Relevant bibliographies by topics / Prostate Carcinogenesis

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Prostate Carcinogenesis'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "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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Dissertations / Theses on the topic "Prostate Carcinogenesis"

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Gao, Meiling. "Role of Sprouty2 in prostate carcinogenesis." Thesis, University of Glasgow, 2011. http://theses.gla.ac.uk/3090/.

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Prostate cancer (PC) is the most common cancer in men. In the UK alone, there are over 30,000 men diagnosed with PC every year. Loss of SPRY2 and activation of receptor tyrosine kinases are common events in PC. However, the molecular basis of their interaction and clinical impact remains to be fully examined. SPRY2 loss may functionally synergise with aberrant cellular signalling to drive PC and to promote treatment resistant disease. Using a combination of in vitro, pre-clinical in vivo models and clinical PC, this thesis shows the impact of SPRY2 loss upon activation of the ErbB signalling system via a positive feedback regulation of the ErbB-PI3K/AKT cascade. Loss of SPRY2 resulted in hyper-activation of PI3K/AKT signalling to drive proliferation and invasion by enhanced internalisation of EGFR/HER2 and their sustained localisation and signalling at the early endosome in a PTEN-dependent manner. This involves activation of p38 MAPK by PI3K to facilitate clathrin-mediated ErbB receptor endocytosis. Furthermore, this thesis suggests a critical role of PI3K/AKT in PC whereby in vitro and in vivo inhibition of PI3K suppresses proliferation and invasion, supporting PI3K/AKT as a target for therapy particularly in patients with PTEN-haploinsufficiency, low SPRY2 and ErbB expressing tumours. In conclusion, SPRY2 is an important tumour suppressor in PC; its loss drives the PI3K/AKT pathway via functional interaction with the ErbB system.
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Nelson, Adam William. "Estrogen receptor beta modulates prostate carcinogenesis." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/267736.

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Prostate cancer (PC) is characterised by dependence upon androgen receptor (AR) as its driving oncogene. When organ-confined, radical treatment can be curative, however there is no cure for advanced, castration-resistant prostate cancer (CRPC). There is therefore a need to better understand the biology of PC, and how influencing AR can modify disease progression. Estrogen is essential for prostate carcinogenesis with evidence from epidemiological, in vitro, human tissue and animal studies. Most suggests that estrogen receptor beta (ERβ) is tumour-suppressive, but trials of ERβ-selective agents have not improved clinical outcomes. ERβ has also been implicated as an oncogene, therefore its role remains unclear. Additional evidence suggests interplay between ERβ and AR, the mechanisms of which are uncertain. The study hypothesis ‘ERβ is an important modulator of prostate carcinogenesis’ was developed to establish whether targeting ERβ could affect PC progression. Much of the confusion around ERβ stems from use of inadequately validated antibodies and cell line models. The first phase of this work was to test ERβ antibodies using an ERβ-inducible cell system. Eight ERβ antibodies were assessed by multiple techniques, showing that commonly used antibodies are either non-specific or only specific in one modality. Two reliable antibodies were identified. Next, cell lines previously used to study ERβ were assessed using validated antibodies and independent approaches. No ERβ expression was detected; an important finding that casts doubt on previously published ERβ biology. Subsequently, a PC cell line with inducible ERβ expression (LNCaP-ERβ) was developed and validated to enable controlled experiments on the effects of ERβ on proliferation, gene expression and ERβ/AR genomic cross-talk. Phase three of this work focused on ERβ biology in PC and its relationship to AR. Interrogation of clinical datasets showed that greater ERβ expression associated with favourable prognosis. Gene expression data from men treated with androgen deprivation therapy revealed that AR represses ERβ. This was confirmed in vitro. The LNCaP-ERβ cell line was treated with androgen and/or ERβ-selective estrogen. Activated ERβ in the presence of androgen-stimulated AR inhibited cell proliferation and down-regulated androgen-dependent genes. Genome-wide mapping of ERβ binding sites reveals that ERβ antagonises AR through competition for shared DNA binding sites. In conclusion, ERβ expression is down-regulated by AR during malignant transformation of prostate epithelium. We reveal an antagonistic relationship between ERβ and AR whereby sustaining or replacing ERβ may inhibit tumour growth through down-regulation of AR-target genes. In future, an ERβ-selective compound may be used to slow or abrogate PC progression.
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Roberts, Kristen M. "Dietary Bioactives and Human Prostate Carcinogenesis." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1429195549.

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Wang, Wanzhong. "Inflammation and prostatic carcinogenesis : a morphological study of the human prostate /." Göteborg : Dept. of Urology, Institute of Clinical Sciences, Sahlgrenska University Hospital, The Sahlgrenska Academy at Göteborg University, 2007. http://hdl.handle.net/2077/9634.

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Xiao, Hong. "Distribution of Metal Ions in Prostate and Urine during Prostate Carcinogenesis." University of Cincinnati / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1310410436.

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Kwan, Pak-shing, and 關百誠. "Roles of Daxx in mitosis and prostate carcinogenesis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43085337.

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Kwan, Pak-shing. "Roles of Daxx in mitosis and prostate carcinogenesis." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43085337.

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Bantval, Rao Roheet. "Understanding the role of huntingtin interacting protein 1 (HIP1) in prostate carcinogenesis and cancer progression." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608064.

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Uegaki, Masayuki. "Downregulation of RalGTPase-activating protein promotes invasion of prostatic epithelial cells and progression from intraepithelial neoplasia to cancer during prostate carcinogenesis." Kyoto University, 2019. http://hdl.handle.net/2433/245310.

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Ling, Ming-tat Patrick, and 凌明達. "The role of Id-1 in prostate development and carcinogenesis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B31244506.

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Books on the topic "Prostate Carcinogenesis"

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Jonathan J. Li Satyabrata Nandi. Hormonal Carcinogenesis: Proceedings of the First International Symposium. Springer, 2011.

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National Cancer Institute (U.S.). Division of Cancer Biology, Diagnosis, and Centers, ed. Estrogens as endogenous carcinogens in the breast and prostate: [a symposium held at Westfields International Conference Center, Chantilly, Virginia, March 15-17, 1998]. Bethesda, MD: National Cancer Institute, 2000.

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J, Li Jonathan, and International Symposium on Hormonal Carcinogenesis (5th : 2006 : Montpellier, France), eds. Hormonal carcinogenesis V. New York, NY: Springer, 2008.

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J, Li Jonathan, and International Symposium on Hormonal Carcinogenesis (5th : 2006 : Montpellier, France), eds. Hormonal carcinogenesis V. New York, NY: Springer, 2008.

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(Editor), Jonathan J. Li, Sara A. Li (Editor), and Antonio Llombart-Bosch (Editor), eds. Hormonal Carcinogenesis IV. Springer, 2004.

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Vukovic, Bisera. Role of telomere length and chromosomal instability in prostatic carcinogenesis. 2006.

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(Editor), W. Jonat, M. Kaufmann (Editor), and K. Munk (Editor), eds. Hormone-Dependent Tumors: Basic Research and Clinical Studies : 9th International Expert Meeting of the Dr. Mildred Scheel Stiftung Fur Krebsforschung, ... 19 (Contributions to Oncology, Vol 50). S. Karger AG (Switzerland), 1995.

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Book chapters on the topic "Prostate Carcinogenesis"

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Muniyan, Sakthivel, Yu-Wei Chou, Shou-Qiang Ou-Yang, and Ming-Fong Lin. "Human Prostatic Acid Phosphatase in Prostate Carcinogenesis." In Prostate Cancer, 323–48. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6828-8_12.

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Mulholland, David J., Jing Jiao, and Hong Wu. "Hormone Refractory Prostate Cancer: Lessons Learned from the PTEN Prostate Cancer Model." In Hormonal Carcinogenesis V, 87–95. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-69080-3_8.

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Stanford, Janet L. "Prostate Cancer, Androgens, and Estrogens." In Hormonal Carcinogenesis III, 87–96. New York, NY: Springer New York, 2001. http://dx.doi.org/10.1007/978-1-4612-2092-3_7.

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Nelson, William G., Srinivasan Yegnasubramanian, Patrick J. Bastian, Masashi Nakayama, and Angelo M. De Marzo. "Somatic DNA Methylation Changes and Prostatic Carcinogenesis." In Prostate Cancer, 301–15. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-224-3_17.

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Agoulnik, Irina U., and Nancy L. Weigel. "Androgen Receptor Coactivators and Prostate Cancer." In Hormonal Carcinogenesis V, 245–55. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-69080-3_23.

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Ostrander, Elanie A., and Bo Johannesson. "Prostate Cancer Susceptibility Loci: Finding the Genes." In Hormonal Carcinogenesis V, 179–90. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-69080-3_17.

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Wang, Diping, and Donald J. Tindall. "Androgen Action During Prostate Carcinogenesis." In Methods in Molecular Biology, 25–44. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-243-4_2.

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Shirai, Tomoyuki, Seiko Tamano, Shogo Iwasaki, and Nobuyuki Ito. "Enhancement of Prostate Carcinogenesis in Rats by Testosterone and Prolactin." In Hormonal Carcinogenesis, 27–32. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4613-9208-8_4.

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Buchanan, Grant, and Wayne D. Tilley. "Androgen Receptor Structure and Function in Prostate Cancer." In Hormonal Carcinogenesis III, 333–41. New York, NY: Springer New York, 2001. http://dx.doi.org/10.1007/978-1-4612-2092-3_32.

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Mohler, James L. "Castration-Recurrent Prostate Cancer Is Not Androgen-Independent." In Hormonal Carcinogenesis V, 223–34. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-69080-3_21.

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Conference papers on the topic "Prostate Carcinogenesis"

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Cheng, Siyuan, Shu Yang, Zachary M. Connelly, Fenghua Chen, and Xiuping Yu. "Abstract 4302: AR signaling promotes prostate carcinogenesis." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4302.

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Cheng, Siyuan, Shu Yang, Zachary M. Connelly, Fenghua Chen, and Xiuping Yu. "Abstract 4302: AR signaling promotes prostate carcinogenesis." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4302.

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Suman, Suman, Trinath P. Das, Houda Alatassi, Murali K. Ankem, and Chendil Damodaran. "Abstract 5251: Chemoprevention of cadmium induced prostate carcinogenesis." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-5251.

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Nelson, William G., Michael C. Haffner, Martin J. Aryee, David M. Esopi, William B. Isaacs, G. Steven Bova, Alan K. Meeker, George Netto, Angelo M. De Marzo, and Srinivasan Yegnasubramanian. "Abstract CN05-04: Early molecular changes in prostate carcinogenesis." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Nov 7-10, 2010; Philadelphia, PA. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1940-6207.prev-10-cn05-04.

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Thapa, Dinesh, Addanki P. Kumar, and Rita Ghosh. "Abstract 2061: Implication of NQO1 knockdown on prostate carcinogenesis." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2061.

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Shannon, Brian D., and Laurie E. Littlepage. "Abstract 4212: ADAM10/Kuzbanian is upregulated during neuroendocrine prostate carcinogenesis." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4212.

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Li, Yan, and James C. Fleet. "Abstract 2398: Gene expression profiling of TgAPT121mouse prostate reveals biological processes associated with early prostate carcinogenesis." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2398.

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Xing, Changsheng, Xiaoying Fu, Xiaodong Sun, and Jin-Tang Dong. "Abstract 60: KLF5 deletion promotes but does not initiate prostate carcinogenesis." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-60.

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Spees, Colleen K., Jennifer M. Thomas-Ahner, Hseuh-Li Tan, Jun-Ge Yu, Justin B. Smolinski, Pavlo L. Kovalenko, James C. Fleet, and Steven K. Clinton. "Abstract 2403: Characterization of p53 in transgenic mouse prostate carcinogenesis models." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2403.

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Pramanik, Kartick C., Michael Schlicht, Maarten Bosland, Chang Jiang, Yibin Deng, and Junxuan Lu. "Abstract 1264: Studying senescence in prostate of selenium treated rats undergoing carcinogen-induced, androgen-promoted prostate carcinogenesis." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1264.

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Reports on the topic "Prostate Carcinogenesis"

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Bianchi-Frias, Daniella. The Aged Microenvironment Influences Prostate Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, December 2009. http://dx.doi.org/10.21236/ada542443.

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Bianchi-Frias, Daniella. The Aged Microenvironment Influences Prostate Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, December 2007. http://dx.doi.org/10.21236/ada479324.

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Hunag, Haojie. CBP and p27KIP1 in Prostate Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, February 2008. http://dx.doi.org/10.21236/ada482547.

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Bianchi-Frias, Daniella. The Aged Microenvironment Influences Prostate Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, December 2008. http://dx.doi.org/10.21236/ada500681.

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Nelson, Joel B. Cell Lineage Analysis of Mouse Prostate Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, July 2014. http://dx.doi.org/10.21236/ada609597.

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Taylor, Renea. Role of Tumor Stroma in Prostate Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, March 2006. http://dx.doi.org/10.21236/ada446857.

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Nelson, Joel B. Cell Lineage Analysis of Mouse Prostate Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada591013.

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De Marzo, Angelo M. Interaction Between Dietary Factors and Inflammation in Prostate Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, December 2008. http://dx.doi.org/10.21236/ada494446.

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Ouyang, Xuesong. Isolation of Target Genes for NKX3.1 in Prostate Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, March 2004. http://dx.doi.org/10.21236/ada426046.

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DeMarzo, Angelo M. Interactions between Dietary Factors and Inflammation in Prostate Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, December 2006. http://dx.doi.org/10.21236/ada468039.

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