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Relevant bibliographies by topics / Prostate cancer; epigenetic modification

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

Author: Grafiati

Published: 10 December 2022

Last updated: 31 July 2025

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

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Zhang, Shouyi, Tao Shen, and Yu Zeng. "Epigenetic Modifications in Prostate Cancer Metastasis and Microenvironment." Cancers 15, no. 8 (2023): 2243. http://dx.doi.org/10.3390/cancers15082243.

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The gradual evolution of prostate tissue from benign tumor to malignant lesion or distant metastasis is driven by intracellular epigenetic changes and the tumor microenvironment remodeling. With the continuous study of epigenetic modifications, these tumor-driving forces are being discovered and are providing new treatments for cancer. Here we introduce the classification of epigenetic modification and highlight the role of epigenetic modification in tumor remodeling and communication of the tumor microenvironment.

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Albany, Costantine, Ajjai S. Alva, Ana M. Aparicio, et al. "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 ce

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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,

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Zeng, Yaohui, Cai Lv, Bangbei Wan, and Binghao Gong. "The current landscape of m6A modification in urological cancers." PeerJ 11 (September 7, 2023): e16023. http://dx.doi.org/10.7717/peerj.16023.

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N6-methyladenosine (m6A) methylation is a dynamic and reversible procession of epigenetic modifications. It is increasingly recognized that m6A modification has been involved in the tumorigenesis, development, and progression of urological tumors. Emerging research explored the role of m6A modification in urological cancer. In this review, we will summarize the relationship between m6A modification, renal cell carcinoma, bladder cancer, and prostate cancer, and discover the biological function of m6A regulators in tumor cells. We will also discuss the possible mechanism and future application

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Zheng, Jianghua, Jinglong Wang, Xueqing Sun, et al. "HIC1 Modulates Prostate Cancer Progression by Epigenetic Modification." Clinical Cancer Research 19, no. 6 (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, et al. "Epigenetic modifications in prostate cancer." Epigenomics 6, no. 4 (2014): 415–26. http://dx.doi.org/10.2217/epi.14.34.

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Ippolito, Luigi, Giuseppina Comito, Matteo Parri, et al. "Lactate Rewires Lipid Metabolism and Sustains a Metabolic–Epigenetic Axis in Prostate Cancer." Cancer Research 82, no. 7 (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 a

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Zaalberg, Anniek, Elisabeth Pottendorfer, Wilbert Zwart, and Andries M. Bergman. "It Takes Two to Tango: The Interplay between Prostate Cancer and Its Microenvironment from an Epigenetic Perspective." Cancers 16, no. 2 (2024): 294. http://dx.doi.org/10.3390/cancers16020294.

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Prostate cancer is the second most common cancer in men worldwide and is associated with high morbidity and mortality. Consequently, there is an urgent unmet need for novel treatment avenues. In addition to somatic genetic alterations, deviations in the epigenetic landscape of cancer cells and their tumor microenvironment (TME) are critical drivers of prostate cancer initiation and progression. Unlike genomic mutations, epigenetic modifications are potentially reversible. Therefore, the inhibition of aberrant epigenetic modifications represents an attractive and exciting novel treatment strate

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Orea, María J., Javier C. Angulo, Ana González-Corpas, et al. "Claudin-3 Loss of Expression Is a Prognostic Marker in Castration-Resistant Prostate Cancer." International Journal of Molecular Sciences 24, no. 1 (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

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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 compo

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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 suppresse

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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

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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 inte

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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 b

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ROSTI, VALENTINA. "Chromatin solubility as a novel determinant of epigenome dysfunction in prostate cancer." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2022. http://hdl.handle.net/10281/382306.

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Il carcinoma prostatico (PCa) è il secondo tumore maschile più ricorrente, spesso caratterizzato da un esito sfavorevole a causa della sua elevata eterogeneità clinica e molecolare e della sua frequente multifocalità. Sempre più grandi sforzi della ricerca epigenetica si concentrano nel rilevamento di nuovi biomarcatori in grado di migliorare la diagnosi e la prognosi del PCa. Tra i livelli epigenetici, l'architettura nucleare della cromatina rispetta regole precise che garantiscono il corretto funzionamento del genoma e il mantenimento dell'identità cellulare, e il suo rimodellamento è emers

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BANDINI, MARCO. "Development of a novel signature integrating clinical, imaging and epigenetic information to tailor pelvic nodal treatment in prostate cancer." Doctoral thesis, Università Vita-Salute San Raffaele, 2023. https://hdl.handle.net/20.500.11768/136959.

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Radical prostatectomy (RP) is a treatment option for men with localized prostate cancer. Extended pelvic lymph node dissection (ePLND) at the time of RP is recommended only in patients at risk of lymph node invasion (LNI), where a more accurate disease staging can tailor further adjuvant treatments. The risk of LNI is assessed through preoperative models, such as the Briganti nomograms, which are based on clinical features. They allow for sparing ePLND in a significant proportion of patients, but their accuracy is still suboptimal. Unfortunately, ePLND is associated with significant risks of c

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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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Rubino, M. "EPIGENETIC MODIFICATIONS ABOLISH THE EXPRESSION OF THE LONG PENTRAXIN PTX3 IN HUMAN TUMORS." Doctoral thesis, Università degli Studi di Milano, 2015. http://hdl.handle.net/2434/254345.

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PTX3 is a fluid-phase pattern recognition receptor that participates in innate immunity and inflammation by modulating complement activation, leukocyte recruitment, extracellular matrix deposition and angiogenesis. PTX3 is a biomarker of inflammatory conditions in different pathologies in humans, including acute myocardial infarction to autoimmune diseases, infections and cancer associated inflammation. Moreover, in vivo studies indicate that PTX3 is involved in cancer development, possibly by regulating inflammation. Several tumors lack PTX3 expression, such as human esophageal squamous cell

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Books on the topic "Prostate cancer; epigenetic modification"

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INTEGRATIVE GENETIC AND EPIGENETIC STUDIES FOR PROSTATE CANCER GENES: PROSTATE CANCER GENES AT CHROMOSOME 8P. LAP LAMBERT Academic Publishing, 2011.

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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 lesio

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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. Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-2864-9_14.

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Xu, Chenxi, Shuai Zhao, and Ling Cai. "Epigenetic (De)regulation in Prostate Cancer." In Cancer Treatment and Research. Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-45654-1_10.

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Valdés-Mora, Fátima, and Clare Stirzaker. "Epigenetic Alterations in Primary Prostate Cancer." In Molecular Pathology Library. 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. 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. 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. 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. 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. 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. 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. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-53082-6_10.

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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, et al. "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, et al. "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, et al. "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, et al. "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, 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. Defense Technical Information Center, 2006. http://dx.doi.org/10.21236/ada484222.

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Shurin, Michael R. Epigenetic Regulation of Chemokine Expression in Prostate Cancer. Defense Technical Information Center, 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. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada430193.

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Battaglia, Sebastiano. Targeting LSD1 Epigenetic Signature in Castration-Recurrent Prostate Cancer. Defense Technical Information Center, 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. Defense Technical Information Center, 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. Defense Technical Information Center, 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. Defense Technical Information Center, 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. Defense Technical Information Center, 2013. http://dx.doi.org/10.21236/ada580104.

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

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

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