Fetal Prostate Growth and Development

Xia, Tongli; Blackburn, Will R.; Gardner, William A.

doi:10.3109/15513819009067141

Cited by 28 publications

(31 citation statements)

References 22 publications

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“…prostate duct formation with ducts invaginating from the urethra and ending in solid epithelial buds, consistent with the 'bud' stage of prostate development as described by Xia et al [7], and usually seen between 20 and 30 weeks of gestation ( fig. 2).…”

Section: Resultssupporting

confidence: 52%

“…This prostatic development is dependent on epithelial-mesenchymal interaction, and it has been suggested that it is the mesenchyme that mediates epithelial growth and is the target and mediator of androgenic effects on the developing prostate epithelium [14]. Prostate glandular development has been divided into three stages: (1) 'bud' stage (20-30 weeks) with simple, solid cellular buds at the end of the ducts; (2) 'bud-tubule' stage (30-36 weeks) with recognizable cellular buds and acinar structures in both inner and peripheral zones, and (3) 'acinotubular' stage (37-41 weeks) in which lobular clusters are identified [7]. Since all our control cases were less than 24 weeks estimated gestational age, they showed prostatic tissue in the 'bud' stage of development.…”

Section: Discussionmentioning

confidence: 99%

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Fetal Obstructive Uropathy in Trisomy Syndromes

Qureshi¹,

Jacques²,

Feldman³

et al. 2000

Fetal Diagn Ther

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Fetal obstructive uropathy has seldom been described in trisomy syndromes, and its relationship to these syndromes remains unclear. Five trisomic male fetuses, four with trisomy 18 and one with trisomy 21, were identified out of 110 fetuses evaluated for fetal obstructive uropathy. We performed detailed examination on the urinary tracts of four of these fetuses, three with trisomy 18 and one with trisomy 21, following termination in the second trimester. All four had a markedly distended urinary bladder (megacystis), abdominal wall distension, and a small, poorly developed urethra thoughout its full length. All four also had poor development of the prostate with virtual absence of glandular development, as compared to age-matched controls. Posterior urethral valves were not identified in any case. Three of the fetuses (two with trisomy 18 and one with trisomy 21) had unilateral or bilateral hydroureters, and resulting renal tubulocystic or glomerulocystic change. Review of this database reveals an unexpectedly high frequency of trisomies, particularly trisomy 18, suggesting that the relationship may not be coincidental. Abnormal prostate development may be causally related to fetal obstructive uropathies and may be an under-recognized trait in trisomy syndromes. Karyotypic analysis of all fetuses with obstructive uropathy is important since in utero surgical intervention may be contraindicated in cases of fetal aneuploidy.

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Section: Resultssupporting

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Fetal Obstructive Uropathy in Trisomy Syndromes

Qureshi¹,

Jacques²,

Feldman³

et al. 2000

Fetal Diagn Ther

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“…Ducts bud off of the urothelium of the prostatic urethra, initially beginning around the 10th postconceptional week (7 . Fetal prostatic embryogenesis has been previously described (74). We found a similar sequential development of prostatic glands, initially forming posteriorly, then laterally, and finally anteriorly.…”

Section: Discussionmentioning

confidence: 69%

Prostate Development in Prune Belly Syndrome (PBS) and Posterior Urethral Valves (PUV): Etiology of PBS-Lower Urinary Tract Obstruction or Primary Mesenchymal Defect?

et al. 1991

Pediatric Pathology

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Prune belly syndrome (PBS) has been recognized since 1950 as the triad of absent abdominal wall musculature, undescended testes, and urinary tract anomalies. The etiology, however, remains uncertain. Theories of mesenchymal maldevelopment, obstruction, and genetic origin have been proposed. To evaluate the role of lower urinary tract obstruction as it relates to prostatic development and PBS, we studied the lower urinary tract of 15 cases of PBS, 8 cases of posterior urethral valves (PUV), and 34 age-matched controls. It is generally accepted that prostatic growth and development are dependent on mesenchymal-epithelial interactions. We evaluated the mesenchymal and epithelial differentiation and relationships, and found distinctly different and consistent abnormalities between PBS and PUV as compared with one another and controls. The findings suggest that in PBS, prostatic growth and development are hindered because of destruction or absence of the appropriate primitive mesenchyme. Our studies could not definitely exclude very early obstruction as a cause of the findings because of lack of appropriate fetal material.

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“…This period was chosen for tissue acquisition because it is an important period of organogenesis in human fetal prostate 12 . De Paepe et al provides a detailed description of tissue procurement 22 .…”

Section: Methodsmentioning

confidence: 99%

A Human Fetal Prostate Xenograft Model of Developmental Estrogenization

et al. 2015

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Prostate cancer is a common disease in older men. Rodent models have demonstrated that an early and later-life exposure to estrogen can lead to cancerous lesions, and implicated hormonal dysregulation as an avenue for developing future prostate neoplasia. This study utilizes a human fetal prostate xenograft model to study the role of estrogen in the progression of human disease. Histopathological lesions were assessed in 7, 30, 90, 200, and 400-day human prostate xenografts. Gene expression for cell cycle, tumor suppressors, and apoptosis-related genes (i.e. CDKN1A, CASP9, ESR2, PTEN, and TP53) were performed for 200-day estrogen-treated xenografts. Glandular hyperplasia was observed in xenografts given both an initial and secondary exposure to estradiol in both 200 and 400-day xenografts. Persistent estrogenic effects were verified using immunohistochemical markers for cytokeratin 10, p63, and estrogen receptor-α. This model provides data on the histopathological state of the human prostate following estrogenic treatment, which can be utilized in understanding the complicated pathology associated with prostatic disease and early- and later-life estrogenic exposures.

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Fetal Prostate Growth and Development

Cited by 28 publications

References 22 publications

Fetal Obstructive Uropathy in Trisomy Syndromes

Fetal Obstructive Uropathy in Trisomy Syndromes

Prostate Development in Prune Belly Syndrome (PBS) and Posterior Urethral Valves (PUV): Etiology of PBS-Lower Urinary Tract Obstruction or Primary Mesenchymal Defect?

A Human Fetal Prostate Xenograft Model of Developmental Estrogenization

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