostate gland (intermediate cells) that have both structural and functional characteristics common to basal and luminal cells, which may be identified in various conditions; and prostate NE cells may have the same common origin as other exocrine cells, and share the same differentiation pathway. A stem cell model is proposed in which both exocrine and endocrine cells are derived from a subpopulation of basal cells (stem cell) that give rise to luminal cells through intermediate cells (pluripotent amplifying cells). These cells are also probably highly implicated in the early development of prostate benign and malignant neoplasia.</p>","PeriodicalId":77436,"journal":{"name":"The Prostate. Supplement","volume":"8 ","pages":"62-73"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20607782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Provocative aspects of androgen genetics.","authors":"T R Brown","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Androgens play a key role in prostate structure and function, leading to the hypothesis that effects of the hormone are an important component in the development of prostatic disease. Differences in serum testosterone levels and 5alpha-reductase activities between ethnic and racial groups have been implicated in the variable incidence of prostate cancer among certain populations. Androgen receptors transduce the steroid signal within cells, but attempts to correlate differences in receptor levels with prostatic disease have been unsuccessful. However, molecular studies of androgen receptor gene structure have recently provided new insights toward defining a genetic basis for the pathology associated with three diseases--spinal bulbar muscular atrophy, breast carcinoma, and prostate cancer--affecting middle-aged and older men. In summary, epidemiologic data on androgen biosynthesis, metabolism, and action of androgens and molecular genetic analysis of gene structure have led to a new understanding of the interrelationships between environmental and genetic factors that may impact on the incidence of certain pathologic conditions in men.</p>","PeriodicalId":77436,"journal":{"name":"The Prostate. Supplement","volume":"6 ","pages":"9-12"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19607836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Androgen regulation of gene expression.","authors":"J E Perry,&nbsp;M E Grossmann,&nbsp;D J Tindall","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Androgen receptors are important transcription factors regulating the expression of a number of genes in androgen-responsive cells and may play a role in prostate cancer. This article describes transcriptional suppressors and other transcription factors which may play important roles in modulating the expression of androgen receptors.</p>","PeriodicalId":77436,"journal":{"name":"The Prostate. Supplement","volume":"6 ","pages":"79-81"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19609762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Growth factors as mediators of androgen action during male urogenital development.","authors":"G R Cunha","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Studies on the developing prostate and seminal vesicle suggests that androgens act via mesenchymal androgen receptors to elicit synthesis and secretion of keratinocyte growth factor and probably other paracrine factors that regulate epithelial growth and morphogenesis. Clearly, the overall regulation of prostatic epithelial growth and ductal branching morphogenesis is complex and multifactorial, involving the interaction of both positive and negative regulators, extracellular matrix, cell surface receptors for growth factors, and vascularization. Future progress in our understanding of normal and abnormal prostatic growth will certainly be dependent upon the utilization of appropriate, biologically relevant models to examine the respective roles of these complex developmental process.</p>","PeriodicalId":77436,"journal":{"name":"The Prostate. Supplement","volume":"6 ","pages":"22-5"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19608656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNA methylation, molecular genetic, and linkage studies in prostate cancer.","authors":"D F Jarrard,&nbsp;G S Bova,&nbsp;W B Isaacs","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Molecular biologic studies have now identified a number of important genetic and epigenetic mechanisms that cause alterations in growth and differentiation genes in prostate cancer. In addition to DNA deletion and point mutation, DNA methylation represents a new paradigm for the inactivation of tumor suppressor or growth suppressor genes. The identification of new genes, including a prostate cancer susceptibility locus, may furnish further insight into the molecular characteristics of prostate cancer and permit the early identification of affected individuals.</p>","PeriodicalId":77436,"journal":{"name":"The Prostate. Supplement","volume":"6 ","pages":"36-44"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19609755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of androgen in prostate growth and regression: stromal-epithelial interaction.","authors":"C Lee","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The prostate is a secretory gland in which secretions produced by its cells are transported through the ductal system and discharged into the urethra. Each prostatic ductal system can be traced from the opening in the urethra as a single tubular structure from which branches and sub-branches are formed in a manner like the branching pattern of a tree. Owing to the distance from the urethral orifice, regions of the prostatic ductal system can be classed into the proximal, intermediate, and distal regions. In the distal region, the tips of the ductal system (equivalent to the top of the tree), the epithelial cells are tall and columnar in shape, and active in cell division. Cells of the intermediate region (equivalent to the majority of the body of the tree) are also of tall and columnar type but are mitotically quiescent. Cells in this region are the only ones that have the ability to secrete. Cell death is not evident in these two regions. Cells in the proximal region, a region that is immediately adjacent to the urethra (equivalent to the tree trunk) are low cuboidal or flat in shape and are actively undergoing cell death. These observations indicate that cells in different regions of the prostatic ductal system are not the same, even though they are exposed to the same circulating level of androgen. The recognition of this regional heterogeneity in cell shape and activity in the ductal system has advanced our understanding of the basic biology of the prostate. For example, our understanding of the cellular mechanism of action of androgen in the prostate should be re-evaluated. In the past, the convention concept of androgen action has been a stimulatory one, and a depletion of this androgenic support leads to prostatic cell death. The recognition of a regional heterogeneity in cellular activity has created a situation in which all prostatic cells in the same prostatic ductal system are exposed to the same level of circulating androgen. However, these cells are not responding to the same amount of androgen in the same manner: some are multiplying while others are dying. These observations indicate that the effect of androgen vary according to the location of prostatic cells in the ductal system. A new concept of the role of androgen in prostatic growth, differentiation, and cell death is discussed.</p>","PeriodicalId":77436,"journal":{"name":"The Prostate. Supplement","volume":"6 ","pages":"52-6"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19609757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Benign prostatic hyperplasia: a review of its histogenesis and natural history.","authors":"J E Oesterling","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Although the exact etiology of benign prostatic hyperplasia (BPH) is not well-defined, it is thought to occur as a result of epithelial-stromal interactions in the appropriate hormonal milieu. Benign prostatic hyperplasia originates in the periurethral and transition zones of the prostate in a microscopic (histologically identifiable) state as early as the third decade of life. With advancing age and the presence of androgens, approximately 50% of microscopic BPH will develop into macroscopic (palpably enlarged prostate) BPH. However, clinically significant BPH, necessitating treatment, will develop in only 50% of men with an enlarged prostate gland. In the United States, the estimated risk of a 50-year old man undergoing therapeutic intervention in his lifetime is approximately 40%. If left untreated, a significant number of symptomatic patients will remain stable or improve without adverse sequelae.</p>","PeriodicalId":77436,"journal":{"name":"The Prostate. Supplement","volume":"6 ","pages":"67-73"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19609760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic regulation of androgen action.","authors":"P J Kallio,&nbsp;J J Pakvimo,&nbsp;O A Janne","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The androgen receptor (AR) belongs to the superfamily of nuclear receptors that employ complex genetic mechanisms to guide the development and physiological functions of different target tissues. Upon interaction with its cognate hormone, AR activates or represses gene transcription through association with specific DNA elements and/or proteins. This review summarize briefly our current view of androgen action, with a special emphasis on genetic factors that may modulate the response.</p>","PeriodicalId":77436,"journal":{"name":"The Prostate. Supplement","volume":"6 ","pages":"45-51"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19609756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroendocrine differentiation and hormone-refractory prostate cancer.","authors":"P A Abrahamsson","doi":"10.1002/(sici)1097-0045(1996)6+<3::aid-pros2>3.0.co;2-t","DOIUrl":"https://doi.org/10.1002/(sici)1097-0045(1996)6+<3::aid-pros2>3.0.co;2-t","url":null,"abstract":"<p><p>There is an intriguing link between differentiation of neuroendocrine cells and tumor progression in prostate cancer. Neuroendocrine differentiation appears to be associated with the androgen-independent state, for which there is currently no successful therapy. However, the role of the neuroendocrine cells is complex, both in the normal prostate and in the pathway toward malignancy. One important area of research is to investigate the hormones expressed by prostatic neuroendocrine cells and, in particular, to elucidate their significance to androgen independence. It is hoped that an understanding of the specific roles of hormones such as somatostatin, bombesin, and serotonin in prostate cancer may lead to improved therapeutic approaches.</p>","PeriodicalId":77436,"journal":{"name":"The Prostate. Supplement","volume":"6 ","pages":"3-8"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/(sici)1097-0045(1996)6+<3::aid-pros2>3.0.co;2-t","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19608658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"5alpha-reductase inhibitors/finasteride.","authors":"E Stoner","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Benign prostatic hyperplasia (BPH) is a disease diagnosed by the presence of prostatic enlargement and lower-tract urinary obstruction. Finasteride (Proscar), is a potent and specific inhibitor of 5alpha-reductase, which inhibits the conversion of testosterone (T) to dihydrotestosterone (DHT) an important promoter of prostatic growth. It has provided a new therapeutic alternative for the treatment of BPH. The safety and efficacy of finasteride in the treatment of symptomatic BPH have been demonstrated by two multi-center placebo-controlled studies. After 12 months of treatment with 5 mg finasteride daily, prostate volume, DHT and prostate-specific antigen (PSA) levels were reduced and maximum urinary flow rates and symptom scores were improved. Finasteride was well-tolerated. Upon completion of the controlled studies, patients were eligible to enter an open-label extension study in which all patients received 5 mg finasteride. Approximately half of the 543 patients randomized to the 5 mg finasteride group in the controlled studies have now been treated with 5 mg finasteride continuously for 3 years. The data provided by this group of patients on the long-term safety and efficacy of finasteride in the treatment of symptomatic BPH are reviewed.</p>","PeriodicalId":77436,"journal":{"name":"The Prostate. Supplement","volume":"6 ","pages":"82-7"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19609763","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}