Improved Cloning Efficiency by Chemically Induced Metabolic Reprogramming of Donor Cells Used for Porcine Somatic Cell Nuclear Transfer
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Histone Deacetylase Inhibitors: an Attractive Therapeutic Strategy Against Breast Cancer
ANTICANCER RESEARCH 37 : 35-46 (2017) doi:10.21873/anticanres.11286 Review Histone Deacetylase Inhibitors: An Attractive Therapeutic Strategy Against Breast Cancer CHRISTOS DAMASKOS 1,2* , SERENA VALSAMI 3* , MICHAEL KONTOS 4* , ELEFTHERIOS SPARTALIS 2, THEODOROS KALAMPOKAS 5, EMMANOUIL KALAMPOKAS 6, ANTONIOS ATHANASIOU 4, DEMETRIOS MORIS 7, AFRODITE DASKALOPOULOU 2,8 , SPYRIDON DAVAKIS 4, GERASIMOS TSOUROUFLIS 1, KONSTANTINOS KONTZOGLOU 1, DESPINA PERREA 2, NIKOLAOS NIKITEAS 2 and DIMITRIOS DIMITROULIS 1 1Second Department of Propedeutic Surgery, 4First Department of Surgery, Laiko General Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece; 2N.S. Christeas Laboratory of Experimental Surgery and Surgical Research, Medical School, National and Kapodistrian University of Athens, Athens, Greece; 3Blood Transfusion Department, Aretaieion Hospital, Medical School, National and Kapodistrian Athens University, Athens, Greece; 5Assisted Conception Unit, Second Department of Obstetrics and Gynecology, Aretaieion Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece; 6Gynaecological Oncology Department, University of Aberdeen, Aberdeen, U.K.; 7Lerner Research Institute, Cleveland Clinic, Cleveland, OH, U.S.A; 8School of Biology, National and Kapodistrian University of Athens, Athens, Greece Abstract. With a lifetime risk estimated to be one in eight in anticipate further clinical benefits of this new class of drugs, industrialized countries, breast cancer is the most frequent -
Epigenetic Reprogramming of Tumor-Associated Fibroblasts in Lung Cancer: Therapeutic Opportunities
cancers Review Epigenetic Reprogramming of Tumor-Associated Fibroblasts in Lung Cancer: Therapeutic Opportunities Jordi Alcaraz 1,2,3,*, Rafael Ikemori 1 , Alejandro Llorente 1 , Natalia Díaz-Valdivia 1 , Noemí Reguart 2,4 and Miguel Vizoso 5,* 1 Unit of Biophysics and Bioengineering, Department of Biomedicine, School of Medicine and Health Sciences, Universitat de Barcelona, 08036 Barcelona, Spain; [email protected] (R.I.); [email protected] (A.L.); [email protected] (N.D.-V.) 2 Thoracic Oncology Unit, Hospital Clinic Barcelona, 08036 Barcelona, Spain; [email protected] 3 Institute for Bioengineering of Catalonia (IBEC), The Barcelona Institute for Science and Technology (BIST), 08028 Barcelona, Spain 4 Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), 08036 Barcelona, Spain 5 Division of Molecular Pathology, Oncode Institute, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands * Correspondence: [email protected] (J.A.); [email protected] (M.V.) Simple Summary: Lung cancer is the leading cause of cancer death among both men and women, partly due to limited therapy responses. New avenues of knowledge are indicating that lung cancer cells do not form a tumor in isolation but rather obtain essential support from their surrounding host tissue rich in altered fibroblasts. Notably, there is growing evidence that tumor progression and even the current limited responses to therapies could be prevented by rescuing the normal behavior of fibroblasts, which are critical housekeepers of normal tissue function. For this purpose, it is key Citation: Alcaraz, J.; Ikemori, R.; to improve our understanding of the molecular mechanisms driving the pathologic alterations of Llorente, A.; Díaz-Valdivia, N.; fibroblasts in cancer. -
Genome-Wide Meta-Analysis of Common Variant Differences Between Men and Women
Human Molecular Genetics, 2012, Vol. 21, No. 21 4805–4815 doi:10.1093/hmg/dds304 Advance Access published on July 27, 2012 Genome-wide meta-analysis of common variant differences between men and women Vesna Boraska1,2,∗, Ana Jeroncˇic´ 3, Vincenza Colonna1,5, Lorraine Southam1, Dale R. Nyholt 6, Nigel William Rayner1,7,8, John R.B. Perry7,9,10, Daniela Toniolo11, Eva Albrecht12, Wei Ang13, StefaniaBandinelli14, MajaBarbalic15, IneˆsBarroso1,16, Jacques S.Beckmann18,19, ReinerBiffar20, Dorret Boomsma22, Harry Campbell23, Tanguy Corre11, Jeanette Erdmann24,25,To˜ nu Esko27,28,29, Krista Fischer27, Nora Franceschini30, Timothy M. Frayling9, Giorgia Girotto31, Juan R. Gonzalez32,33, Tamara B. Harris34, Andrew C. Heath35, Iris M. Heid36,37, Wolfgang Hoffmann21, Albert Hofman38,40, Momoko Horikoshi7,8, Jing Hua Zhao17, Anne U. Jackson41,42, Jouke-Jan Hottenga22, Antti Jula43, Mika Ka¨ho¨ nen44,46, Kay-Tee Khaw47, Lambertus A. Kiemeney48, Norman Klopp52, Zolta´n Kutalik18,54, Vasiliki Lagou7,8, Downloaded from Lenore J.Launer34, TerhoLehtima¨ki45,46, Mathieu Lemire55, Marja-LiisaLokki56, Christina Loley26, Jian’an Luan17, Massimo Mangino10, Irene Mateo Leach58, Sarah E. Medland6, Evelin Mihailov28, Grant W. Montgomery6, Gerjan Navis59, John Newnham13, Markku S. Nieminen61, Aarno Palotie1,57,62,63, Kalliope Panoutsopoulou1, Annette Peters53, Nicola Pirastu31, http://hmg.oxfordjournals.org/ Ozren Polasˇek4, Karola Rehnstro¨ m1,57, Samuli Ripatti57, Graham R.S. Ritchie1,64, Fernando Rivadeneira38,39,40, Antonietta Robino31, Nilesh J. Samani65, So-Youn Shin1, Juha Sinisalo61, Johannes H. Smit66, Nicole Soranzo1,10, Lisette Stolk39,40, Dorine W. Swinkels49, Toshiko Tanaka68, Alexander Teumer69, Anke To¨ njes70,71, Michela Traglia11, Jaakko Tuomilehto72,73,74,75, Armand Valsesia18,54,76, Wiek H. -
Mechanisms and Clinical Significance of Histone Deacetylase Inhibitors: Epigenetic Glioblastoma Therapy
ANTICANCER RESEARCH 35: 615-626 (2015) Review Mechanisms and Clinical Significance of Histone Deacetylase Inhibitors: Epigenetic Glioblastoma Therapy PHILIP LEE1*, BEN MURPHY1*, RICKEY MILLER1*, VIVEK MENON1*, NAREN L. BANIK1,2, PIERRE GIGLIO1,3, SCOTT M. LINDHORST1, ABHAY K. VARMA1, WILLIAM A. VANDERGRIFT III1, SUNIL J. PATEL1 and ARABINDA DAS1 1Department of Neurology and Neurosurgery & MUSC Brain & Spine Tumor Program Medical University of South Carolina, Charleston, SC, U.S.A.; 2Ralph H. Johnson VA Medical Center, Charleston, SC, U.S.A.; 3Department of Neurological Surgery Ohio State University Wexner Medical College, Columbus, OH, U.S.A. Abstract. Glioblastoma is the most common and deadliest glioblastoma therapy, explain the mechanisms of therapeutic of malignant primary brain tumors (Grade IV astrocytoma) effects as demonstrated by pre-clinical and clinical studies in adults. Current standard treatments have been improving and describe the current status of development of these drugs but patient prognosis still remains unacceptably devastating. as they pertain to glioblastoma therapy. Glioblastoma recurrence is linked to epigenetic mechanisms and cellular pathways. Thus, greater knowledge of the Glioblastoma (GBM) is the most common malignant adult cellular, genetic and epigenetic origin of glioblastoma is the brain tumor. Standard-of-care treatment includes surgery, key for advancing glioblastoma treatment. One rapidly radiation and temozolomide; however, this still yields poor growing field of treatment, epigenetic modifiers; histone prognosis for patients (1). Targeting of key epigenetic deacetylase inhibitors (HDACis), has now shown much enzymes, oncogenes and pathways specific to glioblastoma promise for improving patient outcomes through regulation cells by the drugs is very challenging, which has therefore of the acetylation states of histone proteins (a form of resulted in low potency in clinical trials (2). -
Direct Amidation to Access 3-Amido-1,8-Naphthalimides Including Fluorescent Scriptaid Analogues As HDAC Inhibitors
cells Article Direct Amidation to Access 3-Amido-1,8-Naphthalimides Including Fluorescent Scriptaid Analogues as HDAC Inhibitors Kyle N. Hearn 1,2, Trent D. Ashton 1,3,4 , Rameshwor Acharya 5, Zikai Feng 5 , Nuri Gueven 5 and Frederick M. Pfeffer 1,* 1 School of Life and Environmental Sciences, Deakin University, Waurn Ponds, VIC 3216, Australia 2 STEM College, RMIT University, Melbourne, VIC 3000, Australia; [email protected] 3 Walter and Eliza Hall Institute of Medical Research, Parkville, VIC 3052, Australia; [email protected] 4 Department of Medical Biology, The University of Melbourne, Parkville, VIC 3010, Australia 5 School of Pharmacy and Pharmacology, College of Health and Medicine, University of Tasmania, Hobart, TAS 7001, Australia; [email protected] (R.A.); [email protected] (Z.F.); [email protected] (N.G.) * Correspondence: [email protected] Abstract: Methodology to access fluorescent 3-amido-1,8-naphthalimides using direct Buchwald– Hartwig amidation is described. The protocol was successfully used to couple a number of substrates (including an alkylamide, an arylamide, a lactam and a carbamate) to 3-bromo-1,8-naphthalimide in good yield. To further exemplify the approach, a set of scriptaid analogues with amide substituents at the 3-position were prepared. The new compounds were more potent than scriptaid at a number of histone deacetylase (HDAC) isoforms including HDAC6. Activity was further confirmed in a whole cell tubulin deacetylation assay where the inhibitors were more active than the established Citation: Hearn, K.N.; Ashton, T.D.; HDAC6 selective inhibitor Tubastatin. -
Letters to the Editor SHOX Point Mutations in Dyschondrosteosis
J Med Genet 2001;38:323–351 323 Letters to the Editor J Med Genet: first published as 10.1136/jmg.38.5.323 on 1 May 2001. Downloaded from SHOX point mutations in dyschondrosteosis Céline Huber, Veronica Cusin, Martine Le Merrer, Michèle Mathieu, Véronique Sulmont, Nathalie Dagoneau, Arnold Munnich, Valérie Cormier-Daire Dyschondrosteosis (DCS) has been recently Table 2 SHOX point mutations identified in DCS patients ascribed to mutations of the SHOX gene on the pseudoautosomal region of the X and Y chro- Sequence change Exon Protein eVect mosomes.12 Most cases are accounted for by Family 4 106–107 del CG 2 77X large scale deletions3–7 and only two point Family 5 334 C→T 3 Q112X Family 6 445 G→T 3 E149X mutations have been hitherto identified in exon Family 7 481 ins GT 3 181X 4 (R195 X and Y199X12). Here, we show that Family 8 517 C→T 4 R173C point mutations in various regions of the 1 SHOX gene also play an important role in the one nonsense mutation ). Studying eight addi- pathogenesis of the disease. tional DCS families, we describe here three A total of 22 aVected subjects belonging to deletions and five point mutations of SHOX. Taken together, these data suggest that SHOX eight families were included in the study. deletion is the most frequent common disease Inclusion criteria for aVected status were short causing mechanism in DCS (10/16, 62.5%) stature (2 SD below normal) with short and that point mutations also account for a sig- forelimbs and distal radioulnar deformity on nificant fraction of our patients (6/16, 37.5%). -
Histone Deacetylase Inhibitors for the Treatment of Myelodysplastic Syndrome and Acute Myeloid Leukemia
Leukemia (2011) 25, 226–235 & 2011 Macmillan Publishers Limited All rights reserved 0887-6924/11 www.nature.com/leu REVIEW Histone deacetylase inhibitors for the treatment of myelodysplastic syndrome and acute myeloid leukemia A Quinta´s-Cardama1,3, FPS Santos1,2,3 and G Garcia-Manero1 1Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA and 2Hematology Department, Hospital Israelita Albert Einstein, Sa˜o Paulo, Brazil Epigenetic changes have been identified in recent years as drugs whose mechanism of action has been linked to modula- important factors in the pathogenesis of myelodysplastic tion of gene transcription have taken center stage of both syndrome (MDS) and acute myeloid leukemia (AML). Histone clinical and preclinical research in AML and MDS.8 deacetylase inhibitors (HDACIs) regulate the acetylation of histones as well as other non-histone protein targets. Treat- Histone deacetylase inhibitors (HDACIs) represent one class ment with HDACIs results in chromatin remodeling that permits of gene expression modulating drugs, which is currently being re-expression of silenced tumor suppressor genes in cancer developed for therapy of several types of cancer.9 HDACIs were cells, which, in turn, can potentially result in cellular differ- initially developed as putative epigenetic agents, owing to their entiation, inhibition of proliferation and/or apoptosis. Several ability to modify acetylation status of histones and induce gene classes of HDACIs are currently under development for the expression.10 Typically, optimal gene expression occurs when treatment of patients with MDS and AML. Although modest 11 clinical activity has been reported with the use of HDACIs as histones are in a state of maximal acetylation. -
China Japan United States Europe
Inhibitor United States China Toll Free: +1 877 796-6397 Toll Free: 400-668-6834 Fax: +1 832 582-8590 Fax: 021-68591981 E-mail: [email protected] E-mail: [email protected] Europe Japan Tel: +49-89-46148500 Tel: + 81 3-5632-9610 Fax: +49-89-461485022 Fax: + 81 3-5632-9619 E-mail: [email protected] E-mail: [email protected] Protein Tyrosine Kinase PI3K/Akt/mTOR MAPK Inhibitors Cytoskeletal Signaling Selleck Chemicals supplies over 3,000 Apoptosis + inhibitors used in the study of cell 3000 Epigenetics Cell Cycle Inhibitors signaling pathways. Ubiquitin Signaling DNA Damage Stem Others Cells Neuronal Signaling Product Citations Selleck products have been cited in more than 12000 studies from various SCI journals. (Cell, Nature, Science: 61 studies) Compound Libraries Bioactive Compound Library 2659 compounds Nature. 2017, 541(7638):481-487. Nature. 2015, 521(7552):357-61. Science. 2016, 354(6315). Nature. 2017, 10.1038/nature21064. Nature. 2015, 521(7552):316-21. Science. 2016, 353(6302):929-32. Kinase Inhibitor Library Nature. 2016, 540(7631):119-123. Nature. 2015, 520(7549):683-7. Science. 2016, 352(6283):353-8. 430 inhibitors Nature. 2016, 539(7629):437-442. Nature. 2015, 520(7547):368-72. Science. 2016, 352(6282):189-96. Nature. 2016, 539(7628):304-308. Nature. 2015, 519(7543):370-3. Science. 2016, 351(6277):aad3680. FDA-approved Drug Library 1443 compounds Nature. 2016, 539(7627):54-58. Nature. 2015, 518(7538):254-7. Science. 2013, 341(6146):651-4. Nature. 2016, 538(7626):477-482. Nature. 2015, 517(7536):583-8. -
Characterizing Heterogeneous Cellular Responses to Perturbations
Characterizing heterogeneous cellular responses to perturbations Michael D. Slacka,b, Elisabeth D. Martineza,c, Lani F. Wua,b,1, and Steven J. Altschulera,b,1 aDepartment of Pharmacology, bGreen Center for Systems Biology, Simmons Cancer Center, and the cHamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, TX 75390 Edited by Alfred G. Gilman, University of Texas Southwestern Medical Center, Dallas, TX, and approved October 16, 2008 (received for review July 20, 2008) Cellular populations have been widely observed to respond hetero- rithms to identify phenotypic ‘‘stereotypes’’ within the overall geneously to perturbation. However, interpreting the observed het- population and assign probabilities to cells belonging to subpopu- erogeneity is an extremely challenging problem because of the lations modeled on these stereotypes. Subpopulation identification complexity of possible cellular phenotypes, the large dimension of is based on application of a Gaussian mixture model (GMM), which potential perturbations, and the lack of methods for separating has been applied recently in the context of online phenotype meaningful biological information from noise. Here, we develop an discovery (30). Finally, for each population (or condition), we image-based approach to characterize cellular phenotypes based on estimated the fraction of cells in each subpopulation and summa- patterns of signaling marker colocalization. Heterogeneous cellular rized the results as a probability vector. The resulting ‘‘subpopula- populations are characterized as mixtures of phenotypically distinct tion profiles’’ are human- and machine-interpretable and enable the subpopulations, and responses to perturbations are summarized comparison of heterogeneous responses across multiple physiolog- succinctly as probabilistic redistributions of these mixtures. We apply ical, pathological, or environmental perturbations. -
S13229-020-00387-6.Pdf
Cavallo et al. Molecular Autism (2020) 11:88 https://doi.org/10.1186/s13229-020-00387-6 RESEARCH Open Access High-throughput screening identifes histone deacetylase inhibitors that modulate GTF2I expression in 7q11.23 microduplication autism spectrum disorder patient-derived cortical neurons Francesca Cavallo1†, Flavia Troglio2†, Giovanni Fagà3,4, Daniele Fancelli3,4, Reinald Shyti2, Sebastiano Trattaro1,2, Matteo Zanella2,10, Giuseppe D’Agostino2,11, James M. Hughes2,12, Maria Rosaria Cera3,4, Maurizio Pasi3,4, Michele Gabriele2,13, Maddalena Lazzarin1, Marija Mihailovich1,2, Frank Kooy9, Alessandro Rosa5,6, Ciro Mercurio3,4, Mario Varasi3,4 and Giuseppe Testa2,7,8* Abstract Background: Autism spectrum disorder (ASD) is a highly prevalent neurodevelopmental condition afecting almost 1% of children, and represents a major unmet medical need with no efective drug treatment available. Duplication at 7q11.23 (7Dup), encompassing 26–28 genes, is one of the best characterized ASD-causing copy number variations and ofers unique translational opportunities, because the hemideletion of the same interval causes Williams–Beuren syndrome (WBS), a condition defned by hypersociability and language strengths, thereby providing a unique refer- ence to validate treatments for the ASD symptoms. In the above-indicated interval at 7q11.23, defned as WBS critical region, several genes, such as GTF2I, BAZ1B, CLIP2 and EIF4H, emerged as critical for their role in the pathogenesis of WBS and 7Dup both from mouse models and human studies. Methods: We performed a high-throughput screening of 1478 compounds, including central nervous system agents, epigenetic modulators and experimental substances, on patient-derived cortical glutamatergic neurons dif- ferentiated from our cohort of induced pluripotent stem cell lines (iPSCs), monitoring the transcriptional modulation of WBS interval genes, with a special focus on GTF2I, in light of its overriding pathogenic role. -
Histone Deacetylase Inhibitor Scriptaid Reactivates Latent HIV-1 Promoter by Inducing Histone Modification in in Vitro Latency Cell Lines
265-272.qxd 18/6/2010 08:23 Ì ™ÂÏ›‰·265 INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 26: 265-272, 2010 265 Histone deacetylase inhibitor Scriptaid reactivates latent HIV-1 promoter by inducing histone modification in in vitro latency cell lines HAO YING, YUHAO ZHANG, SHIGUAN LIN, YEFEI HAN and HUAN-ZHANG ZHU State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai 200433, P.R. China Received March 2, 2010; Accepted April 13, 2010 DOI: 10.3892/ijmm_00000461 Abstract. Human immunodeficiency virus type 1 (HIV-1) completely eradicate HIV-1 (1,2). It is now widely believed latency remains a major problem for the eradication of viruses that the presence of a long-lived, stable population of latently in infected individuals undergoing highly active anti-retroviral infected resting memory CD4+ T cells is a major barrier to therapy. By inhibiting HIV-1 gene expression and virus virus eradication (3-5). These latently infected cells can go production, histone deacetylase (HDAC) may contribute to the dormant, and remain in the peripheral circulation and other quiescence of HIV-1 within resting CD4+ T cells. A novel tissues for years despite effective HAART (5). The decay rate HDAC inhibitor, Scriptaid, has been found to have robust of the HIV-1 latent reservoir has been found to be so low that activity and lower toxicity compared to trichostatin A (TSA). their eradication during a human lifespan is unlikely (6,7). We therefore investigated Scriptaid for its capability to reverse Therefore, any curative AIDS therapy should provide a solution HIV-1 latency by inducing HIV-1 activation in the Jurkat T to the HIV-1 latency hurdle (3,6). -
Anti-Tumor Activity of Phenoxybenzamine and Its Inhibition of Histone Deacetylases
Touro Scholar NYMC Faculty Publications Faculty 6-13-2018 Anti-Tumor Activity of Phenoxybenzamine and Its Inhibition of Histone Deacetylases Mario A. Inchiosa New York Medical College Follow this and additional works at: https://touroscholar.touro.edu/nymc_fac_pubs Part of the Enzymes and Coenzymes Commons, and the Pharmacology Commons Recommended Citation Inchiosa, M. A. (2018). Anti-Tumor Activity of Phenoxybenzamine and Its Inhibition of Histone Deacetylases. PLoS One, 13 (6), 0198514-0198514. https://doi.org/10.1371/journal.pone.0198514 This Article is brought to you for free and open access by the Faculty at Touro Scholar. It has been accepted for inclusion in NYMC Faculty Publications by an authorized administrator of Touro Scholar. For more information, please contact [email protected]. RESEARCH ARTICLE Anti-tumor activity of phenoxybenzamine and its inhibition of histone deacetylases Mario A. Inchiosa, Jr.* Departments of Pharmacology and Anesthesiology, New York Medical College, Valhalla, New York, United States of America * [email protected] a1111111111 a1111111111 Abstract a1111111111 a1111111111 The principal finding from this study was the recognition that the α-adrenergic antagonist, a1111111111 phenoxybenzamine, possesses histone deacetylase inhibitory activity. Phenoxybenzamine is approved by the United States Food and Drug Administration for the treatment of hyper- tensive crises associated with tumors of the adrenal medulla, pheochromocytomas. It has several ªoff labelº indications relative to its capacity to relax vascular smooth muscle and OPEN ACCESS smooth muscle of the urogenital tract. The drug also has a long history of apparent efficacy Citation: Inchiosa MA, Jr. (2018) Anti-tumor in ameliorating, and perhaps reversing, the severe symptoms of neuropathic pain syn- activity of phenoxybenzamine and its inhibition of dromes.