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Artículos de revistas sobre el tema "Pharmacoepigenetic"

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Autor: Grafiati

Publicado: 1 de abril de 2023

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1

Cacabelos, Ramón. "The PharmacoEpiGenetic Connection". Current Pharmacogenomics and Personalized Medicine 17, n.º 2 (28 de octubre de 2020): 72–75. http://dx.doi.org/10.2174/187569211702200921093217.

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2

Karaglani, Makrina, Georgia Ragia, Maria Panagopoulou, Ioanna Balgkouranidou, Evangelia Nena, George Kolios, Nikolaos Papanas, Vangelis Manolopoulos y Ekaterini Chatzaki. "Search for Pharmacoepigenetic Correlations in Type 2 Diabetes Under Sulfonylurea Treatment". Experimental and Clinical Endocrinology & Diabetes 127, n.º 04 (2 de febrero de 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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3

Yahaya, M. A. F., S. Z. I. Zolkiffly, M. A. M. Moklas, H. Abdul Hamid, J. Stanslas, M. Zainol y M. Z. Mehat. "Possible Epigenetic Role of Vitexin in Regulating Neuroinflammation in Alzheimer’s Disease". Journal of Immunology Research 2020 (10 de marzo de 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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4

Sun, Yan y Robert Davis. "Rapid Collection of Biospecimens by Automated Identification of Patients Eligible for Pharmacoepigenetic Studies". Journal of Personalized Medicine 3, n.º 4 (26 de septiembre de 2013): 263–74. http://dx.doi.org/10.3390/jpm3040263.

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5

Ingelman-Sundberg, Magnus, Sarah C. Sim, Alvin Gomez y Cristina Rodriguez-Antona. "Influence of cytochrome P450 polymorphisms on drug therapies: Pharmacogenetic, pharmacoepigenetic and clinical aspects". Pharmacology & Therapeutics 116, n.º 3 (diciembre de 2007): 496–526. http://dx.doi.org/10.1016/j.pharmthera.2007.09.004.

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6

Gomez, Alvin y Magnus Ingelman-Sundberg. "Pharmacoepigenetic aspects of gene polymorphism on drug therapies: effects of DNA methylation on drug response". Expert Review of Clinical Pharmacology 2, n.º 1 (enero de 2009): 55–65. http://dx.doi.org/10.1586/17512433.2.1.55.

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7

Khatami, Fatemeh, Mohammad R. Mohajeri-Tehrani y 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, n.º 6 (3 de septiembre de 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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8

Cacabelos, Ramón, Juan Carril, Natalia Cacabelos, Aleksey Kazantsev, Alex Vostrov, Lola Corzo, Pablo Cacabelos y Dmitry Goldgaber. "Sirtuins in Alzheimer’s Disease: SIRT2-Related GenoPhenotypes and Implications for PharmacoEpiGenetics". International Journal of Molecular Sciences 20, n.º 5 (12 de marzo de 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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9

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, n.º 3 (10 de agosto de 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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10

Cacabelos, Ramon. "Pharmacogenomics of Cognitive Dysfunction and Neuropsychiatric Disorders in Dementia". International Journal of Molecular Sciences 21, n.º 9 (26 de abril de 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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11

Peedicayil, Jacob. "Pharmacoepigenetics and Pharmacoepigenomics: An Overview". Current Drug Discovery Technologies 16, n.º 4 (11 de diciembre de 2019): 392–99. http://dx.doi.org/10.2174/1570163815666180419154633.

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Background: The rapid and major advances being made in epigenetics are impacting pharmacology, giving rise to new sub-disciplines in pharmacology, pharmacoepigenetics, the study of the epigenetic basis of variation in response to drugs; and pharmacoepigenomics, the application of pharmacoepigenetics on a genome-wide scale. Methods: This article highlights the following aspects of pharmacoepigenetics and pharmacoepigenomics: epigenetic therapy, the role of epigenetics in pharmacokinetics, the relevance of epigenetics to adverse drug reactions, personalized medicine, drug addiction, and drug resistance, and the use of epigenetic biomarkers in drug therapy. Results: Epigenetics is having an increasing impact on several areas of pharmacology. Conclusion: Pharmacoepigenetics and pharmacoepigenomics are new sub-disciplines in pharmacology and are likely to have an increasing impact on the use of drugs in clinical practice.

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12

Swathy, Babu y Moinak Banerjee. "Haloperidol induces pharmacoepigenetic response by modulating miRNA expression, global DNA methylation and expression profiles of methylation maintenance genes and genes involved in neurotransmission in neuronal cells". PLOS ONE 12, n.º 9 (8 de septiembre de 2017): e0184209. http://dx.doi.org/10.1371/journal.pone.0184209.

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13

Peedicayil, Jacob. "Pharmacoepigenetics and pharmacoepigenomics". Pharmacogenomics 9, n.º 12 (diciembre de 2008): 1785–86. http://dx.doi.org/10.2217/14622416.9.12.1785.

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14

Buzinschi, Sorin. "Pharmacogenetics, epigenetics and pharmacoepigenetics". Romanian Journal of Pharmaceutical Practice 13, n.º 2 (30 de junio de 2020): 50–52. http://dx.doi.org/10.37897/rjphp.2020.2.2.

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15

Mateo Leach, Irene, Pim van der Harst y Rudolf A. de Boer. "Pharmacoepigenetics in Heart Failure". Current Heart Failure Reports 7, n.º 2 (21 de abril de 2010): 83–90. http://dx.doi.org/10.1007/s11897-010-0011-y.

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16

Candelaria, M., E. de la Cruz-Hernández, E. Pérez-Cárdenas, C. Trejo-Becerril, O. Gutiérrez-Hernández y A. Dueñas-González. "Pharmacogenetics and pharmacoepigenetics of gemcitabine". Medical Oncology 27, n.º 4 (10 de noviembre de 2009): 1133–43. http://dx.doi.org/10.1007/s12032-009-9349-y.

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17

Esteller, M. "9 Pharmacoepigenetics and epigenetic drugs". European Journal of Cancer Supplements 8, n.º 7 (noviembre de 2010): 13. http://dx.doi.org/10.1016/s1359-6349(10)71712-2.

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18

Majchrzak-Celińska, Aleksandra y Wanda Baer-Dubowska. "Pharmacoepigenetics: an element of personalized therapy?" Expert Opinion on Drug Metabolism & Toxicology 13, n.º 4 (28 de noviembre de 2016): 387–98. http://dx.doi.org/10.1080/17425255.2017.1260546.

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19

Lopomo, Angela y Fabio Coppedè. "Pharmacoepigenetics and pharmacoepigenomics of gastrointestinal cancers". Expert Review of Gastroenterology & Hepatology 12, n.º 1 (11 de septiembre de 2017): 49–62. http://dx.doi.org/10.1080/17474124.2017.1374853.

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20

Hack, Laura M., Gabriel R. Fries, Harris A. Eyre, Chad A. Bousman, Ajeet B. Singh, Joao Quevedo, Vineeth P. John, Bernhard T. Baune y Boadie W. Dunlop. "Moving pharmacoepigenetics tools for depression toward clinical use". Journal of Affective Disorders 249 (abril de 2019): 336–46. http://dx.doi.org/10.1016/j.jad.2019.02.009.

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21

Chu, Shih-Kai y Hsin-Chou Yang. "Interethnic DNA methylation difference and its implications in pharmacoepigenetics". Epigenomics 9, n.º 11 (noviembre de 2017): 1437–54. http://dx.doi.org/10.2217/epi-2017-0046.

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22

Lauschke, Volker M., Isabel Barragan y Magnus Ingelman-Sundberg. "Pharmacoepigenetics and Toxicoepigenetics: Novel Mechanistic Insights and Therapeutic Opportunities". Annual Review of Pharmacology and Toxicology 58, n.º 1 (6 de enero de 2018): 161–85. http://dx.doi.org/10.1146/annurev-pharmtox-010617-053021.

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23

Gomez, A. y M. Ingelman-Sundberg. "Pharmacoepigenetics: Its Role in Interindividual Differences in Drug Response". Clinical Pharmacology & Therapeutics 85, n.º 4 (25 de febrero de 2009): 426–30. http://dx.doi.org/10.1038/clpt.2009.2.

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24

Fornaro, Lorenzo. "Pharmacoepigenetics in gastrointestinal tumors em MGMT em methylation and beyond". Frontiers in Bioscience 8, n.º 1 (2016): 170–80. http://dx.doi.org/10.2741/758.

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25

Fornaro, Lorenzo. "Pharmacoepigenetics in gastrointestinal tumors em MGMT em methylation and beyond". Frontiers in Bioscience 8, n.º 1 (2016): 170–80. http://dx.doi.org/10.2741/e758.

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26

Gutierrez-Camino, Angela, Maitane Umerez, Borja Santos, Idoia Martin-Guerrero, Nagore García de Andoin, Ana Sastre, Aurora Navajas, Itziar Astigarraga y Africa Garcia-Orad. "Pharmacoepigenetics in childhood acute lymphoblastic leukemia: involvement of miRNA polymorphisms in hepatotoxicity". Epigenomics 10, n.º 4 (abril de 2018): 409–17. http://dx.doi.org/10.2217/epi-2017-0138.

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27

Kovács, Erika Rozália, Sára Tóth y Dániel János Erdélyi. "Az etopozid szervezeten belüli eloszlásában és metabolizmusában szerepet játszó epigenetikai hatások". Orvosi Hetilap 159, n.º 32 (agosto de 2018): 1295–302. http://dx.doi.org/10.1556/650.2018.31162.

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Abstract: Etoposide is a topoisomerase II inhibitor antitumor agent which is widely used in the treatment of several hematologic malignancies and solid tumors. The therapeutic index of etoposide is quite high, thus its application causes several short-term and long-term side effects which can decrease the chance to cure patients. Drug dosing is based on body surface area calculation; recommendations for individual dosing do not exist yet. The biotransformation and transportation of etoposide are carried out by enzymes and transporters as reported in pharmacogenomic studies published in this area. Nowadays pharmacoepigenetics research has come to the fore. The authors wish to give an insight into the research of the epigenetical changes of the etoposide pathways, especially focusing on published findings on enzymes and transporters with pharmacokinetic relevance. In the future, epigenetical changes of the etoposide pathway might have a great role in diagnostics, prognostics and personalized medicine. Orv Hetil. 2018; 159(32): 1295–1302.

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28

Domschke, Katharina, Nicola Tidow, Kathrin Schwarte, Christiane Ziegler, Klaus-Peter Lesch, Jürgen Deckert, Volker Arolt, Peter Zwanzger y Bernhard T. Baune. "Pharmacoepigenetics of depression: no major influence of MAO-A DNA methylation on treatment response". Journal of Neural Transmission 122, n.º 1 (10 de mayo de 2014): 99–108. http://dx.doi.org/10.1007/s00702-014-1227-x.

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29

Yu, A. M., Y. Tian, M. J. Tu, P. Y. Ho y J. L. Jilek. "MicroRNA Pharmacoepigenetics: Posttranscriptional Regulation Mechanisms behind Variable Drug Disposition and Strategy to Develop More Effective Therapy". Drug Metabolism and Disposition 44, n.º 3 (13 de noviembre de 2015): 308–19. http://dx.doi.org/10.1124/dmd.115.067470.

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30

Knothe, Claudia, Bruno G. Oertel, Alfred Ultsch, Mattias Kettner, Peter Harald Schmidt, Cora Wunder, Stefan W. Toennes, Gerd Geisslinger y Jörn Lötsch. "Pharmacoepigenetics of the role of DNA methylation in μ-opioid receptor expression in different human brain regions". Epigenomics 8, n.º 12 (diciembre de 2016): 1583–99. http://dx.doi.org/10.2217/epi-2016-0072.

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31

Nasr, Rihab, Fatima Sleiman, Zeinab Awada y Natalie K. Zgheib. "The pharmacoepigenetics of drug metabolism and transport in breast cancer: review of the literature and in silico analysis". Pharmacogenomics 17, n.º 14 (septiembre de 2016): 1573–85. http://dx.doi.org/10.2217/pgs-2016-0081.

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32

Glavaski, Mila y Karmen Stankov. "Epigenetics in disease etiopathogenesis". Genetika 51, n.º 3 (2019): 975–94. http://dx.doi.org/10.2298/gensr1903975g.

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The term epigenetics refers to heritable changes in gene expression that are not caused by modifications in DNA sequence. Epigenetic changes are DNA methylation, histone modifications, nucleosome positioning, and non-coding RNA (including microRNA) mediated modifications. Epigenetic mechanisms are involved in malignant diseases, imprinting defects, and some hereditary diseases. Recent research explained the role of epigenetic disorders in infections, autoimmune, neurodegenerative and bone diseases, as well as in psoriasis, endometriosis, and polycystic ovary syndrome. Epigenetic modifications have a potential clinical application as diagnostic and prognostic biomarkers, and also as therapeutic targets in oncology, endocrinology, cardiology, and neuropsychiatry. Stress, anxiety, depression, emotions and many other psychological factors may affect epigenetic mechanisms. Influence of preconception parental stress exposure transmits to the next generation through epigenetic changes, as direct results of prenatal and postnatal environmental factors. Epigenetic changes identify environmental factors which affect health and cause disease onset. Milk is the sophisticated system of communication between mother and infant, operating via epigenetic mechanisms. Lifelong consumption of bovine milk causes epigenetic disorders. Recent studies provide important information about the role of bioactive dietary nutrients which modify epigenome in malignancy prevention and therapy. Any interruption in the balance of intestinal microbiota initiates aberrant epigenetic modifications. Epigenetic patterns act as the ?molecular watches? and they play the central role in the establishment of biological rhythms. Epigenetic mechanisms can determine the result of assisted reproductive technology and genetic engineering. The extensive research about the association of epigenetics and pharmacology led to the development of pharmacoepigenetics. All these results emphasize the importance of further research which will take into account all factors that may affect epigenetic mechanisms.

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Gojo, Ivana, Jan H. Beumer, Keith Pratz, Jiuping Ji, Lihua Wang, Michelle A. Rudek, Michael A. McDevitt et al. "A Phase 1 Study of the PARP Inhibitor Veliparib in Combination with Temozolomide in Acute Leukemias". Blood 126, n.º 23 (3 de diciembre de 2015): 1361. http://dx.doi.org/10.1182/blood.v126.23.1361.1361.

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Abstract Among mechanisms underlying cytotoxic drug resistance is activation of diverse DNA damage response (DDR) pathways. Poly(ADP-ribose) polymerases (PARP)-1/2 facilitate both single- and double-strand break (DSB) repair and play a key role in the base excision repair (BER) of chemotherapy-damaged DNA. The PARP inhibitor veliparib (V) potentiates the cytotoxicity of different chemotherapeutics, including temozolomide (TEM). TEM induces distinct alkylating events in neoplastic cells whose ultimate outcome depends on the interaction of BER, mismatch repair (MMR), O(6)-methylguanine-DNA methyltransferase (MGMT), and DSB repair. While clinical activity of TEM has been mainly observed in MGMT-deficient AML, V potentiated cytotoxicity of TEM in leukemia cells in vitro in the setting of MGMT overexpression or deficient MMR pathway (Mol Cancer Ther, 2009). Methods: We conducted a Phase I study to determine maximum tolerated dose (MTD) and recommended Phase II dose (RP2D) of V+TEM, using a 3+3 dose escalation. Patients (pts) ≥60 years (yrs) with newly diagnosed poor cytogenetic-risk AML/ALL who were not candidates for intensive therapy, or ≥18 yrs with relapsed/refractory AML/ALL, secondary AML (therapy-related or arising from MDS or MPN), and CMMoL-2 were eligible. Any number of prior regimens, including allogeneic transplant (alloSCT), were allowed. V was given orally day (d)1 once, then twice a day on d4-12 at one of 6 dose levels (DL) (DL1A-B 20mg; DL2-DL3-DL4-DL5-DL6: 40-80-120-150-200 mg). TEM was given orally once a day on d3-9 (DL1A 150 mg/m2/d; DL1B-DL6 200 mg/m2/d). 28-day cycles (cy) were repeated depending on response/tolerability (4-6 weeks delay allowed) with V on d1-8 and TEM d1-5. TEM was taken on empty stomach with antiemetics and V was taken irrespective of meals. Results: Forty-nine pts with median age 69 yrs (range, 22-88; 47% ≥70) were treated. Of 47 AML pts, 29 (62%) had secondary AML and 27 (57%) adverse karyotype. Median number of prior treatments for AML was 1 (range, 0-6): 18 (38%) had median 1 prior therapy (range, 1-3) for MDS; 30 (64%), 9 (18%), 34 (69%) received hypomethylating agents, alloSCT and intensive chemotherapy, respectively. Overall 42 (85%) pts were refractory to their last treatment. Pts received a median of 1 (range, 1-7) cy of therapy. Two did not complete cy 1, pt withdrawal d5 and progressive fungal pneumonia d9 with death d15 of progressive disease (PD). The MTD/RP2D was defined at V 150 mg and TEM 200 mg/m2; 2 of 4 pts treated at V 200 mg and TEM 200 mg/m2 developed dose-limiting toxicity of grade (gr) 3 oral mucositis/esophagitis. The most frequent drug-related toxicities (NCI CTC v4) were gr 1/2 nausea/vomiting (39%), fatigue (26%), oropharyngeal mucositis (26%), constipation (12%), and diarrhea (10%). Other common toxicities were infectious, including febrile neutropenia (29%), pneumonia (20%), bacteremia (18%). One (2%) pt died ≤d30 and 12 (24%) ≤d60 mainly of PD (1 pt fungal pneumonia before count recovery d31). Overall response rate was 33% (complete remission (CR), hematologic improvement (HI)/stable disease) with 8 (16%) pts achieving CR (1 CRi). Median overall survival was 5.03 months, for all responders 11.58 months, and for CR pts 19.89 months (Fig 1). Responses occurred at all DLs. Three CR pts underwent alloSCT; 2 remain in CR at ~3 yrs. Pharmacokinetics (PK): V or TEM PKs were not altered with co-administration. There was a correlation between the DLT of mucositis and V single (Cmax P=0.005; AUC P=0.009) and multiple dose exposure (Cmax P = 0.02; AUC P=0.03). Pharmacodynamics and pharmacoepigenetics: Four of 39 pts examined had MGMT methylation (3 CR; 75%) and 2 had BRCA-1 methylation (1 HI) in peripheral blood (PB) or bone marrow (BM) mononuclear cells (MC). Defective FancD2 pathway was observed in the BMMC of 19/19 pts using FancD2 ubiquitylation assays but did not correlate with response. V reduced PAR levels by >75% in PBMC of most pts and in the presence of TEM. Induction of γ-H2AX in CD34+ cells was seen upon V/V+TEM treatment. Conclusion: V plus TEM demonstrated safety and activity in this resistant and elderly leukemia population. Response rate was higher in MGMT methylated pts, but responses were also seen in pts who had no MGMT methylation, had failed multiple therapies, had secondary AML and/or adverse karyotype. Future clinical study should aim to identify pts with defective DDR pathways who are most likely to respond to this therapeutic approach. Figure 1. Figure 1. Disclosures Off Label Use: Temozolomide is not approved for AML. Beumer:Millenium: Other: Research support. Gore:Celgene: Consultancy, Honoraria, Research Funding.

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Fisher, Virginia A., Lan Wang, Xuan Deng, Chloé Sarnowski, L. Adrienne Cupples y Ching-Ti Liu. "Do changes in DNA methylation mediate or interact with SNP variation? A pharmacoepigenetic analysis". BMC Genetics 19, S1 (septiembre de 2018). http://dx.doi.org/10.1186/s12863-018-0635-6.

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Olstad, Emilie Willoch, Hedvig Marie Egeland Nordeng y Kristina Gervin. "Prenatal medication exposure and epigenetic outcomes: a systematic literature review and recommendations for prenatal pharmacoepigenetic studies". Epigenetics, 29 de abril de 2021, 1–24. http://dx.doi.org/10.1080/15592294.2021.1903376.

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Montoya, Tatiana, María Luisa Castejón, Rocío Muñoz-García y Catalina Alarcón-de-la-Lastra. "Epigenetic linkage of systemic lupus erythematosus and nutrition". Nutrition Research Reviews, 16 de agosto de 2021, 1–59. http://dx.doi.org/10.1017/s0954422421000287.

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Abstract The term “epigenetics” refers to a series of meiotically/mitotically inheritable alterations in gene expression, related to environmental factors, without disruption on DNA sequences of bases. Recently, the pathophysiology of autoimmune diseases (ADs) has been closely linked to epigenetic modifications. Actually, epigenetic mechanisms can modulate gene expression or repression of targeted cells and tissues involved in autoimmune/inflammatory conditions acting as keys effectors in regulation of adaptive and innate responses. ADs, as systemic lupus erythematosus (SLE), a rare disease that still lacks effective treatment, is characterized by epigenetic marks in affected cells. Taking into account that epigenetic mechanisms have been proposed as a winning strategy in the search of new more specific and personalized therapeutics agents. Thus, pharmacology and pharmacoepigenetic studies about epigenetic regulations of ADs may provide novel individualized therapies. Focussing in possible implicated factors on development and predisposition of SLE, diet is feasibly one of the most important factors since it is linked directly to epigenetic alterations and these epigenetic changes may augment or diminish the risk of SLE. Nevertheless, several studies have guaranteed that dietary therapy could be a promise to SLE patients via prophylactic actions deprived of side effects of pharmacology, decreasing co-morbidities and improving lifestyle of SLE sufferers. Herein, we review and discuss the cross-link between epigenetic mechanisms on SLE predisposition and development, as well as the influence of dietary factors on regulation epigenetic modifications that would eventually make a positive impact on SLE patients.

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Zhou, Jiaqi, Miao Li, Xueying Wang, Yuwen He, Yan Xia, John A. Sweeney, Richard F. Kopp, Chunyu Liu y Chao Chen. "Drug Response-Related DNA Methylation Changes in Schizophrenia, Bipolar Disorder, and Major Depressive Disorder". Frontiers in Neuroscience 15 (13 de mayo de 2021). http://dx.doi.org/10.3389/fnins.2021.674273.

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Pharmacotherapy is the most common treatment for schizophrenia (SCZ), bipolar disorder (BD), and major depressive disorder (MDD). Pharmacogenetic studies have achieved results with limited clinical utility. DNA methylation (DNAm), an epigenetic modification, has been proposed to be involved in both the pathology and drug treatment of these disorders. Emerging data indicates that DNAm could be used as a predictor of drug response for psychiatric disorders. In this study, we performed a systematic review to evaluate the reproducibility of published changes of drug response-related DNAm in SCZ, BD and MDD. A total of 37 publications were included. Since the studies involved patients of different treatment stages, we partitioned them into three groups based on their primary focuses: (1) medication-induced DNAm changes (n = 8); (2) the relationship between DNAm and clinical improvement (n = 24); and (3) comparison of DNAm status across different medications (n = 14). We found that only BDNF was consistent with the DNAm changes detected in four independent studies for MDD. It was positively correlated with clinical improvement in MDD. To develop better predictive DNAm factors for drug response, we also discussed future research strategies, including experimental, analytical procedures and statistical criteria. Our review shows promising possibilities for using BDNF DNAm as a predictor of antidepressant treatment response for MDD, while more pharmacoepigenetic studies are needed for treatments of various diseases. Future research should take advantage of a system-wide analysis with a strict and standard analytical procedure.

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Ling, Charlotte. "Pharmacoepigenetics in type 2 diabetes: is it clinically relevant?" Diabetologia, 21 de marzo de 2022. http://dx.doi.org/10.1007/s00125-022-05681-x.

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AbstractData generated over nearly two decades clearly demonstrate the importance of epigenetic modifications and mechanisms in the pathogenesis of type 2 diabetes. However, the role of pharmacoepigenetics in type 2 diabetes is less well established. The field of pharmacoepigenetics covers epigenetic biomarkers that predict response to therapy, therapy-induced epigenetic alterations as well as epigenetic therapies including inhibitors of epigenetic enzymes. Not all individuals with type 2 diabetes respond to glucose-lowering therapies in the same way, and there is therefore a need for clinically useful biomarkers that discriminate responders from non-responders. Blood-based epigenetic biomarkers may be useful for this purpose. There is also a need for a better understanding of whether existing glucose-lowering therapies exert their function partly through therapy-induced epigenetic alterations. Finally, epigenetic enzymes may be drug targets for type 2 diabetes. Here, I discuss whether pharmacoepigenetics is clinically relevant for type 2 diabetes based on studies addressing this topic.

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Smith, Delaney A., Marie C. Sadler y Russ B. Altman. "Promises and Challenges in Pharmacoepigenetics". Cambridge Prisms: Precision Medicine, 9 de febrero de 2023, 1–24. http://dx.doi.org/10.1017/pcm.2023.6.

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Saiyed, Atiyabanu N., Abhay R. Vasavada y S. R. Kaid Johar. "Recent trends in miRNA therapeutics and the application of plant miRNA for prevention and treatment of human diseases". Future Journal of Pharmaceutical Sciences 8, n.º 1 (1 de abril de 2022). http://dx.doi.org/10.1186/s43094-022-00413-9.

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Abstract Background Researchers now have a new avenue to investigate when it comes to miRNA-based therapeutics. miRNAs have the potential to be valuable biomarkers for disease detection. Variations in miRNA levels may be able to predict changes in normal physiological processes. At the epigenetic level, miRNA has been identified as a promising candidate for distinguishing and treating various diseases and defects. Main body In recent pharmacology, plants miRNA-based drugs have demonstrated a potential role in drug therapeutics. The purpose of this review paper is to discuss miRNA-based therapeutics, the role of miRNA in pharmacoepigenetics modulations, plant miRNA inter-kingdom regulation, and the therapeutic value and application of plant miRNA for cross-kingdom approaches. Target prediction and complementarity with host genes, as well as cross-kingdom gene interactions with plant miRNAs, are also revealed by bioinformatics research. We also show how plant miRNA can be transmitted from one species to another by crossing kingdom boundaries in this review. Despite several unidentified barriers to plant miRNA cross-transfer, plant miRNA-based gene regulation in trans-kingdom gene regulation may soon be valued as a possible approach in plant-based drug therapeutics. Conclusion This review summarised the biochemical synthesis of miRNAs, pharmacoepigenetics, drug therapeutics and miRNA transkingdom transfer.

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Imani, Saber, Matteo Becatti y Md Asaduzzaman Khan. "Editorial: Molecular Targeted Therapy in Oncology: Lessons From Pharmacogenetics and Pharmacoepigenetics". Frontiers in Molecular Biosciences 9 (15 de marzo de 2022). http://dx.doi.org/10.3389/fmolb.2022.822188.

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"Pharmacoepigenetics explores the epigenetic contribution to anti-cancer agent-induced cytotoxicities". Stem Cell Epigenetics, 2 de mayo de 2015. http://dx.doi.org/10.14800/sce.359.

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Nuotio, Marja-Liisa, Heini Sánez Tähtisalo, Alexandra Lahtinen, Kati Donner, Frej Fyhrquist, Markus Perola, Kimmo K. Kontula y Timo P. Hiltunen. "Pharmacoepigenetics of hypertension: genome-wide methylation analysis of responsiveness to four classes of antihypertensive drugs using a double-blind crossover study design". Epigenetics, 25 de febrero de 2022, 1–14. http://dx.doi.org/10.1080/15592294.2022.2038418.

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