Journal articles: 'Prostate Carcinogenesis'

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Rhim, Johng S., and Hsiang-fu Kung. "Human Prostate Carcinogenesis." Critical Reviews™ in Oncogenesis 8, no. 4 (1997): 305–28. http://dx.doi.org/10.1615/critrevoncog.v8.i4.20.

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de Bono, Johann S., Christina Guo, Bora Gurel, Angelo M. De Marzo, Karen S. Sfanos, Ram S. Mani, Jesús Gil, Charles G. Drake, and Andrea Alimonti. "Prostate carcinogenesis: inflammatory storms." Nature Reviews Cancer 20, no. 8 (June 16, 2020): 455–69. http://dx.doi.org/10.1038/s41568-020-0267-9.

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Nakai, Yasutomo, and Norio Nonomura. "Inflammation and prostate carcinogenesis." International Journal of Urology 20, no. 2 (July 31, 2012): 150–60. http://dx.doi.org/10.1111/j.1442-2042.2012.03101.x.

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De Marzo, Angelo M., Elizabeth A. Platz, Siobhan Sutcliffe, Jianfeng Xu, Henrik Grönberg, Charles G. Drake, Yasutomo Nakai, William B. Isaacs, and William G. Nelson. "Inflammation in prostate carcinogenesis." Nature Reviews Cancer 7, no. 4 (April 2007): 256–69. http://dx.doi.org/10.1038/nrc2090.

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Bruckheimer, Elizabeth M., and Natasha Kyprianou. "Apoptosis in prostate carcinogenesis." Cell and Tissue Research 301, no. 1 (March 30, 2000): 153–62. http://dx.doi.org/10.1007/s004410000196.

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Leung, G., I. F. F. Benzie, A. Cheung, S. W. Tsao, and Y. C. Wong. "No effect of a high-fat diet on promotion of sex hormone-induced prostate and mammary carcinogenesis in the Noble rat model." British Journal of Nutrition 88, no. 4 (October 2002): 399–409. http://dx.doi.org/10.1079/bjn2002673.

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Results of international correlation and migrant studies suggest that dietary fat promotes carcinogenesis in hormone-sensitive sites, but this is disputed. In the present study, we used a Noble rat model of sex hormone-induced cancers to examine the effect of a high-fat diet on the incidence and latency of prostate and mammary cancer in male (n 139) and female (n 72) animals respectively. We also measured α-tocopherol levels in female breast tissue to determine whether a high intake of polyunsaturated fatty acids depletes antioxidant defence in target tissues, providing a possible potentiating mechanism for carcinogenesis. Results showed a very high incidence of hormone-induced adenocarcinomas of prostate and mammary gland, irrespective of diet. There was no difference in the pattern of carcinogenesis in different prostatic locations, weight of the prostate, or weight gain between male rats on the high-fat diet compared with the control (standard, low-fat) diet. In female rats, the incidence of mammary cancer and the body-weight gain were the same in both dietary groups, and breast α-tocopherol was also unaffected by dietary fat intake. Our present results are supportive of recent cohort studies that reported no significant association between intake of fat and the development of human prostate and breast cancer, and do not support a role for dietary fat in promoting sex hormone-induced prostate and mammary carcinogenesis.

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Hu, Dan-Ping, Wen-Yang Hu, Lishi Xie, Ye Li, Lynn Birch, and Gail S. Prins. "Actions of Estrogenic Endocrine Disrupting Chemicals on Human Prostate Stem/Progenitor Cells and Prostate Carcinogenesis." Open Biotechnology Journal 10, no. 1 (March 31, 2016): 76–97. http://dx.doi.org/10.2174/1874070701610010076.

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Substantial evidences from epidemiological and animal-based studies indicate that early exposure to endocrine disrupting chemicals (EDCs) during the developmental stage results in a variety of disorders including cancer. Previous studies have demonstrated that early estrogen exposure results in life-long reprogramming of the prostate gland that leads to an increased incidence of prostatic lesions with aging. We have recently documented that bisphenol A (BPA), one of the most studied EDCs with estrogenic activity has similar effects in increasing prostate carcinogenic potential, supporting the connection between EDCs exposure and prostate cancer risk. It is well accepted that stem cells play a crucial role in development and cancer. Accumulating evidence suggest that stem cells are regulated by extrinsic factors and may be the potential target of hormonal carcinogenesis. Estrogenic EDCs which interfere with normal hormonal signaling may perturb prostate stem cell fate by directly reprogramming stem cells or breaking down the stem cell niche. Transformation of stem cells into cancer stem cells may underlie cancer initiation accounting for cancer recurrence, which becomes a critical therapeutic target of cancer management. We therefore propose that estrogenic EDCs may influence the development and progression of prostate cancer through reprogramming and transforming the prostate stem and early stage progenitor cells. In this review, we summarize our current studies and have updated recent advances highlighting estrogenic EDCs on prostate carcinogenesis by possible targeting prostate stem/progenitor cells. Using novel stem cell assays we have demonstrated that human prostate stem/progenitor cells express estrogen receptors (ER) and are directly modulated by estrogenic EDCs. Moreover, employing anin vivohumanized chimeric prostate model, we further demonstrated that estrogenic EDCs initiate and promote prostatic carcinogenesis in an androgen-supported environment. These findings support our hypothesis that prostate stem/progenitor cells may be the direct targets of estrogenic EDCs as a consequence of developmental exposure which carry permanent reprogrammed epigenetic and oncogenic events and subsequently deposit into cancer initiation and progression in adulthood.

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Wang, Zhuohua, Gail S. Prins, Karen T. Coschigano, John J. Kopchick, Jeffrey E. Green, Vera H. Ray, Samad Hedayat, Konstantin T. Christov, Terry G. Unterman, and Steven M. Swanson. "Disruption of Growth Hormone Signaling Retards Early Stages of Prostate Carcinogenesis in the C3(1)/T Antigen Mouse." Endocrinology 146, no. 12 (December 1, 2005): 5188–96. http://dx.doi.org/10.1210/en.2005-0607.

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Recent epidemiological studies suggest that elevated serum titers of IGF-I, which are, to a large degree, regulated by GH, are associated with an increase in prostate cancer risk. The purpose of the current study was to develop the first animal models to directly test the hypothesis that a normal, functional GH/IGF-I axis is required for prostate cancer progression. The GH receptor (GHR) gene-disrupted mouse (Ghr−/−), which has less than 10% of the plasma IGF-I found in GHR wild-type mice, was crossed with the C3(1)/T antigen (Tag) mouse, which develops prostatic intraepithelial neoplasia driven by the large Tag that progress to invasive prostate carcinoma in a manner similar to the process observed in humans. Progeny of this cross were genotyped and Tag/Ghr+/+ and Tag/Ghr−/− mice were killed at 9 months of age. Seven of eight Tag/Ghr+/+ mice harbored prostatic intraepithelial neoplasia lesions of various grades. In contrast, only one of the eight Tag/Ghr−/− mice exhibited atypia (P < 0.01, Fischer’s exact test). Disruption of the GHR gene altered neither prostate androgen receptor expression nor serum testosterone titers. Expression of the Tag oncogene was similar in the prostates of the two mouse strains. Immunohistochemistry revealed a significant decrease in prostate epithelial cell proliferation and an increase in basal apoptotic indices. These results indicate that disruption of GH signaling significantly inhibits prostate carcinogenesis.

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Joshua, A. M., B. Vukovic, I. Braude, A. Evans, J. Srigley, and J. A. Squire. "Telomere dysfunction in prostatic carcinogenesis." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 10021. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.10021.

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10021 Background: Telomeres are composed of tandemly repeated DNA sequences (TTAGGG) and specific binding proteins located at the ends of eukaryotic chromosomes. They stabilize chromosomal ends; telomere shortening is an important mechanism of genomic instability and can lead to end-to-end chromosomal fusion, rearrangements and cell death. Here we evaluate the hypothesis that telomere shortening contributes to the development of prostate cancer (CaP). Methods: We used telomeric, centromeric and chromosome specific peptide-nucleic acid probes with z-stacked quantitative fluorescence in-situ hybridisation analysis to initially analyse 15 radical prostatectomy specimens and then subsequently sextant core biopsies from 80 men obtained in 1998–2001 containing high-grade prostate intraepithelial neoplasia (HPIN) only. The biopsy cohort outcome is blinded to prevent experimental bias and has a minimum follow-up of 2 years with 41 men diagnosed subsequently with CaP and 39 men without CaP on rebiopsy. Regions of interest were identifying with an overlying haematoxylin and eosin slide. Results: We found a significant decrease in telomere length in both HPIN and CaP in comparison to normal prostatic epithelium accompanied by elevated rates of aneusomy. Telomere erosion in HPIN was more common in regions of the prostate-containing CaP. We now have analyzed ∼4000 cells of matching HPIN and surrounding stroma. Preliminary analysis demonstrated that the median telomere length in HPIN is approximately 27% of the surrounding stroma with upper and lower quartiles being 16% and 38% respectively. Logistic regression analysis is in progress to determine whether the length of the shortest telomeres or the average telomeric length in a sample predicts for subsequent diagnosis of CaP. Secondary analyses are examining the effect of telomere length on the interval to the diagnosis of CaP, the effect of age on telomere length and the eventual Gleason score. Conclusions: Analysis of telomere length holds great promise for developing improved prognostic markers in prostatic carcinogenesis. This is a first of its kind study in the field. No significant financial relationships to disclose.

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Lara, P. "Molecular biology of prostate carcinogenesis." Critical Reviews in Oncology/Hematology 32, no. 3 (December 1999): 197–208. http://dx.doi.org/10.1016/s1040-8428(99)00041-4.

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Fowler, Jackson E., and Steven A. Bigler. "Racial differences in prostate carcinogenesis." Urologic Clinics of North America 29, no. 1 (February 2002): 183–91. http://dx.doi.org/10.1016/s0094-0143(02)00003-4.

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Shirai, Tomoyuki, Satoru Takahashi, Lin Cui, Mitsuru Futakuchi, Koji Kato, Seiko Tamano, and Katsumi Imaida. "Experimental prostate carcinogenesis — rodent models." Mutation Research/Reviews in Mutation Research 462, no. 2-3 (April 2000): 219–26. http://dx.doi.org/10.1016/s1383-5742(00)00039-9.

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Omabe, Maxwell, and Martin Ezeani. "Infection, inflammation and prostate carcinogenesis." Infection, Genetics and Evolution 11, no. 6 (August 2011): 1195–98. http://dx.doi.org/10.1016/j.meegid.2011.03.002.

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De Marzo, Angelo M., Yasutomo Nakai, and William G. Nelson. "Inflammation, atrophy, and prostate carcinogenesis." Urologic Oncology: Seminars and Original Investigations 25, no. 5 (September 2007): 398–400. http://dx.doi.org/10.1016/j.urolonc.2007.05.007.

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Abate-Shen, Cory, and Michael M. Shen. "Mouse models of prostate carcinogenesis." Trends in Genetics 18, no. 5 (May 2002): S1—S5. http://dx.doi.org/10.1016/s0168-9525(02)02683-5.

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Hussain, Tajamul, Sanjay Gupta, and Hasan Mukhtar. "Cyclooxygenase-2 and prostate carcinogenesis." Cancer Letters 191, no. 2 (March 2003): 125–35. http://dx.doi.org/10.1016/s0304-3835(02)00524-4.

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McLean, Dalton T., Douglas W. Strand, and William A. Ricke. "Prostate cancer xenografts and hormone induced prostate carcinogenesis." Differentiation 97 (September 2017): 23–32. http://dx.doi.org/10.1016/j.diff.2017.08.005.

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Cunha, Gerald R., Y. Z. Wang, Simon W. Hayward, and Gail P. Risbridger. "Estrogenic effects on prostatic differentiation and carcinogenesis." Reproduction, Fertility and Development 13, no. 4 (2001): 285. http://dx.doi.org/10.1071/rd01010.

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Estrogens, alone or in combination with androgens, can induce aberrant growth and/or malignancy of the prostate gland. Squamous metaplasia is an abnormal form of prostatic epithelial differentiation elicited by exogenous estrogen alone. Estrogens elicit their effects via estrogen receptors (ER) in the prostate. Experiments using ERα and ERβ null mice demonstrated that ERα, but not ERβ is essential in the induction of prostatic squamous metaplasia. To determine the respective roles of epithelial versus stromal ERα in this response, the following tissue recombinants were constructed with prostatic epithelium (PRE) and stroma (S) from wild-type (wt) and ERα knockout (αERKO) mice: wt-S + wt-PRE, · αERKO-S + αERKO-PRE, wt-S + αERKO-PRE and αERKO-S + wt-PRE. A metaplastic response to diethylstilbestrol (DES) was only observed in wt-S + wt-PRE tissue recombinants. Tissue recombinants containing αERKO-PRE and/or αERKO-S (ERKO-S + αERKO-PRE, wt-S + αERKO-PRE and αERKO-S + wt-PRE) failed to respond to DES. Therefore, full and uniform epithelial squamous metaplasia requires ERα in both the epithelium and stroma. Estradiol (E2) in combination with testosterone (T) was shown to be effective in inducing prostatic carcinogenesis in a tissue recombinant model composed of rat urogenital sinus mesenchyme plus mouse prostatic epithelium. A particularly efficient model of prostatic carcinogenesis in mice involves T + E2 treatment of mice bearing grafts of wild-type rat urogenital mesenchyme (rUGM) plus retinoblastoma gene (Rb) knockout (Rb-KO) prostatic epithelium (rUGM + Rb-KO-PRE). Such rUGM + Rb-KO-PRE tissue recombinants developed hyperplasia, atypical hyperplasia and invasive prostatic carcinoma with high efficiency. During carcinogenesis in rUGM + Rb-KO-PRE tissue recombinants, epithelial E-cadherin almost totally disappeared and epithelial PCNA labeling was elevated. These epithelial changes were associated with almost total loss of smooth muscle cells in the stroma. The results of this study demonstrate that the absence of the Rb tumor suppressor gene predisposes prostatic epithelial cells to hormonal carcinogenesis.

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Chen, James Lin, Kristen Otto, and Donald Vander Griend. "Role of homeobox pathway in prostate carcinogenesis." Journal of Clinical Oncology 30, no. 5_suppl (February 10, 2012): 126. http://dx.doi.org/10.1200/jco.2012.30.5_suppl.126.

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126 Background: Identifying aberrant activity of developmental pathways in prostate cancer provides therapeutic opportunities. To this end, despite a shared embryonic origin and similarities to prostate cancer in histology and androgen dependence, seminal vesicle cancer is exceptionally rare. Genomic pathway analyses of their critical developmental differences may reveal uncharacterized oncogenic pathways. Previous attempts to do so have used whole tissue preparations. We hypothesized that careful gene profiling of pure primary epithelial cultures from normal prostate and seminal vesicles would reduce confounding noise during analysis and provide more robust pathway prioritization. Methods: Paired normal prostate and seminal vesicle epithelium cultures were created from three de-identified patients. Derived gene expression profiles were grouped into cancer biomodules using a protein-protein network algorithm to analyze their relationship to known oncogenes. Each resultant biomodule was assayed for its prognostic ability in independent Kaplan-Meier analyses of prostate cancer patients for time to recurrence and overall survival. Protein products from prioritized biomodule genes were then evaluated in vitro. Results: Gene expression profiling and protein network prioritization resulted in three cancer biomodules. Survival analysis revealed that the embryonic developmental biomodule centered on homeobox genes Meis1, Meis2 and Pbx1 to have clinical import. This homeobox biomodule detected a survival difference in a set of active surveillance patients (n=172, p=0.05) and identified men who were more likely to recur biochemically post-prostatectomy (n=78, p=0.02). We analyzed in vitro protein expression of Meis1, Meis2, Pbx1 and confirmed decreased gene expression in independent datasets of prostate cancer versus normal tissue. Conclusions: The Meis1/Meis2/Pbx1 biomodule may explain key differences in seminal vesicle and normal prostate epithelium development. In contrast to other cancers, Meis1, Meis2, and Pbx1 may play a tumor suppressor role in prostate cancer. Thus deregulation of this biomodule may be critical in prostate cancer oncogenesis.

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Rojas-Armas, Juan Pedro, Jorge Luis Arroyo-Acevedo, José Manuel Ortiz-Sánchez, Miriam Palomino-Pacheco, Oscar Herrera-Calderón, James Calva, Agustín Rojas-Armas, Hugo Jesús Justil-Guerrero, Américo Castro-Luna, and Julio Hilario-Vargas. "Cordia lutea L. Flowers: A Promising Medicinal Plant as Chemopreventive in Induced Prostate Carcinogenesis in Rats." Evidence-Based Complementary and Alternative Medicine 2020 (May 26, 2020): 1–8. http://dx.doi.org/10.1155/2020/5062942.

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The objective of this study was to evaluate the chemopreventive effect of the ethanolic extract of Cordia lutea flowers (EECL) on N-methyl-N-nitrosourea- (MNU), cyproterone-, and testosterone-induced prostate cancer in rats. 40 Holtzman male rats were used and assigned to 5 groups (n = 8). In Group I, rats received normal saline (10 mL/Kg); Group II: rats were induced for prostate cancer with cyproterone, testosterone, and NMU; Groups III, IV, and V: rats received EECL daily, at doses of 50, 250, and 500 mg/kg body weight, respectively. After the period of treatment, animals were sacrificed by an overdose of pentobarbital and blood samples were collected for determination of prostate-specific antigen (PSA). The prostate was dissected and weighed accurately. The ventral lobe of the prostate was processed for histopathology analysis. The somatic prostate index decreased with EECL at dependent dose, from 0.34 ± 0.04 to 0.23 ± 0.05 (P<0.05). The PSA levels also decreased significantly at doses of 250 and 500 mg/kg. Histopathological analysis showed a decrease in the number of prostatic layers with high-grade prostatic intraepithelial neoplasia (HG-PIN) and low-grade prostatic intraepithelial neoplasia (LG-PIN) at the dose of 500 mg/kg. The ethanolic extract of Cordia lutea flowers had a chemopreventive effect on induced prostate cancer in rats.

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Lotan, Yair, Xiao C. Xu, Moshe Shalev, Reuben Lotan, Russell Williams, Thomas M. Wheeler, Timothy C. Thompson, and Dov Kadmon. "Differential Expression of Nuclear Retinoid Receptors in Normal and Malignant Prostates." Journal of Clinical Oncology 18, no. 1 (January 1, 2000): 116. http://dx.doi.org/10.1200/jco.2000.18.1.116.

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PURPOSE: To determine (1) whether nuclear retinoic acid receptors (RARs) and retinoid X receptors (RXRs) are differentially expressed in normal and in cancerous human prostate tissues and (2) whether oral fenretinide therapy impacts the expression of these receptors in prostate cancer. PATIENTS AND METHODS: In situ hybridization with antisense riboprobes was used to probe for RAR and RXR transcripts in prostate tissues in a two-phased study: (1) expression of retinoid receptors in eight normal prostates was compared with their expression in 10 randomly picked radical prostatectomy specimens (group A); (2) expression of retinoid receptors was determined in 22 radical prostatectomy specimens from participants in a clinical study (group B). Twelve patients received oral fenretinide 200 mg/d, and 10 received placebo pills for 28 days before surgery. RESULTS: RARα, RARγ, RXRα, and RXRγ mRNAs were detected in most normal and cancerous prostates. In group A, RARβ mRNA was expressed in only four of 10 malignant prostates but was present in seven of eight benign prostates (P = .05). RXRβ mRNA was expressed in four of eight benign prostates and in zero of 10 malignant prostates (P = .023). In group B prostates, RARβ and RXRβ mRNAs were markedly reduced in all cancers and in the adjacent, nonmalignant tissue. There were no differences between receptor expression in the fenretinide-treated group and the placebo group. CONCLUSION: RARβ and RXRβ mRNAs are selectively lost in both prostate cancer and adjacent morphologically normal prostatic tissue, supporting the concept of a field of carcinogenesis. One month of oral fenretinide (200 mg/d) did not influence the expression of retinoid receptors in prostate cancer.

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De Stefani, Eduardo, Luis Fierro, Enrique Barrios, and Alvaro Ronco. "Tobacco, Alcohol, Diet and Risk of prostate Cancer." Tumori Journal 81, no. 5 (September 1995): 315–20. http://dx.doi.org/10.1177/030089169508100503.

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A hospital-based case-control study of the association between tobacco smoking, alcohol drinking and several relevant dietary items and prostate cancer was carried out in the National Cancer Institute of Uruguay between January 1988 and December 1994. The sample included 156 patients with histologically proven prostatic cancer and 302 controls with a variety of neoplastic and non-neoplastic diseases. The results showed increased risks of prostate cancer associated with beer drinking, meat, milk and fruit consumption, after adjusting for major confounders. The possible role of N-nitroso compounds from beer in prostatic carcinogenesis is discussed.

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Cai, Tommaso, Raffaella Santi, Irene Tamanini, Ilaria Camilla Galli, Gianpaolo Perletti, Truls E. Bjerklund Johansen, and Gabriella Nesi. "Current Knowledge of the Potential Links between Inflammation and Prostate Cancer." International Journal of Molecular Sciences 20, no. 15 (August 6, 2019): 3833. http://dx.doi.org/10.3390/ijms20153833.

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Inflammation is inherent in prostatic diseases and it is now accepted that it may facilitate cellular proliferation in both benign and malignant conditions. The strong relationship between prostatic inflammation and pathogenesis of benign prostatic hyperplasia (BPH) is supported by epidemiologic, histopathologic and molecular evidence. Contrariwise, the role of inflammation in prostate carcinogenesis is still controversial, although current data indicate that the inflammatory microenvironment can regulate prostate cancer (PCa) growth and progression. Knowledge of the complex molecular landscape associated with chronic inflammation in the context of PCa may lead to the introduction and optimization of novel targeted therapies. In this perspective, evaluation of the inflammatory component in prostate specimens could be included in routine pathology reports.

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Kambhampati, Suman,. "Growth factors involved in prostate carcinogenesis." Frontiers in Bioscience 10, no. 1-3 (2005): 1355. http://dx.doi.org/10.2741/1625.

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Conlon, Lauren E., Matthew A. Wallig, and John W. Erdman. "Pelleting Diets Impairs TRAMP Prostate Carcinogenesis." Food and Nutrition Sciences 08, no. 02 (2017): 212–26. http://dx.doi.org/10.4236/fns.2017.82014.

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Lomshakov, Andrey, Vadim Astashov, Oleg Zayko, and Ilya Pushkar. "Lymphoid organs in experimental prostate carcinogenesis." Archiv Euromedica 9, no. 3 (December 24, 2019): 17–19. http://dx.doi.org/10.35630/2199-885x/2019/9/3.5.

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Palapattu, Ganesh S., Siobhan Sutcliffe, Patrick J. Bastian, Elizabeth A. Platz, Angelo M. De Marzo, William B. Isaacs, and William G. Nelson. "Prostate carcinogenesis and inflammation: emerging insights." Carcinogenesis 26, no. 7 (October 21, 2004): 1170–81. http://dx.doi.org/10.1093/carcin/bgh317.

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CARRUBA, GIUSEPPE, ROSALBA STEFANO, LETIZIA COCCIADIFERRO, FRANCESCA SALADINO, ANTONIETTA CRISTINA, ERIK TOKAR, SALMAAN T. A. QUADER, MUKTA M. WEBBER, and LUIGI CASTAGNETTA. "Intercellular Communication and Human Prostate Carcinogenesis." Annals of the New York Academy of Sciences 963, no. 1 (January 24, 2006): 156–68. http://dx.doi.org/10.1111/j.1749-6632.2002.tb04107.x.

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Meyer, Hellmuth-Alexander, Isabelle Ahrens-Fath, Anette Sommer, and Bernard Haendler. "Novel molecular aspects of prostate carcinogenesis." Biomedicine & Pharmacotherapy 58, no. 1 (January 2004): 10–16. http://dx.doi.org/10.1016/j.biopha.2003.11.001.

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Wang, Zhuohua, Raul M. Luque, Rhonda D. Kineman, Vera H. Ray, Konstantin T. Christov, Daniel D. Lantvit, Tomoyuki Shirai, et al. "Disruption of Growth Hormone Signaling Retards Prostate Carcinogenesis in the Probasin/TAg Rat." Endocrinology 149, no. 3 (December 13, 2007): 1366–76. http://dx.doi.org/10.1210/en.2007-1410.

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We asked whether down-regulation of GH signaling could block carcinogenesis in the Probasin/TAg rat, a model of aggressive prostate cancer. The Spontaneous Dwarf rat, which lacks GH due to a mutation (dr) in its GH gene, was crossed with the Probasin/TAg rat, which develops prostate carcinomas at 100% incidence by 15 wk of age. Progeny were heterozygous for the TAg oncogene and homozygous for either the wild-type GH gene (TAg/Gh+/+) or the dr mutation (TAg/Ghdr/dr). Prostate tumor incidence and burden were significantly reduced, and tumor latency was delayed in TAg/Ghdr/dr rats relative to TAg/Gh+/+ controls. At 25 wk of age, loss of GH resulted in a 20 and 80% decrease in the area of microinvasive carcinoma in the dorsal and lateral lobes, respectively. By 52 wk of age, invasive prostate adenocarcinomas were observed in all TAg/Gh+/+ rats, whereas the majority of TAg/Ghdr/dr did not develop invasive tumors. Suppression of carcinogenesis could not be attributed to alterations in prostate expression of TAg or androgen receptor or changes in serum testosterone levels. As carcinogenesis progressed in TAg/Gh+/+ rats, prostate GHR mRNA and protein expression increased significantly, but prostate IGF-I receptor mRNA and protein levels dropped. Furthermore, serum IGF-I and prostate IGF-I levels did not change significantly over the course of carcinogenesis. These findings suggest that GH plays a dominant role in progression from latent to malignant prostate cancer driven by the powerful probasin/TAg fusion gene in rats and suggest that GH antagonists may be effective at treating human prostate cancer.

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Omabe, Maxwell, Kenneth Omabe, Martin Okwuegbu, Ogo Grace, and Desmond Uchenna Okoro. "Exposure of Prostate to Lipopolysaccharide and Hypoxia Potentiates Neoplastic Behavior and Risk for Prostate Carcinogenesis In Vivo." International Scholarly Research Notices 2014 (August 17, 2014): 1–6. http://dx.doi.org/10.1155/2014/420429.

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A number of studies showed that men from tropical countries have higher burden of prostate cancer similar to data from USA. We developed a translational model to examine whether exposure to microbial inflammation-inducing molecule lipopolysacchride LPS was associated with prostatic cell transformation to more proliferative phenotype as indicated by PSA secretion. Immunocompetent adult mice were divided into two groups; the first group received a local prostate inoculation with E. coli, while the second group received inoculation with sterile solution of saline as vehicle. At the end of 6 days, the PSA values were measured and compared. In the second experiment, two groups of animals were involved. The test group received two drops of the hydrogen peroxide orally for six to seven days to induce hypoxia, while the control group received normal saline. Blood samples were evaluated for serum level of PSA. Result showed a 2-fold increase in level of PSA compared to the control mice in the E. coli inoculated-LPS exposed animals. In addition, exposure of the animals to hypoxic stress resulted in 3.5 fold increase in the serum PSA compared to the control group, which was found to be statistically significant (P<0.0001). In conclusion, our data shows that chronic prostatic infection and exposure to inflammatory stimulus, especially LPS, may alter the phenotype of prostate epithelial cells for increased PSA secretion, a known cancer-like behavior; this is mediated by compromised redox state and oxidative stress injury. We propose that exposure of the prostate epithelial cells to lipopolysaccharide (LPS) promotes chronic inflammation and risk of neoplastic behavior of the prostate in vivo; this may explain the high rate of prostate cancer in tropics.

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Geraghty, Connor, Jennifer Thomas-Ahner, Remy Powell, Nathan Schmidt, Chureeporn Chitchumroonchokchai, Ken Riedl, Lindsey Solden, et al. "Dietary Tomato Varieties Similarly Inhibit Prostate Carcinogenesis in the TRAMP Model in Association with Distinct Transcriptomic and Metabolomic Profiles." Current Developments in Nutrition 4, Supplement_2 (May 29, 2020): 326. http://dx.doi.org/10.1093/cdn/nzaa044_025.

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Abstract Objectives Lycopene intake is associated with reduced risk of prostate cancer, especially lethal disease. Tangerine tomatoes contain highly bioavailable lycopene isomers, compared to red tomatoes, but impact of isomers on cancer preventive bioactivity are unknown. Our goals are: (1) to determine if feeding tomato containing diets with differing lycopene isomers inhibit transgenic adenocarcinoma of the mouse prostate (TRAMP) carcinogenesis, and (2) to determine key early metabolic and transcriptional pathways through which tomatoes act to prevent carcinogenesis. Methods We examine prostate carcinogenesis in the TRAMP model, comparing two tomatoes with distinct lycopene isomer profiles: all-trans-lycopene-rich red tomatoes and cis-lycopene-isomer-rich tangerine tomatoes. Weanling TRAMP and wild type (WT) mice were fed AIN-93 G control, 10% tangerine tomato + AIN-93 G (w/w), or 10% red tomato + AIN-93 G (w/w) diet until 10 or 18 wks. At 10 wks., prostate RNA-seq and plasma metabolomics were performed on TRAMP and WT samples. At 18 wks., plasma carotenoid analysis and histopathology was performed on TRAMP mice. Results At 18 wks., plasma lycopene concentrations were 2.84-fold greater in tangerine tomato-fed mice than red tomato-fed mice (p < 0.0001), yet both red and tangerine tomato diets similarly prevent carcinoma incidence compared to the control diet by 43% and 36% respectively (p < 0.001, both vs. control). Our investigation of early carcinogenesis (10 wks.) shows that both tomato diets similarly impact the plasma metabolome, and we define prostate transcriptomic profiles mediated by TRAMP genotype, such as inflammation- and immune-regulated pathways, that are inhibited by dietary tomato. We identify an inflammatory gene panel (Olr1, Il1a, Cscl9, and Ccl22) which is inhibited by tomato diets. In a human prostate cancer database, higher expression of this gene panel is associated with a more aggressive phenotype. Conclusions Together, our results implicate red and tangerine tomatoes as potentially beneficial for the inhibition of early prostate carcinogenesis through the modulation of transcriptional programs centered on inflammation and the immune response. Our findings support efforts to test novel tomato products for the inhibition of human prostate carcinogenesis. Funding Sources AICR, NIH P30, USDA NNF.

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Knouf, Emily C., Michael J. Metzger, Patrick S. Mitchell, Jason D. Arroyo, John R. Chevillet, Muneesh Tewari, and A. Dusty Miller. "Multiple Integrated Copies and High-Level Production of the Human Retrovirus XMRV (Xenotropic Murine Leukemia Virus-Related Virus) from 22Rv1 Prostate Carcinoma Cells." Journal of Virology 83, no. 14 (April 29, 2009): 7353–56. http://dx.doi.org/10.1128/jvi.00546-09.

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ABSTRACT The human retrovirus XMRV (xenotropic murine leukemia virus-related virus) is associated with prostate cancer, most frequently in humans with a defect in the antiviral defense protein RNase L, suggesting a role for XMRV in prostate carcinogenesis. However, XMRV has not been found in prostate carcinoma cells. Here we show that 22Rv1 prostate carcinoma cells produce high-titer virus that is nearly identical in properties and sequence to XMRV isolated by others and consist primarily of a single clone of cells with at least 10 integrated copies of XMRV, warranting further study of a possible role for XMRV integration in carcinogenesis.

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Benbrahim-Tallaa, Lamia, and Michael Waalkes. "Inorganic arsenic and human prostate cancer." Ciência & Saúde Coletiva 14, no. 1 (February 2009): 307–18. http://dx.doi.org/10.1590/s1413-81232009000100037.

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We critically evaluated the etiologic role of inorganic arsenic in human prostate cancer. We assessed data from relevant epidemiologic studies concerning environmental inorganic arsenic exposure. Whole animal studies were evaluated as were in vitro model systems of inorganic arsenic carcinogenesis in the prostate. Multiple studies in humans reveal an association between environmental inorganic arsenic exposure and prostate cancer mortality or incidence. Many of these human studies provide clear evidence of a dose-response relationship. Relevant whole animal models showing a relationship between inorganic arsenic and prostate cancer are not available. However, cellular model systems indicate arsenic can induce malignant transformation of human prostate epithelial cells in vitro. Arsenic also appears to impact prostate cancer cell progression by precipitating events leading to androgen independence in vitro. Available evidence in human populations and human cells in vitro indicates that the prostate is a target for inorganic arsenic carcinogenesis. A role for this common environmental contaminant in human prostate cancer initiation and/or progression would be very important.

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Esmat, Amr Y., Fawzia M. Refaie, Mohamed H. Shaheen, and Mahmoud M. Said. "Chemoprevention of Prostate Carcinogenesis by DFMO and/or Finasteride Treatment in Male Wistar Rats." Tumori Journal 88, no. 6 (November 2002): 513–21. http://dx.doi.org/10.1177/030089160208800616.

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In the present study the chemopreventive activities of DFMO, the irreversible inhibitor of ornithine decarboxylase, and finasteride, the inhibitor of prostatic 5a-reductase, against the development of chemically induced prostate adenocarcinoma by methylnitrosourea/testosterone propionate in male Wistar rats were investigated. According to histological examination, oral administration of DFMO and finasteride, either alone or combined, for two months to MNU/TP-inoculated rats reduced the tumor incidence to 11.11%, 10% and 10%, respectively, compared to tumored controls (64.3%). DFMO and/or finasteride treatment resulted in significant reductions in the wet weight of the prostate gland and seminal vesicles and its ratio relative to the total body weight, as well as the levels of prostate total protein, DNA, RNA and DNA/RNA ratio, compared to tumored controls. However, the effect of the combined treatment was of no statistical significance compared to single DFMO or finasteride treatment, as demonstrated by the non-significant differences between the mean values of most of the studied parameters. The tumor chemopreventive activity and the prostate growth inhibitory effect of DFMO and finasteride were due to suppression of prostate polyamine synthesis. ANOVA test revealed that the relative weight of the prostate as well as blood and tissue polyamine levels could be used as significant endpoint biomarkers for DFMO and finasteride as cancer chemopreventive agents.

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Tam, Neville N. C., Carol Y. Y. Szeto, Johannes M. Freudenberg, Amy N. Fullenkamp, Mario Medvedovic, and Shuk-Mei Ho. "Research Resource: Estrogen-Driven Prolactin-Mediated Gene-Expression Networks in Hormone-Induced Prostatic Intraepithelial Neoplasia." Molecular Endocrinology 24, no. 11 (November 1, 2010): 2207–17. http://dx.doi.org/10.1210/me.2010-0179.

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Abstract Cotreatment with testosterone (T) and 17β-estradiol (E2) is an established regimen for inducing of prostatic intraepithelial neoplasia (PIN) and prostate cancer in rodent models. We previously used the pure antiestrogen ICI 182,780 (ICI) and bromocriptine, a dopamine receptor agonist, to inhibit PIN induction and systemic hyperprolactinemia in Noble rats and found that the carcinogenic action of T+E2 is mediated directly by the effects of E2 on the prostate and/or indirectly via E2-induced hyperprolactinemia. In this study, we delineate the specific action(s) of E2 and prolactin (PRL) in early prostate carcinogenesis by an integrated approach combining global transcription profiling, gene ontology, and gene-network mapping. We identified 2504 differentially expressed genes in the T+E2-treated lateral prostate. The changes in expression of a subset of 1990 genes (∼80%) were blocked upon cotreatment with ICI and bromocriptine, respectively, whereas those of 262 genes (∼10%) were blocked only by treatment with ICI, suggesting that E2-induced pituitary PRL is the primary mediator of the prostatic transcriptional response to the altered hormone milieu. Bioinformatics analyses identified hormone-responsive gene networks involved in immune responses, stromal tissue remodeling, and the ERK pathway. In particular, our data suggest that IL-1β may mediate, at least in part, hormone-induced changes in gene expression during PIN formation. Together, these data highlight the importance of pituitary PRL in estrogen-induced prostate tumorigenesis. The identification of both E2- and pituitary PRL-responsive genes provides a comprehensive resource for future investigations of the complex mechanisms by which changes in the endocrine milieu contribute to prostate carcinogenesis in vivo.

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Huynh, HT, L. Alpert, DW Laird, G. Batist, L. Chalifour, and MA Alaoui-Jamali. "Regulation of the gap junction connexin 43 gene by androgens in the prostate." Journal of Molecular Endocrinology 26, no. 1 (February 1, 2001): 1–10. http://dx.doi.org/10.1677/jme.0.0260001.

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Androgens play an important role in prostate gland development and function, and have been implicated in prostate carcinogenesis. We report the regulation of the gap junctional intercellular communication gene connexin 43 (Cx43) by androgens in the prostate gland. In rat ventral prostate tissue, only trace levels of Cx43 mRNA were detected. Castration, however, resulted in a high increase in Cx43 mRNA and protein. Cx32 was unchanged. Castration-induced Cx43 mRNA and protein were abolished by administration of dihydrotestosterone (DHT). Following castration, prostate weights were approximately 16% of sham-treated controls. However, DHT replacement resulted in prostate weights which were not different from sham-treated controls. Under similar castration conditions, Cx43 induction coincided with pronounced apoptosis in the prostate gland cells, and DHT prevented the induction of apoptosis. Given the physiological role of gap junctions and androgens in the regulation of prostate tissue homeostasis, our observations are relevant to the understanding of androgen-dependent prostate carcinogenesis.

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Culig, Zoran. "miRNA as Regulators of Prostate Carcinogenesis and Endocrine and Chemoresistance." Current Cancer Drug Targets 21, no. 4 (May 27, 2021): 283–88. http://dx.doi.org/10.2174/1568009620666210108103134.

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More therapy options are available for advanced prostate cancer, including novel inhibitors of androgen synthesis, anti-androgens, chemotherapeutics and targeted therapies. Although patients ´ survival has been improved, management of castration therapy-resistant prostate cancer remains a challenge. Regulation of cellular events in cancer by small non-coding miRNAs is, therefore, an area of special interest. Overexpression of selected miRNA may lead to androgen independence and prostate cancer progression. miRNA may be considered also a biomarker in patients with prostate cancer. In contrast, diminished expression of tumor-suppressive miRNA in prostate cancer leads to enhanced proliferation, reduced apoptosis, increased migration, invasion and epithelial- to-mesenchymal transition. miRNA may be directly involved in the regulation of chemosensitivity in prostate cancer. Experimental overexpression of selected miRNA in chemoresistant prostate cancer leads to the inhibition of cellular stemness and epithelial-to-mesenchymal transition. Reduction of tumor-suppressive miRNA may also lead to hyperactivity of signaling pathways such as that of the epidermal growth factor receptor and mitogen-activated protein kinase. Although considerable progress on miRNA research in prostate cancer has been achieved, therapeutic effects could be improved on the basis of the development of novel delivery methods.

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Van Haute, Carl, Dirk De Ridder, and Bernd Nilius. "TRP Channels in Human Prostate." Scientific World JOURNAL 10 (2010): 1597–611. http://dx.doi.org/10.1100/tsw.2010.149.

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This review gives an overview of morphological and functional characteristics in the human prostate. It will focus on the current knowledge about transient receptor potential (TRP) channels expressed in the human prostate, and their putative role in normal physiology and prostate carcinogenesis. Controversial data regarding the expression pattern and the potential impact of TRP channels in prostate function, and their involvement in prostate cancer and other prostate diseases, will be discussed.

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Bosland, MaartenC, and AbeerM Mahmoud. "Hormones and prostate carcinogenesis: Androgens and estrogens." Journal of Carcinogenesis 10, no. 1 (2011): 33. http://dx.doi.org/10.4103/1477-3163.90678.

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Shukla, Girish C. "Racial disparities disruptive genes in prostate carcinogenesis." Frontiers in Bioscience 9, no. 2 (2017): 244–53. http://dx.doi.org/10.2741/s485.

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Chung, Leland W. K. "THE ROLES OF MYOFIBROBLASTS IN PROSTATE CARCINOGENESIS." Journal of Urology 172, no. 6 Part 1 (December 2004): 2125–26. http://dx.doi.org/10.1097/01.ju.0000145136.48668.41.

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Farnsworth, Wells E. "Prostate Carcinogenesis is an Endogenous, Hypoxic Process." UroOncology 4, no. 2 (June 2004): 77–83. http://dx.doi.org/10.1080/15610950410001720251.

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Asamoto, Makoto, Naomi Hokaiwado, Young-Man Cho, and Tomoyuki Shirai. "A Transgenic Rat Model of Prostate Carcinogenesis." Journal of Toxicologic Pathology 15, no. 3 (2002): 191. http://dx.doi.org/10.1293/tox.15.191.

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Moscatelli, David, and E. Lynette Wilson. "Bmi-1, stem cells and prostate carcinogenesis." Asian Journal of Andrology 13, no. 3 (February 21, 2011): 353–54. http://dx.doi.org/10.1038/aja.2011.7.

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HAYWARD, SIMON W., GERALD R. CUNHA, and RAJVIR DAHIYA. "Normal Development and Carcinogenesis of the Prostate." Annals of the New York Academy of Sciences 784, no. 1 Challenges an (April 1996): 50–62. http://dx.doi.org/10.1111/j.1749-6632.1996.tb16227.x.

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Kolenko, Vladimir, Ervin Teper, Alexander Kutikov, and Robert Uzzo. "Zinc and zinc transporters in prostate carcinogenesis." Nature Reviews Urology 10, no. 4 (March 12, 2013): 219–26. http://dx.doi.org/10.1038/nrurol.2013.43.

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Kharaishvili, Gvantsa, Dana Simkova, Eka Makharoblidze, Katerina Trtkova, Zdenek Kolar, and Jan Bouchal. "WNT SIGNALING IN PROSTATE DEVELOPMENT AND CARCINOGENESIS." Biomedical Papers 155, no. 1 (March 1, 2011): 11–18. http://dx.doi.org/10.5507/bp.2011.016.

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Bosland, Maarten C., Nur Özten, Jillian N. Eskra, and Abeer M. Mahmoud. "A Perspective on Prostate Carcinogenesis and Chemoprevention." Current Pharmacology Reports 1, no. 4 (April 11, 2015): 258–65. http://dx.doi.org/10.1007/s40495-015-0031-0.

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Zaichick, Vladimir. "A Systematic Review of the Antimony Content of the Normal Human Prostate Gland." Journal of Hematology and Oncology Research 4, no. 1 (December 28, 2020): 17–27. http://dx.doi.org/10.14302/issn.2372-6601.jhor-20-3673.

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The prostate gland is subject to various disorders. The etiology and pathogenesis of these diseases remain not well understood. Moreover, despite technological advancements, the differential diagnosis of prostate disorders has become progressively more complex and controversial. It was suggested that the antimony (Sb) level in prostatic tissue plays an important role in prostatic carcinogenesis and its measurement may be useful as a cancer biomarker. These suggestions promoted more detailed studies of the Sb content in the prostatic tissue of healthy subjects. The present study evaluated by systematic analysis the published data for Sb content analyzed in prostatic tissue of “normal” glands. This evaluation reviewed 1998 studies, all of which were published in the years from 1921 to 2020 and were located by searching the databases PubMed, Scopus, ELSEVIER-EMBASE, Cochrane Library, and the Web of Science. The articles were analyzed and “Median of Means” and “Range of Means” were used to examine heterogeneity of the measured Sb content in prostates of apparently healthy men. The objective analysis was performed on data from the 23 studies, which included 1173 subjects. It was found that the range of means of prostatic Sb content reported in the literature for “normal” gland varies widely from 0.0066 mg/kg to 0.071 mg/kg with median of means 0.0085 mg/kg on a wet mass basis. Because of small sample size and high data heterogeneity, we recommend other primary studies be performed.

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Journal articles on the topic 'Prostate Carcinogenesis'

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