Relevant bibliographies by topics / Pharmacoepigenetic

Academic literature on the topic 'Pharmacoepigenetic'

Author: Grafiati
Published: 1 April 2023

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Journal articles on the topic "Pharmacoepigenetic"

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Cacabelos, Ramón. "The PharmacoEpiGenetic Connection." Current Pharmacogenomics and Personalized Medicine 17, no. 2 (October 28, 2020): 72–75. http://dx.doi.org/10.2174/187569211702200921093217.

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Karaglani, Makrina, Georgia Ragia, Maria Panagopoulou, Ioanna Balgkouranidou, Evangelia Nena, George Kolios, Nikolaos Papanas, Vangelis Manolopoulos, and Ekaterini Chatzaki. "Search for Pharmacoepigenetic Correlations in Type 2 Diabetes Under Sulfonylurea Treatment." Experimental and Clinical Endocrinology & Diabetes 127, no. 04 (February 2, 2018): 226–33. http://dx.doi.org/10.1055/s-0043-121265.

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AbstractSulfonylureas are insulin secretagogues which act in pancreatic β cells by blocking the KATP channels encoded by KCNJ11 and ABCC8 genes. In the present study, a pharmacoepigenetic approach was applied for the first time, investigating the correlation of KCNJ11 and ABCC8 gene promoter methylation with sulfonylureas-induced mild hypoglycemic events as well as the KCNJ11 E23K genotype. Sodium bisulfite-treated genomic DNA of 171 sulfonylureas treated T2DM patients previously genotyped for KCNJ11 E23K, including 88 that had experienced drug-associated hypoglycemia and 83 that had never experienced hypoglycemia, were analyzed for DNA methylation of KCNJ11 and ABCC8 gene promoters via quantitative Methylation-Specific PCR. KCNJ11 methylation was detected in 19/88 (21.6%) of hypoglycemic and in 23/83 (27.7%) of non-hypoglycemic patients (p=0.353), while ABCC8 methylation in 6/83 (7.2%) of non-hypoglycemic and none (0/88) of the hypoglycemic patients (p=0.012). Methylation in at least one promoter (KCNJ11 or ABCC8) was significantly associated with non-hypoglycemic patients who are carriers of KCNJ11 EK allele (p=0.030). Our data suggest that ABCC8 but not KCNJ11 methylation is associated to hypoglycemic events in sulfonylureas-treated T2DM patients. Furthermore, it is demonstrated that the KCNJ11 E23K polymorphism in association to either of the two genes’ DNA methylation may have protective role against sulfonylurea-induced hypoglycemia.
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Yahaya, M. A. F., S. Z. I. Zolkiffly, M. A. M. Moklas, H. Abdul Hamid, J. Stanslas, M. Zainol, and M. Z. Mehat. "Possible Epigenetic Role of Vitexin in Regulating Neuroinflammation in Alzheimer’s Disease." Journal of Immunology Research 2020 (March 10, 2020): 1–7. http://dx.doi.org/10.1155/2020/9469210.

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Alzheimer’s disease (AD) has been clinically characterized by a progressive degeneration of neurons which resulted in a gradual and irreversible cognitive impairment. The accumulation of Aβ and τ proteins in the brain contribute to the severity of the disease. Recently, vitexin compound has been the talk amongst researchers due to its pharmacological properties as anti-inflammation and anti-AD. However, the epigenetic mechanism of the compound in regulating the neuroinflammation activity is yet to be fully elucidated. Hence, this review discusses the potential of vitexin compound to have the pharmacoepigenetic property in regulating the neuroinflammation activity in relation to AD. It is with hope that the review would unveil the potential of vitexin as the candidate in treating AD.
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Sun, Yan, and Robert Davis. "Rapid Collection of Biospecimens by Automated Identification of Patients Eligible for Pharmacoepigenetic Studies." Journal of Personalized Medicine 3, no. 4 (September 26, 2013): 263–74. http://dx.doi.org/10.3390/jpm3040263.

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Ingelman-Sundberg, Magnus, Sarah C. Sim, Alvin Gomez, and Cristina Rodriguez-Antona. "Influence of cytochrome P450 polymorphisms on drug therapies: Pharmacogenetic, pharmacoepigenetic and clinical aspects." Pharmacology & Therapeutics 116, no. 3 (December 2007): 496–526. http://dx.doi.org/10.1016/j.pharmthera.2007.09.004.

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Gomez, Alvin, and Magnus Ingelman-Sundberg. "Pharmacoepigenetic aspects of gene polymorphism on drug therapies: effects of DNA methylation on drug response." Expert Review of Clinical Pharmacology 2, no. 1 (January 2009): 55–65. http://dx.doi.org/10.1586/17512433.2.1.55.

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Khatami, Fatemeh, Mohammad R. Mohajeri-Tehrani, and Seyed M. Tavangar. "The Importance of Precision Medicine in Type 2 Diabetes Mellitus (T2DM): From Pharmacogenetic and Pharmacoepigenetic Aspects." Endocrine, Metabolic & Immune Disorders - Drug Targets 19, no. 6 (September 3, 2019): 719–31. http://dx.doi.org/10.2174/1871530319666190228102212.

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Background:Type 2 Diabetes Mellitus (T2DM) is a worldwide disorder as the most important challenges of health-care systems. Controlling the normal glycaemia greatly profit long-term prognosis and gives explanation for early, effective, constant, and safe intervention.Materials and Methods:Finding the main genetic and epigenetic profile of T2DM and the exact molecular targets of T2DM medications can shed light on its personalized management. The comprehensive information of T2DM was earned through the genome-wide association study (GWAS) studies. In the current review, we represent the most important candidate genes of T2DM like CAPN10, TCF7L2, PPAR-γ, IRSs, KCNJ11, WFS1, and HNF homeoboxes. Different genetic variations of a candidate gene can predict the efficacy of T2DM personalized strategy medication.Results:SLCs and AMPK variations are considered for metformin, CYP2C9, KATP channel, CDKAL1, CDKN2A/2B and KCNQ1 for sulphonylureas, OATP1B, and KCNQ1 for repaglinide and the last but not the least ADIPOQ, PPAR-γ, SLC, CYP2C8, and SLCO1B1 for thiazolidinediones response prediction.Conclusion:Taken everything into consideration, there is an extreme need to determine the genetic status of T2DM patients in some known genetic region before planning the medication strategies.
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Cacabelos, Ramón, Juan Carril, Natalia Cacabelos, Aleksey Kazantsev, Alex Vostrov, Lola Corzo, Pablo Cacabelos, and Dmitry Goldgaber. "Sirtuins in Alzheimer’s Disease: SIRT2-Related GenoPhenotypes and Implications for PharmacoEpiGenetics." International Journal of Molecular Sciences 20, no. 5 (March 12, 2019): 1249. http://dx.doi.org/10.3390/ijms20051249.

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Sirtuins (SIRT1-7) are NAD+-dependent protein deacetylases/ADP ribosyltransferases with important roles in chromatin silencing, cell cycle regulation, cellular differentiation, cellular stress response, metabolism and aging. Sirtuins are components of the epigenetic machinery, which is disturbed in Alzheimer’s disease (AD), contributing to AD pathogenesis. There is an association between the SIRT2-C/T genotype (rs10410544) (50.92%) and AD susceptibility in the APOEε4-negative population (SIRT2-C/C, 34.72%; SIRT2-T/T 14.36%). The integration of SIRT2 and APOE variants in bigenic clusters yields 18 haplotypes. The 5 most frequent bigenic genotypes in AD are 33CT (27.81%), 33CC (21.36%), 34CT (15.29%), 34CC (9.76%) and 33TT (7.18%). There is an accumulation of APOE-3/4 and APOE-4/4 carriers in SIRT2-T/T > SIRT2-C/T > SIRT2-C/C carriers, and also of SIRT2-T/T and SIRT2-C/T carriers in patients who harbor the APOE-4/4 genotype. SIRT2 variants influence biochemical, hematological, metabolic and cardiovascular phenotypes, and modestly affect the pharmacoepigenetic outcome in AD. SIRT2-C/T carriers are the best responders, SIRT2-T/T carriers show an intermediate pattern, and SIRT2-C/C carriers are the worst responders to a multifactorial treatment. In APOE-SIRT2 bigenic clusters, 33CC carriers respond better than 33TT and 34CT carriers, whereas 24CC and 44CC carriers behave as the worst responders. CYP2D6 extensive metabolizers (EM) are the best responders, poor metabolizers (PM) are the worst responders, and ultra-rapid metabolizers (UM) tend to be better responders that intermediate metabolizers (IM). In association with CYP2D6 genophenotypes, SIRT2-C/T-EMs are the best responders. Some Sirtuin modulators might be potential candidates for AD treatment.
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Lucafò, Marianna, Daria Sicari, Andrea Chicco, Debora Curci, Arianna Bellazzo, Alessia Di Silvestre, Chiara Pegolo, et al. "miR-331-3p is involved in glucocorticoid resistance reversion by rapamycin through suppression of the MAPK signaling pathway." Cancer Chemotherapy and Pharmacology 86, no. 3 (August 10, 2020): 361–74. http://dx.doi.org/10.1007/s00280-020-04122-z.

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Abstract Glucocorticoids (GCs) are commonly used as therapeutic agents for immune-mediated diseases and leukemia. However, considerable inter-individual differences in efficacy have been reported. Several reports indicate that the inhibitor of mTOR rapamycin can reverse GC resistance, but the molecular mechanism involved in this synergistic effect has not been fully defined. In this context, we explored the differential miRNA expression in a GC-resistant CCRF-CEM cell line after treatment with rapamycin alone or in co-treatment with methylprednisolone (MP). The expression analysis identified 70, 99 and 96 miRNAs that were differentially expressed after treatment with MP, rapamycin and their combination compared to non-treated controls, respectively. Two pathways were exclusively altered as a result of the co-treatment: the MAPK and ErbB pathways. We validated the only miRNA upregulated specifically by the co-treatment associated with the MAPK signaling, miR-331-3p. Looking for miR-331-3p targets, MAP2K7, an essential component of the JNK/MAPK pathway, was identified. Interestingly, MAP2K7 expression was downregulated during the co-treatment, causing a decrease in terms of JNK activity. miR-331-3p in mimic-transfected cells led to a significant decrease in MAP2K7 levels and promoted the reversion of GC resistance in vitro. Interestingly, miR-331-3p expression was also associated with GC-resistance in patient leukemia cells taken at diagnosis. The combination of rapamycin with MP restores GC effectiveness through the regulation of different miRNAs, suggesting the important role of these pharmacoepigenetic factors in GC response.
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Cacabelos, Ramon. "Pharmacogenomics of Cognitive Dysfunction and Neuropsychiatric Disorders in Dementia." International Journal of Molecular Sciences 21, no. 9 (April 26, 2020): 3059. http://dx.doi.org/10.3390/ijms21093059.

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Symptomatic interventions for patients with dementia involve anti-dementia drugs to improve cognition, psychotropic drugs for the treatment of behavioral disorders (BDs), and different categories of drugs for concomitant disorders. Demented patients may take >6–10 drugs/day with the consequent risk for drug–drug interactions and adverse drug reactions (ADRs >80%) which accelerate cognitive decline. The pharmacoepigenetic machinery is integrated by pathogenic, mechanistic, metabolic, transporter, and pleiotropic genes redundantly and promiscuously regulated by epigenetic mechanisms. CYP2D6, CYP2C9, CYP2C19, and CYP3A4/5 geno-phenotypes are involved in the metabolism of over 90% of drugs currently used in patients with dementia, and only 20% of the population is an extensive metabolizer for this tetragenic cluster. ADRs associated with anti-dementia drugs, antipsychotics, antidepressants, anxiolytics, hypnotics, sedatives, and antiepileptic drugs can be minimized by means of pharmacogenetic screening prior to treatment. These drugs are substrates, inhibitors, or inducers of 58, 37, and 42 enzyme/protein gene products, respectively, and are transported by 40 different protein transporters. APOE is the reference gene in most pharmacogenetic studies. APOE-3 carriers are the best responders and APOE-4 carriers are the worst responders; likewise, CYP2D6-normal metabolizers are the best responders and CYP2D6-poor metabolizers are the worst responders. The incorporation of pharmacogenomic strategies for a personalized treatment in dementia is an effective option to optimize limited therapeutic resources and to reduce unwanted side-effects.
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Dissertations / Theses on the topic "Pharmacoepigenetic"

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Chu, Shih-Kai, and 朱是鍇. "Interethnic DNA Methylation Difference and its Implications in Pharmacoepigenetics." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/4t2br8.

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博士
國立陽明大學
生物醫學資訊研究所
106
Using DNA methylation variants for evaluating the drug response and absorption, distribution, metabolism, and excretion (ADME) represents a crucial application in pharmacoepigenetics. However, the influence of the interethnic DNA methylation difference on the application in pharmacoepigenetics has not been studied systematically. In this dissertation, we analyzed the whole DNA methylome and RNA transcriptome data of primary tumor tissues of four cancer types (breast, colon, head and neck, and uterine corpus) from The Cancer Genome Atlas and lymphoblastoid cell lines from the International HapMap Project for African and European ancestry populations. The methylation data were generated by the Infinium HumanMethylation450 BeadChip and the gene expression data by RNA sequencing experiments. After data quality control, regression analyses with batch effect and covariate adjustments identified 307–20,287 ethnicity-associated CpG sites (E-CpGs) in the five datasets. E-CpG sites exhibited similar methylation patterns in the two studied populations; however, the patterns differed between tumor tissues and lymphoblastoid cell lines. E-CpG sites showed tumor-specific patterns of methylation and gene regulation. In addition, we observed that 264 E-CpG sites were associated with the drug response and ADME. For example, cg16919093 on BRCA1 and cg1055436 on FOXL2 were associated with the drug response to breast cancer chemotherapy; cg23283614 on DHRS7 and cg01878807 on DHRS4 were associated Phase I metabolism. We also identified E-CpG sites that triggered gene expression and influenced drug ADME. For example, the interethnic methylation difference for cg27560818 on SLC7A5 partially explained the poorer response to tamoxifen therapy in breast cancer patients with African ancestry than that in breast cancer patients with European ancestry. We also found that a small number of CpG sites exerted both ethnicity and methylation age effects on the drug response. In conclusion, we provide evidence about the influence of interethnic differences in DNA methylation on differential gene regulation and pharmacoepigenetics by tissue types. Ethnicity and tissue types should be carefully accounted for in future clinical practices and pharmacoepigenetics research.
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Books on the topic "Pharmacoepigenetic"

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Pharmacoepigenetics. Elsevier, 2019. http://dx.doi.org/10.1016/c2017-0-00603-1.

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Cacabelos, Ramón. Pharmacoepigenetics. Elsevier Science & Technology, 2019.

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Cacabelos, Ramón. Pharmacoepigenetics. Elsevier Science & Technology Books, 2019.

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Cacabelos, Ramón. Pharmacoepigenetics. Elsevier Science & Technology Books, 2024.

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Imani, Saber, Matteo Becatti, and Md Asaduzzaman Khan, eds. Molecular Targeted Therapy in Oncology: Lessons from Pharmacogenetics and Pharmacoepigenetics. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-855-6.

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Book chapters on the topic "Pharmacoepigenetic"

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Zeitoun, R., E. Abou Diwan, R. Nasr, and N. K. Zgheib. "Pharmacoepigenetic Considerations for the Treatment of Breast Cancer." In Pharmacoepigenetics, 531–39. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-813939-4.00015-2.

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Cacabelos, Ramón, Juan C. Carril, Ana Sanmartín, and Pablo Cacabelos. "Pharmacoepigenetic Processors: Epigenetic Drugs, Drug Resistance, Toxicoepigenetics, and Nutriepigenetics." In Pharmacoepigenetics, 191–424. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-813939-4.00006-1.

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Flanagan, James, and Arturas Petronis. "Pharmacoepigenetics." In Drugs and the Pharmaceutical Sciences, 461–91. CRC Press, 2005. http://dx.doi.org/10.1201/9780849359507.ch20.

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Cacabelos, Ramón, Iván Tellado, and Pablo Cacabelos. "The Epigenetic Machinery in the Life Cycle and Pharmacoepigenetics." In Pharmacoepigenetics, 1–100. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-813939-4.00001-2.

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Majchrzak-Celińska, Aleksandra, and Wanda Baer-Dubowska. "Pharmacoepigenetics: Basic Principles for Personalized Medicine." In Pharmacoepigenetics, 101–12. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-813939-4.00002-4.

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Teijido, Oscar. "Epigenetic Mechanisms in the Regulation of Drug Metabolism and Transport." In Pharmacoepigenetics, 113–28. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-813939-4.00003-6.

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Li, Dongying, William H. Tolleson, Dianke Yu, Si Chen, Lei Guo, Wenming Xiao, Weida Tong, and Baitang Ning. "MicroRNA-Dependent Gene Regulation of the Human Cytochrome P450." In Pharmacoepigenetics, 129–38. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-813939-4.00004-8.

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Cacabelos, Ramón. "Pathoepigenetics: The Role of Epigenetic Biomarkers in Disease Pathogenesis." In Pharmacoepigenetics, 139–89. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-813939-4.00005-x.

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Daifuku, Richard. "Pharmacoepigenetics of Novel Nucleoside DNA Methyltransferase Inhibitors." In Pharmacoepigenetics, 425–35. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-813939-4.00007-3.

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Vilwanathan, Ravikumar, Anusha Chidambaram, and Ramesh Kumar Chidambaram. "Pharmacoepigenetics: Novel Mechanistic Insights in Drug Discovery and Development Targeting Chromatin-Modifying Enzymes." In Pharmacoepigenetics, 437–45. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-813939-4.00008-5.

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Conference papers on the topic "Pharmacoepigenetic"

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Lopez-Lopez, Elixabet, Idoia Martin-Guerrero, Javier Ballesteros, Javier Uriz, Nagore Garcia de Andoin, M. Angeles Piñan, Pura Garcia-Miguel, Aurora Navajas, and Africa Garcia-Orad. "Abstract B31: Pharmacogenetics and pharmacoepigenetics of childhood acute lymphoblastic leukemia." In Abstracts: AACR International Conference on Translational Cancer Medicine--; Mar 21–24, 2010; Amsterdam, The Netherlands. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1078-0432.tcme10-b31.

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