Relevant bibliographies by topics / Prostate cancer; epigenetic modification

Academic literature on the topic 'Prostate cancer; epigenetic modification'

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Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Prostate cancer; epigenetic modification"

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Albany, Costantine, Ajjai S. Alva, Ana M. Aparicio, Rakesh Singal, Sarvari Yellapragada, Guru Sonpavde, and Noah M. Hahn. "Epigenetics in Prostate Cancer." Prostate Cancer 2011 (2011): 1–12. http://dx.doi.org/10.1155/2011/580318.

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Prostate cancer (PC) is the most commonly diagnosed nonskin malignancy and the second most common cause of cancer death among men in the United States. Epigenetics is the study of heritable changes in gene expression caused by mechanisms other than changes in the underlying DNA sequences. Two common epigenetic mechanisms, DNA methylation and histone modification, have demonstrated critical roles in prostate cancer growth and metastasis. DNA hypermethylation of cytosine-guanine (CpG) rich sequence islands within gene promoter regions is widespread during neoplastic transformation of prostate cells, suggesting that treatment-induced restoration of a “normal” epigenome could be clinically beneficial. Histone modification leads to altered tumor gene function by changing chromosome structure and the level of gene transcription. The reversibility of epigenetic aberrations and restoration of tumor suppression gene function have made them attractive targets for prostate cancer treatment with modulators that demethylate DNA and inhibit histone deacetylases.
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Donkena, Krishna Vanaja, Charles Y. F. Young, and Donald J. Tindall. "Oxidative Stress and DNA Methylation in Prostate Cancer." Obstetrics and Gynecology International 2010 (2010): 1–14. http://dx.doi.org/10.1155/2010/302051.

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The protective effects of fruits, vegetables, and other foods on prostate cancer may be due to their antioxidant properties. An imbalance in the oxidative stress/antioxidant status is observed in prostate cancer patients. Genome oxidative damage in prostate cancer patients is associated with higher lipid peroxidation and lower antioxidant levels. Oxygen radicals are associated with different steps of carcinogenesis, including structural DNA damage, epigenetic changes, and protein and lipid alterations. Epigenetics affects genetic regulation, cellular differentiation, embryology, aging, cancer, and other diseases. DNA methylation is perhaps the most extensively studied epigenetic modification, which plays an important role in the regulation of gene expression and chromatin architecture, in association with histone modification and other chromatin-associated proteins. This review will provide a broad overview of the interplay of oxidative stress and DNA methylation, DNA methylation changes in regulation of gene expression, lifestyle changes for prostate cancer prevention, DNA methylation as biomarkers for prostate cancer, methods for detection of methylation, and clinical application of DNA methylation inhibitors for epigenetic therapy.
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Zheng, Jianghua, Jinglong Wang, Xueqing Sun, Mingang Hao, Tao Ding, Dan Xiong, Xiumin Wang, et al. "HIC1 Modulates Prostate Cancer Progression by Epigenetic Modification." Clinical Cancer Research 19, no. 6 (January 22, 2013): 1400–1410. http://dx.doi.org/10.1158/1078-0432.ccr-12-2888.

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Ngollo, Marjolaine, Aslihan Dagdemir, Seher Karsli-Ceppioglu, Gaelle Judes, Amaury Pajon, Frederique Penault-Llorca, Jean-Paul Boiteux, Yves-Jean Bignon, Laurent Guy, and Dominique J. Bernard-Gallon. "Epigenetic modifications in prostate cancer." Epigenomics 6, no. 4 (August 2014): 415–26. http://dx.doi.org/10.2217/epi.14.34.

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Ippolito, Luigi, Giuseppina Comito, Matteo Parri, Marta Iozzo, Assia Duatti, Francesca Virgilio, Nicla Lorito, et al. "Lactate Rewires Lipid Metabolism and Sustains a Metabolic–Epigenetic Axis in Prostate Cancer." Cancer Research 82, no. 7 (February 8, 2022): 1267–82. http://dx.doi.org/10.1158/0008-5472.can-21-0914.

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Abstract Lactate is an abundant oncometabolite in the tumor environment. In prostate cancer, cancer-associated fibroblasts (CAF) are major contributors of secreted lactate, which can be taken up by cancer cells to sustain mitochondrial metabolism. However, how lactate impacts transcriptional regulation in tumors has yet to be fully elucidated. Here, we describe a mechanism by which CAF-secreted lactate is able to increase the expression of genes involved in lipid metabolism in prostate cancer cells. This regulation enhanced intracellular lipid accumulation in lipid droplets (LD) and provided acetyl moieties for histone acetylation, establishing a regulatory loop between metabolites and epigenetic modification. Inhibition of this loop by targeting the bromodomain and extraterminal protein family of histone acetylation readers suppressed the expression of perilipin 2 (PLIN2), a crucial component of LDs, disrupting lactate-dependent lipid metabolic rewiring. Inhibition of this CAF-induced metabolic–epigenetic regulatory loop in vivo reduced growth and metastasis of prostate cancer cells, demonstrating its translational relevance as a therapeutic target in prostate cancer. Clinically, PLIN2 expression was elevated in tumors with a higher Gleason grade and in castration-resistant prostate cancer compared with primary prostate cancer. Overall, these findings show that lactate has both a metabolic and an epigenetic role in promoting prostate cancer progression. Significance: This work shows that stromal-derived lactate induces accumulation of lipid droplets, stimulates epigenetic rewiring, and fosters metastatic potential in prostate cancer.
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Kgatle, Mankgopo M., Asgar A. Kalla, Muhammed M. Islam, Mike Sathekge, and Razia Moorad. "Prostate Cancer: Epigenetic Alterations, Risk Factors, and Therapy." Prostate Cancer 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/5653862.

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Prostate cancer (PCa) is the most prevalent urological cancer that affects aging men in South Africa, and mechanisms underlying prostate tumorigenesis remain elusive. Research advancements in the field of PCa and epigenetics have allowed for the identification of specific alterations that occur beyond genetics but are still critically important in the pathogenesis of tumorigenesis. Anomalous epigenetic changes associated with PCa include histone modifications, DNA methylation, and noncoding miRNA. These mechanisms regulate and silence hundreds of target genes including some which are key components of cellular signalling pathways that, when perturbed, promote tumorigenesis. Elucidation of mechanisms underlying epigenetic alterations and the manner in which these mechanisms interact in regulating gene transcription in PCa are an unmet necessity that may lead to novel chemotherapeutic approaches. This will, therefore, aid in developing combination therapies that will target multiple epigenetic pathways, which can be used in conjunction with the current conventional PCa treatment.
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Orea, María J., Javier C. Angulo, Ana González-Corpas, David Echegaray, Marcos Marvá, María V. T. Lobo, Begoña Colás, and Santiago Ropero. "Claudin-3 Loss of Expression Is a Prognostic Marker in Castration-Resistant Prostate Cancer." International Journal of Molecular Sciences 24, no. 1 (January 2, 2023): 803. http://dx.doi.org/10.3390/ijms24010803.

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Castration-resistant prostate cancer (CRPC) development is the foremost concern after treatment of patients with high risk with locally advanced or metastatic prostate cancer. Androgen receptor (AR) is the main driver of CRPC development, through its interaction with epigenetic modifier genes, placing epigenetics modifications in the forefront of CRPC development. Comparing the DNA methylation and expression profile of androgen-sensitive and -refractory prostate cancer cells, we describe the epigenetic silencing of claudin-3 (CLDN3) in AR positive cells resistant to androgen deprivation (LNCaP-abl). CLDN3 silencing was associated with DNA methylation, loss of histone acetylation and H3K27 methylation, and was re-expressed by the combined treatment with the epigenetic modulators Aza and SAHA. From a functional point of view, CLDN3 loss was associated with increased cellular invasion. Immunohistochemical analysis showed decreased CLDN3 expression in samples from CRPC patients. Interestingly, CLDN3 expression was significantly decreased in samples from patients with high total Gleason score (≥8) and locally advanced tumors. Finally, CLDN3 loss of expression was associated with worse disease-free survival and time to clinical progression. In conclusion, our findings strongly indicate that epigenetic silencing of CLDN3 is a common event in CRPC that could be useful as a molecular marker for the prognosis of prostate cancer patients and to discriminate aggressive from indolent prostate tumors.
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López, Judith, Ana M. Añazco-Guenkova, Óscar Monteagudo-García, and Sandra Blanco. "Epigenetic and Epitranscriptomic Control in Prostate Cancer." Genes 13, no. 2 (February 18, 2022): 378. http://dx.doi.org/10.3390/genes13020378.

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The initiation of prostate cancer has been long associated with DNA copy-number alterations, the loss of specific chromosomal regions and gene fusions, and driver mutations, especially those of the Androgen Receptor. Non-mutational events, particularly DNA and RNA epigenetic dysregulation, are emerging as key players in tumorigenesis. In this review we summarize the molecular changes linked to epigenetic and epitranscriptomic dysregulation in prostate cancer and the role that alterations to DNA and RNA modifications play in the initiation and progression of prostate cancer.
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Bartkowiak-Wieczorek, Joanna, Radosław Kujawski, Anna Bogacz, and Marcin Ożarowski. "An introduction to genetic and epigenetic changes in prostate gland – implications in efficacy of phytotherapy of benign prostatic hyperplasia and prostate cancer." Journal of Medical Science 84, no. 2 (June 30, 2015): 97–103. http://dx.doi.org/10.20883/medical.e23.

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The usage of classical pharmacological treatment of prostate diseases causes the risk of a number of side effects therefore the researchers are looking for new pharmacologically active molecules, including those contained in the plant extracts. The most widely studied is the lipido-sterolic extract from Serenoa repens (saw palmetto), water extract from Camellia sinensis (green tea) and several cruciferous vegetables. The molecular mechanisms underlying of the development and the progression of prostate disorders, especially benign prostatic hyperplasia (BPH) and prostate cancer (PC), remain still poorly understood. The development of pathologically changed prostate cells proliferation involves many factors, including genetic alterations, such as mutations, and epigenetic changes, appear to contribute to the transformation and progression of prostate cancer. In this paper we suggest that the knowledge of epigenetic modifications presented in this paper introduces the new point of view concerning the possibility of action of plant substances used in prevention and symptomatic treatment of BPH and prostate cancer. Thus, identification of the epigenetic modifications involved on the one hand in the development and progression of BPH / PC, on the other influencing the efficacy and safety of potential phytotherapeutics will be helpful in identifying its novel therapeutic strategy.
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Cimadamore, Alessia, Silvia Gasparrini, Marina Scarpelli, Andrea Doria, Roberta Mazzucchelli, Francesco Massari, Liang Cheng, Antonio Lopez-Beltran, and Rodolfo Montironi. "Epigenetic Modifications and Modulators in Prostate Cancer." Critical Reviews™ in Oncogenesis 22, no. 5-6 (2017): 439–50. http://dx.doi.org/10.1615/critrevoncog.2017020964.

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Dissertations / Theses on the topic "Prostate cancer; epigenetic modification"

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Mohamed, M. "Epigenetic biomarkers in prostate cancer." Thesis, Queen's University Belfast, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426926.

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Zhang, Qunshu. "Epigenetic Regulation of Apoptosis in Prostate Cancer." Diss., North Dakota State University, 2015. https://hdl.handle.net/10365/27614.

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Enhancer of zeste homolog 2 (EZH2) is the catalytic subunit of the polycomb repressive complex 2 and suppresses gene expression by catalyzing histone H3 methylation on lysine 27. EZH2 is overexpressed in metastatic prostate cancer and has been shown to promote cell proliferation and metastasis. Here we show that EZH2 also suppresses prostate cancer apoptosis by coordinating the epigenetic silencing of two pro-apoptotic microRNAs, miR-205 and miR-31. We previously reported that miR-205 is silenced in prostate cancer through promoter methylation. In this study, we found that EZH2 suppresses miR-31 expression by trimethylation of H3K27 on the miR-31 promoter. SiRNA knockdown of EZH2 increased miR-31 expression and decreased the anti-apoptotic protein E2F6 (a target of miR-31), resulting in the sensitization of prostate cancer cells to docetaxel-induced apoptosis and vice versa. We further demonstrated that miR-205 silencing is linked to miR-31 silencing through EZH2. Suppression of miR-205 caused an increase of EZH2 protein, which in turn inhibited miR-31 expression and vice versa. Thus, EZH2 integrates the epigenetic silencing of miR-205 and miR-31 to confer resistance to chemotherapy-induced apoptosis. Besides the histone modification by histone methyltransferases (HMTs) such as EZH2, histone deacetylases (HDACs) offer another mechanism to epigenetically regulate gene expressions in cancer. The class I selective inhibitor of HDACs, mocetinostat, has promising antitumor activities in both preclinical studies and the clinical trials. To understand how mocetinostat induces apoptosis in prostate cancer cells, we examined the effects of mocetinostat on miR-31. We found that miR-31 was significantly upregulated by mocetinostat in prostate cancer cells. E2F6 was decreased by mocetinostat treatment. Mocetinostat also increased the expression of pro-apoptotic protein Bad and activated caspase-3 and caspase-9. SiRNA iv knockdown of E2F6 sensitized cancer cells to mocetinostat-induced apoptosis. Importantly, we found the same results in the primary prostate cancer stem cells. Thus, activation of miR-31 and downregulation of E2F6 contribute to mocetinostat-induced apoptosis in prostate cancer. In summary, the epigenetic silencing of miR-31 confers a resistance mechanism for chemotherapy-induced apoptosis in prostate cancer cells. Using mocetinostat to activate miR-31 expression is a novel strategy to overcome resistance to apoptosis and improve response to therapy.
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Chinaranagari, Swathi. "Epigenetic Silencing of ID4 in Prostate Cancer: Mechanistic Insight." DigitalCommons@Robert W. Woodruff Library, Atlanta University Center, 2015. http://digitalcommons.auctr.edu/cauetds/13.

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Inhibitor of DNA binding/differentiation protein 4 (ID4) is a dominant negative regulator of basic helix loop helix (bHLH) family of transcription factors. ID4 shares the homology of HLH domain with other ID proteins (ID1, ID2, and ID3) and lack the basic DNA binding region. Evidence suggested that unlike ID1, ID2 and ID3, ID4 acts as a tumor suppressor in prostate cancer by attenuating cell proliferation and promoting apoptosis. Consistent with these observations ID4 is epigenetically silenced in DU145 prostate cancer cell line. In this study we investigated whether ID4 is also epigenetically silenced in prostate cancer. We also examined association between ID4 promoter hyper-methylation and its expression in prostate cancer cell lines. ID4 protein expression was analyzed in human prostate adenocarcinoma samples by Immunohistochemistry (IHC). ID4 promoter methylation pattern on prostate cancer cell lines was examined by methylation specific PCR. In addition, we performed methylation specific PCR on the human prostate tissues and genomic DNA to correlate cell line studies with clinical studies. IHC demonstrated decreased ID4 protein expression in human prostate tissue samples, whereas higher nuclear ID4 expression was found in normal prostate tissues. ID4 methylation specific PCR (MSP) on prostate cancer cell lines, showed ID4 methylation in DU145, but not in LNCaP and C33 cells. C81 and PC3 cells showed partial methylation. Increased ID4 methylation in C81 as compared to LNCaP suggests its epigenetic silencing as cells acquire androgen independence. Tumors with ID4 promoter hyper-methylation showed distinct loss of ID4 expression. However, the underlying mechanism involved in epigenetic silencing of ID4 is currently unknown. We hypothesized that ID4 promoter methylation is initiated by an EZH2 dependent tri-methylation of histone 3 at lysine 27 (H3K27Me3). ID4 expressing (LNCaP) and non-expressing (DU145 and C81) prostate cancer cell lines were used to investigate EZH2, H3K27Me3 and DNMT1 enrichment on ID4 promoter by Chromatin immuno-precipitation (ChIP). Increased enrichment of EZH2, H3K27Me3 and DNMT1 in DU145 and C81 cell lines was compared to ID4 expressing LNCaP cell line. Knockdown of EZH2 in DU145 cell line led to re-expression of ID4 and decrease in enrichment of EZH2, H3K27Me3 and DNMT1 demonstrating that ID4 is regulated in an EZH2 dependent manner. ChIP on prostate cancer tissue specimens and cell lines suggested EZH2 occupancy and H3K27Me3 marks on the ID4 promoter. Collectively, our data indicate a PRC2 dependent mechanism in ID4 promoter silencing in prostate cancer through recruitment of EZH2 and a corresponding increase in H3K27Me3. Increased EZH2, but decreased ID4 expression in prostate cancer strongly supports this model.
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Taurozzi, Alberto. "Genetic and epigenetic profiling of human prostate cancer cell subsets." Thesis, University of York, 2016. http://etheses.whiterose.ac.uk/17511/.

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Perturbation of androgen signalling drives progression of human prostate cancer (CaP) to castration-resistant prostate cancer (CRPC). Additionally, CaP is initiated and maintained by cancer stem cells (CSC)s which are analogous to normal prostate stem cells (SC)s. This study presents a qPCR assay to detect androgen receptor gene amplification (GAAR), which is the most common mechanism of castration resistance ( > 30%). Also, the epigenetic regulation and function of two SC-silenced genes with tumour-suppressive activity (Latexin (LXN) and Retinoic Acid Receptor Responder 1 (RARRES1)) were interrogated using micro-ChIP, transcriptional profiling and mass spectrometry. Traditionally, GAAR is detected using FISH which is labour-intensive and semi-quantitative, limiting clinical applicability. The mechanism of action of LXN or RARRES1 in CaP is unknown, and epigenetic regulation by DNA methylation has been ruled-out in primary CaP. The qPCR assay can detect GAAR in minor cell populations (~1%) within a heterogeneous sample and also quantifies X chromosome aneuploidy (XCA) - a predictor of poor-prognosis in CaP. GAAR and XCA were detected in near-patient xenografts derived from CRPC-tissue indicating that these abnormalities are present in cells capable of in vivo tumour-reconstitution. Micro-ChIP analysis of fractionated primary CaP cultures identified bivalent chromatin at LXN and RARRES1 promoters. Transcriptomic profiling failed to reveal significant changes in gene expression after transduction with LXN or RARRES1. However, an interactome for LXN and RARRES1 was successfully generated in PC3 cells. Additionally, confocal microscopy of mVenus-tagged LXN revealed a pan-cellular distribution which is reflected in the interactome. Screening for GAAR and XCA, using a high-throughput qPCR assay, could facilitate a targeted-medicine strategy in the treatment of CaP and CRPC. Further investigation of the LXN and RARRES1 interactomes may identify their mechanism(s) of action and the micro-ChIP assay could be used to identify epigenetic-inducers of LXN and RARRES1 which could provide a CSC-targeted strategy for CaP treatment.
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Ribarska, Teodora [Verfasser]. "Expression and epigenetic regulation of imprinted genes in prostate cancer / Teodora Ribarska." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2013. http://d-nb.info/1036727513/34.

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Kadio, Bernard. "A Calcium-Centered Socio-Ecological Model of Prostate Cancer Disparities: Preliminary Studies and Findings." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/40685.

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Western studies have established that men from African descent are disproportionally affected by prostate cancer (PCa). Annual incidence rates in this population vary from 1.5 to 2 times when compared to their counterparts from other racial groups. They also record the worse outcomes in terms of prognosis. Additionally, with the rise of PCa in Subsaharan Africa, new cancer control policies and programs are increasingly demanded. Understanding therefore, factors that underpin racial inequality in distribution and especially why the disease preferentially niches in African males can help better address PCa in both Western and Subsaharan countries. There is also the potential to develop new therapeutic options. A genetic susceptibility was first hypothesized, however available data suggest that they only account for less than 20% of the cases. Current findings from epidemiological and molecular investigations suggest an important role of complex and dynamic environmental interactions involving the different levels of calcium regulation. Using a multi-method design, this research aims at developing an integrative mechanistic model of PCa. We argue that given the versatile and ubiquitous role calcium plays in nutrition, physical environment, and in key cellular processes, that mineral cation is central to prostate tumorigenesis and in shaping its populational distribution. Thus a tree-level investigation was conducted: (i) a critical analysis and synthesis of empirical evidence on calcium interactions with cancer mechanisms (ii) a population-wide prospective cohort study of calcium intake patterns in a group of Subsaharan males in Côte d’Ivoire, namely the African Prostate Cancer Study (APCS) (iii) a proteomics research investigating the responses of prostate cancer cell lines when exposed to a high affinity synthetic calcium binding peptide. This monograph describes the research methods, instruments design and validation and the preliminary findings of the ongoing research, portions of which have already been published, presented at two international cancer seminars or under review. Findings at this stage include: mechanistic models of prostate cancer differential distribution and outcomes, a novel calcium questionnaire specific to African diet, synthesis of a high affinity calcium-binding peptide (Peptide#1). New concepts and constructs related to prostatic carcinogenesis have been developed as well.
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Gupta, Yukti Hari. "An investigation into BORIS expression in prostate cancer cells and its role in epigenetic regulation of the androgen receptor gene." Thesis, University of Essex, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.635911.

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BORIS, a paralogue of the transcription factor CTCF, is a member of the cancer-testis antigen family. BORIS is normally present in the testes; however, it is aberrantly expressed in various tumours and cell lines. The main aim of this study was to investigate BORIS expression in prostate cell lines and tumours, and the importance of BORIS in the regulation of genes in prostate cells, in particular, the androgen receptor CAR) gene, associated with the development of more aggressive prostate tumours.
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Wu, Mengchu. "The Epigenetic Silencing of PMP24 During the Progression of Prostate Cancer from an Androgen-Dependent to Androgen-Independent State in the LNCAP Cell Model: a Dissertation." eScholarship@UMMS, 2005. https://escholarship.umassmed.edu/gsbs_diss/209.

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One important objective of prostate cancer (PCa) research is to understand the molecular basis underlying the progression of these cancers from an androgen dependent to an androgen independent state. Hypermethylation of the promoter CpG islands is associated with the transcriptional silencing of specific gene sets in each tumor type and subtype. Transcriptional silencing of antitumor genes via CpG island hypermethylation could be a mechanism mediating PCa progression from an androgen-dependent to an androgen-independent state. Hypermethylation associated gene silencing has been reported for a great number of genes in PCa with the exception of the genes that undergo methylation associated silencing specifically during cancer development to androgen independence. The first aim of this thesis is to identify novel glenes which undergo DNA hypermethylation associated gene silencing during the cancer progression. The androgen-dependent (AD, as defined as the inability of celill to proliferate in the absence of androgen) PCa cell line LNCaP gives rise to the androgen-independent (AI) subline LNCaPcs generated by maintaining LNCaP in medium with charcoal-stripped (CS) serum for over 30 passages. This LNCaP cell model was used to identify differentially methylated sequences between the two genomes using the Methylation-Sensitive Restriction Fingerprinting (MSRF) technique. One sequence identified is located in a 5' CpG island, which encompasses part of the promoter, exon 1, and part of intron 1, of the Peroxisomal Membrane Protein 24 KD (PMP24) gene. PMP24 is silenced in concert with the hypermethylation of its CpG island in AI LNCaPcsand PC-3 cell lines. The silencing is reactivated by the treatment with a DNA methyltransferase inhibitor, 5-aza-2'-deoxycytidine (5AZAdC). PMP24 is specifically silenced in PCa cancer cell lines and shows potential antitumor properties. These results demonstrate the utility of MSRF in the identification of novel, differentially methylated DNA sequences in the genome and suggest that hypermethylation-mediated silencing of PMP24 is an epigenetic event involved in PCa progression to androgen independence. The next study investigated the molecular mechanism for DNA methylation associated gene silencing of PMP24 in AI LNCaPcs and PC-3 cell lines. We demonstrated that PMP24 transcription is repressed by the disruption of transcription factor binding to a critical cis-element by hypermethylation of its promoter CpG island. We found a CpG containing activator protein 2 (AP-2) cis-element in the intron 1 of PMP24 whose first CpG dinucleotidle is essential for the sequence-specific protein binding and the promoter activity of the gene. We presented first in cellulo evidence that the methylation of AP-2 cis-element alone but not the whole CpG island, using a newly developed methylated oligonucleotides treatment, is sufficient for the downregulation of PMP24. Our study is the first to report that the silencing mechanism for PMP24 in AI LNCaPcs and PC-3 is mediated by the complete methylation of a single GpG site of AP-2 cis-element in the intron 1 part of the CpG island, which interferes with transcription factor binding. Most interestingly, the promoter CpG island of PMP24 is hypermethylated in AD LNCaP cells with the incomplete methylation specifically at the AP-2 cis-element. The silencing of PMP24 in AD LNCaP cells was reactivated not by the 5AZAdC treatment but by the treatment with Trichostatin A (TSA), a histone deacetylase inhibitor. An alternative silencing mechanism for PMP24 other than the interference with transcription factor binding by methylation is therefore likely involved at this androgen-dependent stage. During the androgen ablation process, this mechanism is either evolved by the spread of methylation in the promoter CpG island or selected against, leading to the methylation-dominant silencing mechanism in the AI cells as seen in LNCaPcsand PC-3 cells. Taken together, this thesis emphasized the important role of DNA methylation in the progression of PCa into androgen independence. Particular respect should be paid to the specific CpG dinucleotides in cis-elements critical for the promoter activity, whose complete methylation could dominate the silencing mechanism which is independent of androgen. This thesis also pointed to the importance of monitoring the effects of cell culture on the methylation status of genes. Most importantly, this thesis raised the possibility that the silencing mechanisms for PMP24 could be different in AD LNCaP cells as compared to AI LNCaPcs and PC-3 cells. Either the evolution of such mechanism or the selectivity against it during the androgen ablation process would result in a methylation-dominant silencing mechanism of the genes such as PMP24 in AI cells and may contribute to the overall androgen independence of the cells.
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Siouda, Maha. "Transcriptional regulation and epigenetic repression of the tumor suppressor DOK1 in viral- and non viral-related carcinogenesis." Thesis, Lyon 1, 2013. http://www.theses.fr/2013LYO10163.

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Le suppresseur de tumeur DOK1 (downstream of tyrosine kinases1) est une protéine régulatrice de voies de signalisation impliquées dans des processus cellulaires tel que la prolifération, la migration et l'apoptose. Le rôle suppresseur de tumeur de DOK1 a été démontré dans des modèles animaux. Les souris knock-out pour DOK1 présentent une forte susceptibilité de développer des leucémies, des tumeurs malignes hématologiques, des adénocarcinomes pulmonaires, ainsi que des sarcomes histiocytaires agressifs. En outre, nous avons rapporté précédemment que le gène DOK1 peut être muté et son expression réprimée dans différentes tumeurs malignes humaines, telles que les lignées cellulaires de lymphome de Burkitt (BL) et la leucémie lymphoïde chronique (LLC). Cependant, les mécanismes de dérégulation de DOK1 restent inconnus, notamment dans les processus de carcinogenèse induite ou non par des oncovirus. Dans ce projet de thèse, nous avons d'abord caractérisé le promoteur de DOK1 et le rôle du facteur de transcription E2F1 comme le principal régulateur de l'expression de DOK1. Nous avons démontré pour la première fois la contribution de DOK1 dans la réponse cellulaire au stress par son rôle suppresseur de prolifération cellulaire et promoteur d'apoptose. Nous avons trouvé que l'expression du gène DOK1 est réprimée dans une variété de cancers humains, y compris le cancer de la tête et du cou, les lymphomes de Burkitt et les cancers du poumon. Cette répression est due à l'hyperméthylation aberrante de DOK1. Nous avons donc étudié les événements épigénétiques, qui sont souvent altérés dans les cancers, et leurs implications dans la répression de DOK1 dans les lignes cellulaire cancéreuses de la tête et du cou. Nous nous sommes par la suite intéressés aux mécanismes de dérégulation de DOK1 par le virus d'Epstein Barr dans le cadre de sa propriété oncogénique dans les lymphocytes B humains ainsi que dans les lignes cancéreuses du lymphome de Burkitt. Nos résultats apportent de nouvelles informations sur les mécanismes de régulation de l'expression de DOK1 dans la carcinogenèse induite ou non par des oncovirus, ce qui pourrait le définir comme un biomarqueur potentiel de cancer et comme une cible intéressante pour des thérapies épigénétiques
The newly identified tumor suppressor DOK1 (downstream of tyrosine kinases1) inhibits cell proliferation, negatively regulates MAP kinase activity, opposes leukemogenesis, and promotes cell spreading, motility, and apoptosis. DOK1 also plays a role in the regulation of immune cell activation, including B cells. The tumor suppressor role of DOK1 was demonstrated in animal models. DOK1 knockout mice show a high susceptibility to develop leukemia, hematological malignancies as well as lung adenocarcinomas and aggressive histiocytic sarcoma. In addition, we previously reported that the DOK1 gene can be mutated and its expression is down-regulated in human malignancies such as Burkitt’s lymphoma cell lines (BL) and chronic lymphocytic leukemia (CLL). However, very little is known about the mechanisms underlying DOK1 gene regulation and silencing in viral- and non viral-related tumorigenesis. In the present project, we first characterized the DOK1 promoter. We have shown the role of E2F1 transcription factor as the major regulator of DOK1 expression and how DOK1 plays a role in DNA stress response though opposing cell proliferation and promoting apoptosis. We demonstrated that DOK1 gene expression is repressed in a variety of human cancers, including head and neck, Burkitt’s lymphoma and lung cancers, as a result of aberrant hypermethylation. We investigated the link between the epigenetic events and DOK1 silencing in non viral head and neck cancer cell lines, and by Epstein Barr virus in relation to its oncogenic activity in human B cells and neoplasia such as Burkitt’s lymphoma. These data provide novel insights into the regulation of DOK1 in viral and non viral-related carcinogenesis, and could define it as a potential cancer biomarker and an attractive target for epigeneticbased therapy
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Perriaud, Laury. "Étude systémique des cibles génomiques de la methyl-CpG binding domain protein 2 (MBD2), un répresseur transcriptionnel dépendant de la méthylation de l'ADN : évolution de la distribution de MBD2 dans un modèle syngénique de progression tumorale mammaire." Phd thesis, Université Claude Bernard - Lyon I, 2010. http://tel.archives-ouvertes.fr/tel-00833153.

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Les protéines à " Methyl-CpG-binding domain " (MBD) jouent un rôle important dans l'interprétationde la méthylation de l'ADN conduisant à la répression transcriptionnelle via le recrutement decomplexes remodelant la chromatine. Dans les cancers, MBD2 jouerait un rôle essentiel dans la perted'expression des gènes hyperméthylés. Ainsi, MBD2 serait une cible potentielle pour rétablir, enpartie au moins, leur expression. Caractériser, à l'échelle du génome, la distribution de MBD2 et sesconséquences sur la répression transcriptionnelle au cours de la cancérogenèse est donc une étapeincontournable. (1) L'impact sur l'expression génique de l'inhibition de MBD2 par interférence àl'ARN, a été étudié en utilisant des puces, dans des cellules normales MRC5. La perte de MBD2n'induit pas de surexpression génique globale et la densité en CpG des promoteurs méthylés sembleêtre une composante importante dans la force de répression par MBD2. (2) Les profils de méthylationde l'ADN, de liaisons de MBD2 et de l'ARN polymérase II dans les cellules HeLa ont été analysés parChIP-on-chip avec des puces promoteurs. Ces mêmes approches couplées à l'analyse de l'acétylationdes histones H3 ont été réalisées dans un modèle cellulaire syngénique de progression tumoralemammaire humain. Dans les modèles étudiés, une forte proportion de gènes silencieux et méthylés estliée par MBD2. Les comparaisons entre cellules immortalisées et transformées ne montrent pas dechangements majeurs de la méthylation de l'ADN ou de la répression transcriptionnelle, par contreune redistribution de MBD2 parmi ces sites est observée, suggérant une redondance entre les protéinesliant l'ADN méthylé.
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Books on the topic "Prostate cancer; epigenetic modification"

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Dean, Michael, and Karobi Moitra. Biology of Neoplasia. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0002.

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The term “cancer” encompasses a large heterogeneous group of diseases that involve uncontrolled cell growth, division, and survival, culminating in local invasion and/or distant metastases. Cancer is fundamentally a genetic disease at the cellular level. Tumors occur because clones of abnormal cells acquire multiple lesions in DNA, nearly always involving mutations, chromosomal rearrangements, and extensive alteration of the epigenome. Up to 10% of cancers also involve inherited germline mutations that are moderately to highly penetrant. Cancers begin as localized growths or premalignant lesions that may regress or disappear spontaneously, or progress to a malignant primary tumor. The somatic changes that drive abnormal growth involve activating mutations of specific oncogenes, inactivation of tumor suppressor genes, and/or disruption of epigenetic controls. The latter can result from methylation or the modification of histones and other proteins that affect the remodeling of chromosomes. Numerous non-inherited factors can cause cancer by accelerating these events.
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Book chapters on the topic "Prostate cancer; epigenetic modification"

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Nelson, William G., Michael C. Haffner, Angelo M. De Marzo, and Srinivasan Yegnasubramanian. "Epigenetic Changes in Prostate Cancer." In Prostate Cancer: A Comprehensive Perspective, 169–79. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-2864-9_14.

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Valdés-Mora, Fátima, and Clare Stirzaker. "Epigenetic Alterations in Primary Prostate Cancer." In Molecular Pathology Library, 193–211. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-64096-9_13.

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Chiam, Karen, Tanya Kate Day, and Tina Bianco-Miotto. "Recent Updates on Epigenetic Biomarkers for Prostate Cancer." In Epigenetics and Cancer, 129–50. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6612-9_8.

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Natesan, Ramakrishnan, Shweta Aras, Samuel Sander Effron, and Irfan A. Asangani. "Epigenetic Regulation of Chromatin in Prostate Cancer." In Advances in Experimental Medicine and Biology, 379–407. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-32656-2_17.

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Kumar, Sanjay, James A. Stokes, Udai P. Singh, Kumar S. Bishnupuri, and Manoj K. Mishra. "Enhancer of Zeste Homology 2 (Ezh2), an Epigenetic Regulator: A Possibility for Prostate Cancer Treatment." In Epigenetic Advancements in Cancer, 229–44. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-24951-3_10.

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Celetti, Angela. "Epigenetic Mechanisms: Histone Acetylation, DNA Methylation, miRNA, Chromatin Modifiers." In Prostate Cancer: Shifting from Morphology to Biology, 201–10. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7149-9_12.

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Veltri, Robert W., and Christhunesa S. Christudass. "Nuclear Morphometry, Epigenetic Changes, and Clinical Relevance in Prostate Cancer." In Cancer Biology and the Nuclear Envelope, 77–99. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4899-8032-8_4.

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Savio, Andrea J., and Bharati Bapat. "Beyond the Island: Epigenetic Biomarkers of Colorectal and Prostate Cancer." In Methods in Molecular Biology, 103–24. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1804-1_6.

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Takayama, Ken-ichi, and Satoshi Inoue. "Investigation of Androgen Receptor Signaling Pathways with Epigenetic Machinery in Prostate Cancer." In Molecular Oncology: Underlying Mechanisms and Translational Advancements, 205–22. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-53082-6_10.

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Periyasamy, Loganayaki, Abhaya Krishnan, Mekhala Kumaravel Palanichami, Ilangovan Ramachandran, R. Ileng Kumaran, Jonathan Behlen, Jone Stanley, and Sridhar Muthusami. "Reactive Oxygen Species: Induced Epigenetic Modification in the Expression Pattern of Oncogenic Proteins." In Handbook of Oxidative Stress in Cancer: Therapeutic Aspects, 1–16. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-1247-3_68-1.

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Conference papers on the topic "Prostate cancer; epigenetic modification"

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Singhal, Udit, Anirban Sahu, John R. Prensner, Qi Cao, and Arul M. Chinnaiyan. "Abstract 2869: SChLAP1 mediated epigenetic modifications in prostate cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2869.

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Shankar, Eswar, Omair Iqbal, Natarajan Bhaskaran, Gauri Deb, Gregory T. MacLennan, Pingfu Fu, and Sanjay Gupta. "Abstract 5084: Epigenetic modifications involving reactivation of RECK inhibiting MMP-9 and MMP-2 in prostate cancer." 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.sabcs18-5084.

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Shankar, Eswar, Omair Iqbal, Natarajan Bhaskaran, Gauri Deb, Gregory T. MacLennan, Pingfu Fu, and Sanjay Gupta. "Abstract 5084: Epigenetic modifications involving reactivation of RECK inhibiting MMP-9 and MMP-2 in prostate cancer." 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.am2019-5084.

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Spiliopoulou, Pavlina, Josephine Walton, Suzanne Dowson, Alex Binks, Oliver Maddocks, Peter Adams, and Iain McNeish. "Abstract A37: Epigenetic modification of ovarian cancer immunogenicity." In Abstracts: AACR Special Conference: Addressing Critical Questions in Ovarian Cancer Research and Treatment; October 1-4, 2017; Pittsburgh, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.ovca17-a37.

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Lin, Hui-Yi, Anders Berglund, Thomas Sellers, Ardeshir Hakam, Hyun Park, Julio Pow-Sang, and Jong Y. Park. "Abstract 291: Genomewide scale epigenetic profile and prostate cancer recurrence." 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.am2014-291.

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Puca, Loredana, Dong Gao, Myriam Kossai, Joanna Cyrta, Clarisse Marotz, Juan Miguel Mosquera, Theresa Y. MacDonald, et al. "Abstract B41: Targeting androgen-independent prostate cancer through epigenetic reprogramming." In Abstracts: AACR Special Conference: Chromatin and Epigenetics in Cancer; September 24-27, 2015; Atlanta, GA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.chromepi15-b41.

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Kumar, Devi Sharanya Sampath, and Alan Wells. "Abstract 4016: Epigenetic regulation of CXCR3 splicing in prostate cancer cells." 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.am2012-4016.

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Maitland, Norman James, and John Packer. "Abstract B23: Epigenetic control of prostate epithelial stem cell differentiation." In Abstracts: AACR Special Conference on Developmental Biology and Cancer; November 30 - December 3, 2015; Boston, Massachusetts. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.devbiolca15-b23.

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Battaglia, Sebastiano, Steven Seedhouse, Ellen Karasik, Dominic Smiraglia, and Barbara Foster. "Abstract 3390: Epigenetic corruption of the Vitamin D signaling in prostate cancer." 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.am2014-3390.

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Nelson, William, Michael Haffner, Traci Speed, Byron Lee, and Srinivasan Yegnasubramanian. "Abstract CN01-01: Genetic and epigenetic changes in prostate cancer as targets for prevention." In Abstracts: Frontiers in Cancer Prevention Research 2008. American Association for Cancer Research, 2008. http://dx.doi.org/10.1158/1940-6207.prev-08-cn01-01.

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Reports on the topic "Prostate cancer; epigenetic modification"

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Margueron, Raphael F. An Epigenetic Link to Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, November 2006. http://dx.doi.org/10.21236/ada484222.

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Shurin, Michael R. Epigenetic Regulation of Chemokine Expression in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2006. http://dx.doi.org/10.21236/ada460756.

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Tlsty, Thea D. Modification of Epigenetic Changes in Cancer by the Stromal Environment. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada430193.

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Battaglia, Sebastiano. Targeting LSD1 Epigenetic Signature in Castration-Recurrent Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada612062.

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Park, Jong Y. Genetic and Epigenetic Biomarkers for Recurrent Prostate Cancer After Radiotherapy. Fort Belvoir, VA: Defense Technical Information Center, May 2014. http://dx.doi.org/10.21236/ada609389.

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Case, Adam J., and Frederick E. Domann. Epigenetic Control of Prolyl and Asparaginyl Hydroxylases in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2010. http://dx.doi.org/10.21236/ada542700.

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Case, Adam J. Epigenetic Control of Prolyl and Asparaginyl Hydroxylases in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2009. http://dx.doi.org/10.21236/ada511993.

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Franceschi, Renny T. Epigenetic Control of Prostate Cancer Metastasis: Role of Runx2 Phosphorylation. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada580104.

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Park, Jong. Genetic and Epigenetic Biomarkers for Recurrent Prostate Cancer After Radiotherapy. Fort Belvoir, VA: Defense Technical Information Center, May 2013. http://dx.doi.org/10.21236/ada581491.

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Case, Adam. Epigenetic Control of Prolyl and Asparaginyl Hydroxylases in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada552430.

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