Identification of Multipotent Luminal Progenitor Cells in Human Prostate Organoid Cultures

It has been a decade since it was discovered that primary cilia have an essential role in Hedgehog (Hh) signaling in mammals. This discovery came from screens in the mouse that identified a set of genes that are required for both normal Hh signaling and for the formation of primary cilia. Since then, dozens of mouse mutations have been identified that disrupt cilia in a variety of ways and have complex effects on Hedgehog signaling. Here, we summarize the genetic and developmental studies used to deduce how Hedgehog signal transduction is linked to cilia and the complex effects that perturbation of cilia structure can have on Hh signaling. We conclude by describing the current status of our understanding of the cell-type-specific regulation of ciliogenesis and how that determines the ability of cells to respond to Hedgehog ligands.

https://cshperspectives.cshlp.org/content/early/2016/11/23/cshperspect.a028175.full.pdf

Primary Cilia and Mammalian Hedgehog Signaling.

Molecular signaling pathways that regulate prostate gland development

Ciliary Hedgehog Signaling Restricts Injury-Induced Adipogenesis.

Prostate organogenesis is a complex process that is primarily mediated by the presence of androgens and subsequent mesenchyme-epithelial interactions. The investigation of prostate development is partly driven by its potential relevance to prostate cancer, in particular the apparent re-awakening of key developmental programs that occur during tumorigenesis. However, our current knowledge of the mechanisms that drive prostate organogenesis is far from complete. Here, we provide a comprehensive overview of prostate development, focusing on recent findings regarding sexual dimorphism, bud induction, branching morphogenesis and cellular differentiation.

/pdf/prostate-organogenesis-tissue-induction-hormonal-regulation-1sp0nmro3f.pdf

Prostate organogenesis: tissue induction, hormonal regulation and cell type specification.

Noggin is required for normal lobe patterning and ductal budding in the mouse prostate.

Differential stage-dependent regulation of prostatic epithelial morphogenesis by Hedgehog signaling.

BACKGROUND: In the immediate postoperative period following resection of growth hormone (GH)-secreting pituitary tumors, serum concentrations of GH have limited ability to predict remission of acromegaly. Since many actions of GH actions are mediated by insulin-like growth factor-1 (IGF-I), we aimed to determine the rates of fall of IGF-I during 72 h after surgical resection of pituitary tumors.

METHODS: We studied patients who were undergoing pituitary surgery for acromegaly. IGF-I was measured by LC-MS and GH by immunoassay. Remission was defined by the combination of serum GH <0.4 ng/mL during oral glucose tolerance testing performed 8 weeks after the surgical procedure and normal IGF-I at ≥8 weeks.

RESULTS: During the first 72 h after surgery, the mean (SD) rate of decline of IGF-I was 185 (61) ng/mL per 24 h in those who achieved remission (n = 23), with a mean (SD) apparent half-life of 55 (19) h. IGF-I had decreased to <65% of the preoperative IGF-I on postoperative day 2 in 20 of 23 remission patients (87%) vs none of 5 patients who did not achieve remission. GH was <2.7 ng/mL on day 2 in 21 of 23 remission patients (91%), but in none of the nonremission patients. The combination of IGF-I and GH on day 2 separated the remission and nonremission groups of patients.

CONCLUSIONS: Rapid decline of serum IGF-I during the immediate postoperative period warrants further study as an analytically independent adjunct to GH measurement for early prediction of biochemical remission of acromegaly.

/pdf/decrease-of-serum-igf-i-following-transsphenoidal-pituitary-1sxviewx5w.pdf

Decrease of Serum IGF-I following Transsphenoidal Pituitary Surgery for Acromegaly

Alternate-day fasting for the protection of cognitive impairment in c57BL/6J mice following whole-brain radiotherapy

/pdf/integrin-adjunct-therapy-for-melanoma-1mapnj3azz.pdf

Integrin adjunct therapy for melanoma.

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