Article

McNeal JE Regional morphology and pathology of the prostate

American Journal of Clinical Pathology (Impact Factor: 2.51). 04/1968; 49(3):347-57.
Source: PubMed
2 Followers
 · 
86 Reads
  • Source
    • "Additional views can be found in the " Visible Mouse Project " developed by UC Davis Center for Comparative Medicine[25]. Contrary to mice, men have a prostate without exterior lobation that contains distinct glandular regions, including a peripheral zone (PZ), a central zone (CZ), a transition zone (TZ), and a non-glandular anterior fi bromuscular stroma region, each with characteristic histology[26,27]. Th e PZ is the area that surrounds the proximal prostatic urethra. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Despite substantial similarities in embryological, cellular and molecular biology features, human and mouse prostates differ in organ morphology and tissue architecture. Thus, a clear understanding of the anatomy and histology of the mouse prostate is essential for the identification of urogenital phenotypes in genetically engineered mice, as well as for the study of the etiology, development, and treatment of human prostatic diseases for which mouse models are used. The purpose of this manuscript is to provide a brief guide for the dissection of the mouse prostate and the identification of its different lobes and histology, to both basic researchers and medical pathologists who are unfamiliar with mouse tissues.
    Preview · Article · Feb 2016 · Bosnian journal of basic medical sciences / Udruzenje basicnih mediciniskih znanosti = Association of Basic Medical Sciences
  • Source
    • "Asymptomatic prostatic inflammation is of considerable importance to urologic research because of its association with two of the most common health concerns in urology: prostate cancer and benign prostatic hyperplasia (BPH). Inflammation in the human prostate is extremely common and is associated with dysplastic changes including focal disruption of the epithelium , polymorphisms of epithelial cell nuclei, and increased epithelial proliferation (McNeal 1968; Cotran et al., 1999; DeMarzo et al., 2003). Inflammation is manifested by leukocytic infiltration and the release of proinflammatory cytokines, chemokines, prostanoids, and growth factors. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Prostatic inflammation is of considerable importance to urological research because of its association with benign prostatic hyperplasia and prostate cancer. However, the mechanisms by which inflammation leads to proliferation and growth remain obscure. Here, we show that insulin-like growth factors (IGFs)--previously known as critical developmental growth factors during prostate organogenesis--are induced by inflammation as part of the proliferative recovery to inflammation. Using genetic models and in vivo IGF receptor blockade, we demonstrate that the hyperplastic response to inflammation is dependent upon interleukin-1-driven IGF signaling. We show that human prostatic hyperplasia is associated with IGF pathway activation specifically localized to foci of inflammation. This demonstrates that mechanisms of inflammation-induced epithelial proliferation and hyperplasia involve the induction of developmental growth factors, further establishing a link between inflammatory and developmental signals and providing a mechanistic basis for the management of proliferative diseases by IGF pathway modulation.
    Preview · Article · Oct 2014 · Journal of Pharmacology and Experimental Therapeutics
  • Source
    • "Paradoxically, the age-dependent incidence and associated mortality of prostate cancer between 50 and 60 years of age increase after serum testosterone levels start to decline significantly, particularly after age of 65 (Figure 1A) (Siegel et al., 2014). Prostate adenocarcinomas are slow growing tumors that are characterized by low mitotic index and a long natural history (McNeal, 1968). The progression from normal prostate to prostatic intraepithelial neoplasia (PIN), and eventually to localized adenocarcinoma takes place over several decades (Figure 1B). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Epidemiological data have demonstrated an inverse association between serum vitamin D3 levels, cancer incidence and related mortality. However, the effects of vitamin D on prostate cancer biology and its utility for prevention of prostate cancer progression are not as well-defined. The data are often conflicting: some reports suggest that vitamin D3 induces apoptosis in androgen dependent prostate cancer cell lines, while others suggest that vitamin D3 only induces cell cycle arrest. Recent molecular studies have identified an extensive synergistic crosstalk between the vitamin D- and androgen-mediated mRNA and miRNA expression, adding an additional layer of post-transcriptional regulation to the known VDR- and AR-regulated gene activation. The Warburg effect, the inefficient metabolic pathway that converts glucose to lactate for rapid energy generation, is a phenomenon common to many different types of cancer. This process supports cell proliferation and promotes cancer progression via alteration of glucose, glutamine and lipid metabolism. Prostate cancer is a notable exception to this general process since the metabolic switch that occurs early during malignancy is the reverse of the Warburg effect. This "anti-Warburg effect" is due to the unique biology of normal prostate cells that harbor a truncated TCA cycle that is required to produce and secret citrate. In prostate cancer cells, the TCA cycle activity is restored and citrate oxidation is used to produce energy for cancer cell proliferation. 1,25(OH)2D3 and androgen together modulates the TCA cycle via transcriptional regulation of zinc transporters, suggesting that 1,25(OH)2D3 and androgen maintain normal prostate metabolism by blocking citrate oxidation. These data demonstrate the importance of androgens in the anti-proliferative effect of vitamin D in prostate cancer and highlight the importance of understanding the crosstalk between these two signaling pathways.
    Full-text · Article · May 2014 · Frontiers in Physiology
Show more