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

Author: Grafiati

Published: 10 December 2022

Last updated: 31 July 2025

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1

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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3

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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4

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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6

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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7

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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9

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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11

López, Judith, Ana M. Añazco-Guenkova, Óscar Monteagudo-García, and Sandra Blanco. "Epigenetic and Epitranscriptomic Control in Prostate Cancer." Genes 13, no. 2 (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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12

Abbas, Ata, William Patterson, and Philippe T. Georgel. "The epigenetic potentials of dietary polyphenols in prostate cancer management." Biochemistry and Cell Biology 91, no. 6 (2013): 361–68. http://dx.doi.org/10.1139/bcb-2012-0044.

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Prostate cancer is a disease that is greatly affected by lifestyle, particularly diet, and is more prevalent in US and European countries compared with South and East Asia. Among several known causes and risk factors, nutrition plays an important role in prostate cancer pathogenesis. Various dietary components including polyphenols have been shown to possess anticancer properties. Dietary polyphenols have been the subject of extensive studies for the last decade because of their anticancer and chemopreventive potentials. Besides possessing various antitumor properties, dietary polyphenols also

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13

Cimadamore, Alessia, Silvia Gasparrini, Marina Scarpelli, et al. "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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14

Xu, Songlin, Changfu Li, Lichen Teng, Yongsheng Chen, Dechao Li, and Zhijian Kang. "Advances and Implications of Histone Modifications in Prostate Cancer: A Brief Review." Theoretical and Natural Science 67, no. 1 (2024): 58–63. https://doi.org/10.54254/2753-8818/2024.18074.

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Prostate cancer, a leading cause of cancer-related mortality among men, is increasingly linked to epigenetic changes, particularly histone modifications that affect gene expression and tumor behavior. This review explores recent advances in understanding how aberrant histone acetylation, methylation, and other modifications contribute to prostate cancer progression, metastasis, and therapeutic resistance. By analyzing these modifications' roles in regulating critical pathways, this paper aims to elucidate their diagnostic and therapeutic potential, suggesting that targeted epigenetic therapies

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15

Wu, Peng, Ziyi Cao, and Song Wu. "New Progress of Epigenetic Biomarkers in Urological Cancer." Disease Markers 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/9864047.

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Urological cancers consist of bladder, kidney, prostate, and testis cancers and they are generally silenced at their early stage, which leads to the loss of the best opportunity for early diagnosis and treatment. Desired biomarkers are scarce for urological cancers and current biomarkers are lack of specificity and sensitivity. Epigenetic alterations are characteristic of nearly all kinds of human malignances including DNA methylation, histone modification, and miRNA regulation. Besides, the detection of these epigenetic conditions is easily accessible especially for urine, best target for mon

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16

Yu, Chenglong, Ee Ming Wong, Jihoon Eric Joo, et al. "Epigenetic Drift Association with Cancer Risk and Survival, and Modification by Sex." Cancers 13, no. 8 (2021): 1881. http://dx.doi.org/10.3390/cancers13081881.

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To investigate age- and sex-specific DNA methylation alterations related to cancer risk and survival, we used matched case–control studies of colorectal (n = 835), gastric (n = 170), kidney (n = 143), lung (n = 332), prostate (n = 869) and urothelial (n = 428) cancers, and mature B-cell lymphoma (n = 438). Linear mixed-effects models were conducted to identify age-, sex- and age-by-sex-associated methylation markers using a discovery (controls)-replication (cases) strategy. Replication was further examined using summary statistics from Generation Scotland (GS). Associations between replicated

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17

Inoue, Takahiro, Sho Sekito, Takumi Kageyama, Yusuke Sugino, and Takeshi Sasaki. "Roles of the PARP Inhibitor in BRCA1 and BRCA2 Pathogenic Mutated Metastatic Prostate Cancer: Direct Functions and Modification of the Tumor Microenvironment." Cancers 15, no. 9 (2023): 2662. http://dx.doi.org/10.3390/cancers15092662.

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Cancer cells frequently exhibit defects in DNA damage repair (DDR), leading to genomic instability. Mutations in DDR genes or epigenetic alterations leading to the downregulation of DDR genes can result in increased dependency on other DDR pathways. Therefore, DDR pathways could be a treatment target for various cancers. In fact, polyadenosine diphosphatase ribose polymerase (PARP) inhibitors, such as olaparib (Lynparza®), have shown remarkable therapeutic efficacy against BRCA1/2-mutant cancers through synthetic lethality. Recent genomic analytical advancements have revealed that BRCA1/BRCA2

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18

Sulek, Jay E., Samuel P. Robinson, Albert A. Petrossian, et al. "Role of Epigenetic Modification and Immunomodulation in a Murine Prostate Cancer Model." Prostate 77, no. 4 (2016): 361–73. http://dx.doi.org/10.1002/pros.23275.

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19

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 (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 st

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20

Lopes, Nair, Mariana Brütt Pacheco, Diana Soares-Fernandes, et al. "Hydralazine and Enzalutamide: Synergistic Partners against Prostate Cancer." Biomedicines 9, no. 8 (2021): 976. http://dx.doi.org/10.3390/biomedicines9080976.

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Advanced prostate cancers frequently develop resistance to androgen-deprivation therapy with serious implications for patient survival. Considering their importance in this type of neoplasia, epigenetic modifications have drawn attention as alternative treatment strategies. The aim of this study was to assess the antitumoral effects of the combination of hydralazine, a DNA methylation inhibitor, with enzalutamide, an antagonist of the androgen receptor, in prostate cancer cell lines. Several biological parameters, such as cell viability, proliferation, DNA damage, and apoptosis, as well as clo

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21

Perry, Antoinette S., Ruth Foley, Karen Woodson, and Mark Lawler. "The emerging roles of DNA methylation in the clinical management of prostate cancer." Endocrine-Related Cancer 13, no. 2 (2006): 357–77. http://dx.doi.org/10.1677/erc.1.01184.

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Aberrant DNA methylation is one of the hallmarks of carcinogenesis and has been recognized in cancer cells for more than 20 years. The role of DNA methylation in malignant transformation of the prostate has been intensely studied, from its contribution to the early stages of tumour development to the advanced stages of androgen independence. The most significant advances have involved the discovery of numerous targets such as GSTP1, Ras-association domain family 1A (RASSF1A) and retinoic acid receptor β2 (RARβ2) that become inactivated through promoter hypermethylation during the course of dis

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22

Yasmin, Rehana, Sami Siraj, Amjad Hassan, Abdul Rehman Khan, Rashda Abbasi, and Nafees Ahmad. "Epigenetic Regulation of Inflammatory Cytokines and Associated Genes in Human Malignancies." Mediators of Inflammation 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/201703.

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Inflammation is a multifaceted defense response of immune system against infection. Chronic inflammation has been implicated as an imminent threat for major human malignancies and is directly linked to various steps involved in tumorigenesis. Inflammatory cytokines, interleukins, interferons, transforming growth factors, chemokines, and adhesion molecules have been associated with chronic inflammation. Numerous cytokines are reported to be aberrantly regulated by different epigenetic mechanisms like DNA methylation and histone modifications in tumor tissues, contributing to pathogenesis of tum

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23

Li, Ermao, Yazhi Zhu, Juling Feng, et al. "ALKBH5 Inhibits Cancer Cell Proliferation in Prostate Cancer through KLF4/TERT Signaling." Andrologia 2023 (March 17, 2023): 1–14. http://dx.doi.org/10.1155/2023/8754940.

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N6-methyladenosine (m6A), as a reversible chemical modification of RNA, is a new type of posttranscriptional gene regulation, which plays an important role in cell differentiation and tumorigenesis, and is also a research hotspot in epigenetic transcriptomics in recent years. The purpose of this study was to discuss the action mechanism of m6A demethylase ALKBH5 in the occurrence of prostate cancer (PCa). We found that ALKBH5 was lowly expressed in PCa, and the decreased expression of ALKBH5 was responsible for the poor prognosis of prostate carcinomas. Moreover, ALKBH5 downregulated the expre

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24

Paleati, Nikhila, and Gnanasekar Munirathinam. "Role of Chromatin and Epigenetic Dysregulation in Prostate Cancer: From Development to Progression and Therapeutic Response." Cancers 15, no. 23 (2023): 5638. http://dx.doi.org/10.3390/cancers15235638.

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25

Abbas, Ata, J. Adam Hall, William L. Patterson, et al. "Sulforaphane modulates telomerase activity via epigenetic regulation in prostate cancer cell lines." Biochemistry and Cell Biology 94, no. 1 (2016): 71–81. http://dx.doi.org/10.1139/bcb-2015-0038.

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Epidemiologic studies have revealed that diets rich in sulforaphane (SFN), an isothiocyanate present in cruciferous vegetables, are associated with a marked decrease in prostate cancer incidence. The chemo-preventive role of SFN is associated with its histone de-acetylase inhibitor activity. However, the effect of SFN on chromatin composition and dynamic folding, especially in relation to HDAC inhibitor activity, remains poorly understood. In this study, we found that SFN can inhibit the expression and activity of human telomerase reverse transcriptase (hTERT), the catalytic subunit of telomer

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26

Godbole, Abhijit M., and Vincent C. O. Njar. "New Insights into the Androgen-Targeted Therapies and Epigenetic Therapies in Prostate Cancer." Prostate Cancer 2011 (2011): 1–13. http://dx.doi.org/10.1155/2011/918707.

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Prostate cancer is the most common cancer in men in the United States, and it is the second leading cause of cancer-related death in American men. The androgen receptor (AR), a receptor of nuclear family and a transcription factor, is the most important target in this disease. While most efforts in the clinic are currently directed at lowering levels of androgens that activate AR, resistance to androgen deprivation eventually develops. Most prostate cancer deaths are attributable to this castration-resistant form of prostate cancer (CRPC). Recent work has shed light on the importance of epigen

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27

Hightower, Alexandria J., Suhn K. Rhie, Sara M. Falzarano, and Sarah Buxbaum. "Abstract C045: Investigating molecular and genetic contributions to racial disparities in prostate cancer by integrating multi-omic datasets available in public." Cancer Epidemiology, Biomarkers & Prevention 32, no. 1_Supplement (2023): C045. http://dx.doi.org/10.1158/1538-7755.disp22-c045.

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Abstract African-American males are disproportionately affected by prostate cancer in comparison to other racial and ethnic groups. African-American males have increased risk for the disease, experience higher incidence and mortality rates, and present higher grade and stage prostate tumors than Caucasian men. To determine molecular mechanisms beyond racial disparities in prostate cancer, molecular and genetic profiles of prostate tumor samples from different ethnic groups are developed. For example, DNA sequencing in the form of target-based array or whole exome and genome sequencing revealed

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28

Leal, Alessandro, David Sidransky, and Mariana Brait. "Tissue and Cell-Free DNA-Based Epigenomic Approaches for Cancer Detection." Clinical Chemistry 66, no. 1 (2019): 105–16. http://dx.doi.org/10.1373/clinchem.2019.303594.

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Abstract BACKGROUND Over 9 million people die of cancer each year worldwide, reflecting the unmet need for effective biomarkers for both cancer diagnosis and prognosis. Cancer diagnosis is complex because the majority of malignant tumors present with long periods of latency and lack of clinical presentation at early stages. During carcinogenesis, premalignant cells experience changes in their epigenetic landscapes, such as differential DNA methylation, histone modifications, nucleosome positioning, and higher orders of chromatin changes that confer growth advantage and contribute to determinin

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Kushwaha, Prem Prakash, and Sanjay Gupta. "New insights for drug resistance in metastatic castration-resistant prostate cancer." Cancer Drug Resistance 5, no. 4 (2022): 846–49. http://dx.doi.org/10.20517/cdr.2022.83.

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Prostate cancer is the most common cancer and is the second leading cause of cancer-related deaths among men in the United States. Androgen deprivation therapy (ADT) is the standard treatment for advanced-stage prostate cancer; however, this treatment eventually fails, leading to an incurable disease subtype known as metastatic castration-resistant prostate cancer (mCRPC). There are several molecular mechanisms that facilitate the development of mCRPC engaging androgen receptor (AR) growth axis, including AR amplification, gain of function AR mutations, and AR splice variants that are constitu

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Kauffman, Zachary J., Kevin Koesser, Kyle T. Helzer, et al. "Abstract A057: Microscale analysis of histone modifications in rare cell populations in prostate cancer." Cancer Research 83, no. 11_Supplement (2023): A057. http://dx.doi.org/10.1158/1538-7445.prca2023-a057.

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Abstract Pre-clinical models have identified diverse epigenetic alterations in prostate cancer that associate with treatment resistance and may also be therapeutic targets. However, these assays typically require thousands of cells and are difficult to scale for patient tumor biopsies. This report seeks to adapt the Cleavage Under Targets and Tagmentation (CUT&Tag) assay for use on a microfluidic technology to eliminate cell loss associated with complex, multi-step epigenetic assays to facilitate analysis of low input primary tumor samples. Exclusive Liquid Repellant (ELR) platforms pass m

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Singh, Prashant, and Moray Campbell. "The Interactions of microRNA and Epigenetic Modifications in Prostate Cancer." Cancers 5, no. 4 (2013): 998–1019. http://dx.doi.org/10.3390/cancers5030998.

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32

Wang, Hung-Jung, and Wen-Chi Cheng. "Current advances of targeting epigenetic modifications in neuroendocrine prostate cancer." Tzu Chi Medical Journal 33, no. 3 (2021): 224. http://dx.doi.org/10.4103/tcmj.tcmj_220_20.

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33

Adjakly, Mawussi, Marjolaine Ngollo, Aslihan Dagdemir, et al. "Prostate cancer: The main risk and protective factors – Epigenetic modifications." Annales d'Endocrinologie 76, no. 1 (2015): 25–41. http://dx.doi.org/10.1016/j.ando.2014.09.001.

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34

Bhattacharya, Sreyashi, Ridwan Islam, Sanika Bodas, et al. "Abstract LB037: Chromatin modifications guide Pax5 dependent gene expression in NE like prostate cancer." Cancer Research 82, no. 12_Supplement (2022): LB037. http://dx.doi.org/10.1158/1538-7445.am2022-lb037.

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Abstract Background: Prolonged ablation of androgen receptor pathway in prostate cancer leads to the emergence of therapy resistant neuroendocrine-like (NE-like) aggressive lineage. This NE development is associated with chromatin reprogramming underlying epigenetic alterations and changes in transcriptional network. Clinically, NE development follows a poorer progression with multifaceted therapeutic challenges. Current lack of effective understanding of this NE trans-differentiation process limits the stratification of therapeutic window with further worsened patient management. The followin

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Karan, Dev, Manohar Singh, Seema Dubey, Peter J. Van Veldhuizen, and Yogen Saunthararajah. "DNA Methyltransferase 1 Targeting Using Guadecitabine Inhibits Prostate Cancer Growth by an Apoptosis-Independent Pathway." Cancers 15, no. 10 (2023): 2763. http://dx.doi.org/10.3390/cancers15102763.

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Epigenetic alterations such as DNA methylation and histone modifications are implicated in repressing several tumor suppressor genes in prostate cancer progression. In this study, we determined the anti-prostate cancer effect of a small molecule drug guadecitabine (gDEC) that inhibits/depletes the DNA methylation writer DNA methyltransferase 1 (DNMT1). gDEC inhibited prostate cancer cell growth and proliferation in vitro without activating the apoptotic cascade. Molecular studies confirmed DNMT1 depletion and modulated epithelial-mesenchymal transition markers E-cadherin and β-catenin in sever

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Pasic, Maria D., Ekaterina Olkhov, Bharati Bapat, and George M. Yousef. "Epigenetic regulation of kallikrein-related peptidases: there is a whole new world out there." Biological Chemistry 393, no. 5 (2012): 319–30. http://dx.doi.org/10.1515/hsz-2011-0273.

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AbstractThe human kallikreins are a cluster of 15 kallikreins and kallikrein-related peptidases (KLKs). Evidence shows the involvement of KLKs in a wide range of pathophysiological processes, and underscores their potential contribution to cancer, skin and neurodegenerative disorders. The control ofKLKexpression is not fully elucidated. Understanding the mechanisms controllingKLKexpression is an essential step towards exploring the pathogenesis of several diseases and the use of KLKs as disease biomarkers and/or therapeutic targets. Recently, epigenetic changes (including methylation, histone

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Osterman, Carlos J. Diaz, Anders Berglund, Shannalee Martinez, et al. "Abstract 3675: Epigenetic variations associated with therapy resistance among prostate tumors from Puerto Rican men." Cancer Research 82, no. 12_Supplement (2022): 3675. http://dx.doi.org/10.1158/1538-7445.am2022-3675.

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Abstract Prostate cancer (PCa) is the leading cause of cancer-related death in Puerto Rican (PR) men, a population at higher risk of developing the disease than other Hispanic/Latino groups. But the relationship between this phenomenon and epigenetics, and how this relationship explains PCa racial and ethnic health disparities are controversial. The purpose of this study was to expand on the knowledge regarding epigenetic differences in terms of DNA methylation to enable risk stratification and treatment selection in this genetically admixed population. In addition, we aim to assess differenti

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Moussa, Haboubacar Elhadji Yaou, and Callinis Capo Chichi. "Abstract B052: Prostate cancer prevention is possible thanks to the evaluation of the primary exons of the BRCA1 biomarker in men." Cancer Research 83, no. 11_Supplement (2023): B052. http://dx.doi.org/10.1158/1538-7445.prca2023-b052.

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Abstract Prostate cancer is a public health concern among 50 year old the men worldwide and its incidence keep rising. It is triggered by genome instability or epigenetic modifications impacting DNA repair and tumor suppression genes and proteins. In African countries, little data is available on prostate cancer and the loss of BRCA1 exons responsible for tumor suppression. It is in this context that we undertook this study, the general objective of which is to assess the association between BRCA1 instability in patients with prostate cancer, These men with prostate cancer usually present with

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Gerke, Margo B., Caroline S. Jansen, and Mehmet A. Bilen. "Circulating Tumor DNA in Genitourinary Cancers: Detection, Prognostics, and Therapeutic Implications." Cancers 16, no. 12 (2024): 2280. http://dx.doi.org/10.3390/cancers16122280.

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CtDNA is emerging as a non-invasive clinical detection method for several cancers, including genitourinary (GU) cancers such as prostate cancer, bladder cancer, and renal cell carcinoma (RCC). CtDNA assays have shown promise in early detection of GU cancers, providing prognostic information, assessing real-time treatment response, and detecting residual disease and relapse. The ease of obtaining a “liquid biopsy” from blood or urine in GU cancers enhances its potential to be used as a biomarker. Interrogating these “liquid biopsies” for ctDNA can then be used to detect common cancer mutations,

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Kauffman, Zachary J., Kevin Koesser, Kyle T. Helzer, et al. "Abstract 7023: Application of exclusive liquid repellency for low input CUT&Tag histone analyses in prostate cancer spheroids." Cancer Research 84, no. 6_Supplement (2024): 7023. http://dx.doi.org/10.1158/1538-7445.am2024-7023.

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Abstract Introduction/Background: Epigenetic alterations, including histone modifications and DNA methylation, drive treatment resistance and lethal prostate cancer. However, epigenetic assays typically require thousands of cells and are difficult to scale for patient tumor biopsies. While identifying these alterations is possible in cell lines, these analytes are more difficult to follow in clinical settings. Patient-derived organoids have emerged as viable intermediaries to investigate the changing chromatin landscape during the progression toward treatment-emergent prostate cancer. This rep

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Martin, Francis L. "Epigenetic Influences in the Aetiology of Cancers Arising from Breast and Prostate: A Hypothesised Transgenerational Evolution in Chromatin Accessibility." ISRN Oncology 2013 (February 3, 2013): 1–13. http://dx.doi.org/10.1155/2013/624794.

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Epidemiological studies have consistently supported the notion that environmental and/or dietary factors play a central role in the aetiology of cancers of the breast and prostate. However, for more than five decades investigators have failed to identify a single cause-and-effect factor, which could be implicated; identification of a causative entity would allow the implementation of an intervention strategy in at-risk populations. This suggests a more complex pathoaetiology for these cancer sites, compared to others. When one examines the increases or decreases in incidence of specific cancer

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Taverna, Gianluigi, Mauro Seveso, Guido Giusti, et al. "Senescent Remodeling of the Innate and Adaptive Immune System in the Elderly Men with Prostate Cancer." Current Gerontology and Geriatrics Research 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/478126.

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Despite years of intensive investigation that has been made in understanding prostate cancer, it remains a major cause of death in men worldwide. Prostate cancer emerges from multiple alterations that induce changes in expression patterns of genes and proteins that function in networks controlling critical cellular events. Based on the exponential aging of the population and the increasing life expectancy in industrialized Western countries, prostate cancer in the elderly men is becoming a disease of increasing significance. Aging is a progressive degenerative process strictly integrated with

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Dalpatraj, Nidhi, Ankit Naik та Noopur Thakur. "Combination Treatment of a Phytochemical and a Histone Demethylase Inhibitor—A Novel Approach towards Targeting TGFβ-Induced EMT, Invasion, and Migration in Prostate Cancer". International Journal of Molecular Sciences 24, № 3 (2023): 1860. http://dx.doi.org/10.3390/ijms24031860.

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Minimizing side effects, overcoming cancer drug resistance, and preventing metastasis of cancer cells are of growing interest in current cancer therapeutics. Phytochemicals are being researched in depth as they are protective to normal cells and have fewer side effects. Hesperetin is a citrus bioflavonoid known to inhibit TGFβ-induced epithelial-to-mesenchymal transition (EMT), migration, and invasion of prostate cancer cells. Targeting epigenetic modifications that cause cancer is another class of upcoming therapeutics, as these changes are reversible. Global H3K27me3 levels have been found t

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Kawamoto, Ken, Steven T. Okino, Robert F. Place, et al. "Epigenetic Modifications of RASSF1A Gene through Chromatin Remodeling in Prostate Cancer." Clinical Cancer Research 13, no. 9 (2007): 2541–48. http://dx.doi.org/10.1158/1078-0432.ccr-06-2225.

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Nowacka-Zawisza, Maria, and Ewelina Wiśnik. "DNA methylation and histone modifications as epigenetic regulation in prostate cancer." Oncology Reports 38, no. 5 (2017): 2587–96. http://dx.doi.org/10.3892/or.2017.5972.

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Gonye, Anna, Chi-Ju Kim, Ken Pienta, and Sarah Amend. "Abstract A028: Investigating the epigenetic landscape of chemotherapy-induced polyaneuploid prostate cancer cells." Cancer Research 82, no. 23_Supplement_2 (2022): A028. http://dx.doi.org/10.1158/1538-7445.cancepi22-a028.

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Abstract While localized prostate cancer (PCa) has a high treatment success rate, over 30,000 individuals in the United States and 350,000 men globally die each year from therapy resistant, metastatic PCa. A thorough understanding of the factors contributing to PCa recurrence following development of therapy resistance is acutely needed in order to develop efficacious treatments and disease-management strategies. Our group and others have identified a unique minority population of physically enlarged cancer cells with polyaneuploid genomes, termed polyaneuploid cancer cells (PACCs), in the tum

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Jurkovicova, Dana, Christiana M. Neophytou, Ana Čipak Gašparović, and Ana Cristina Gonçalves. "DNA Damage Response in Cancer Therapy and Resistance: Challenges and Opportunities." International Journal of Molecular Sciences 23, no. 23 (2022): 14672. http://dx.doi.org/10.3390/ijms232314672.

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Resistance to chemo- and radiotherapy is a common event among cancer patients and a reason why new cancer therapies and therapeutic strategies need to be in continuous investigation and development. DNA damage response (DDR) comprises several pathways that eliminate DNA damage to maintain genomic stability and integrity, but different types of cancers are associated with DDR machinery defects. Many improvements have been made in recent years, providing several drugs and therapeutic strategies for cancer patients, including those targeting the DDR pathways. Currently, poly (ADP-ribose) polymera

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Mora-Rodríguez, José María, Belén G. Sánchez, Alba Sebastián-Martín, et al. "Resistance to 2-Hydroxy-Flutamide in Prostate Cancer Cells Is Associated with the Downregulation of Phosphatidylcholine Biosynthesis and Epigenetic Modifications." International Journal of Molecular Sciences 24, no. 21 (2023): 15626. http://dx.doi.org/10.3390/ijms242115626.

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In this study, we examined the metabolic adaptations of a chemoresistant prostate cancer cell line in comparison to a sensitive cell line. We utilized prostate cancer LNCaP cells and subjected them to a stepwise increase in the antiandrogen 2-hydroxy-flutamide (FLU) concentration to generate a FLU-resistant cell line (LN-FLU). These LN-FLU cells displayed characteristics of cancer stem cells, exhibited drug resistance, and showed a significantly reduced expression of Cyclin D1, along with the overexpression of p16, pointing to a proliferation arrest. In comparing the cancer stem-like LN-FLU ce

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Day, Tanya K., and Tina Bianco-Miotto. "Common gene pathways and families altered by DNA methylation in breast and prostate cancers." Endocrine-Related Cancer 20, no. 5 (2013): R215—R232. http://dx.doi.org/10.1530/erc-13-0204.

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Epigenetic modifications, such as DNA methylation, are widely studied in cancer as they are stable and easy to measure genome wide. DNA methylation changes have been used to differentiate benign from malignant tissue and to predict tumor recurrence or patient outcome. Multiple genome wide DNA methylation studies in breast and prostate cancers have identified genes that are differentially methylated in malignant tissue compared with non-malignant tissue or in association with hormone receptor status or tumor recurrence. Although this has identified potential biomarkers for diagnosis and prognos

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Chinenye Mary Okorochi, Frederick Olusegun Akinbo, Gerald Ikechi Eze, et al. "Genetic Mutations in Prostate Cancer: Insights and Implications." World Journal of Advanced Research and Reviews 26, no. 2 (2025): 3744–54. https://doi.org/10.30574/wjarr.2025.26.2.1928.

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This review article aims to provide a comprehensive overview of genetic mutations and alterations in prostate cancer, highlighting their roles in disease development and progression. The scope of the review encompasses common genetic mutations, such as those in the PTEN and TP53 genes, as well as structural alterations like the TMPRSS2-ERG fusion. It also discusses the impact of these genetic changes on cellular functions, including cell cycle regulation and signaling pathways. Major findings indicate that genetic mutations contribute to the uncontrolled proliferation of prostate cells and inf

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