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Journal articles on the topic 'MEL cells; Epigenetic marks'

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Published: 4 June 2021

Last updated: 16 February 2022

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1

Black, Kathryn, Elena Sotillo, Nicole Martinez, et al. "Regulation of CD19 Exon 2 Inclusion in B-Lymphoid Cells By Splicing Factors and Epigenetic Marks." Blood 126, no. 23 (2015): 2425. http://dx.doi.org/10.1182/blood.v126.23.2425.2425.

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Abstract CD19 is expressed broadly on the surface of B-cells during normal development and malignant growth, making it a good target for immunotherapy. While immunotherapies targeting CD19 have had great success against pediatric B-cell acute lymphoblastic leukemia (B-ALL), relapses lacking the CD19 epitope still occur (Maude et al., 2014). We have discovered that alternative splicing of CD19, in particular the skipping of exon 2, is responsible for the loss of CD19 extracellular domains, causing resistance to therapy (Sotillo et al., 2015). Here we investigate the molecular mechanism of CD19

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2

Karkhanis, Vrajesh, Lapo Alinari, Bethany Mundy, et al. "PRMT5 Targets Tumor Suppressor Micro RNAs to Regulate Cyclin D1 and c-MYC in Mantle Cell Lymphoma." Blood 128, no. 22 (2016): 2937. http://dx.doi.org/10.1182/blood.v128.22.2937.2937.

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Abstract Protein arginine methyltransferase-5 (PRMT5), a major type II arginine methyltransferase, is an important epigenetic modifier with oncogene-like properties due to its transcriptional repressive activity. When over-expressed, PRMT5 has been shown to target and silence the expression of multiple regulatory and tumor suppressor genes. Global symmetric dimethylation of arginine residues within the N-terminal of histones (H2A(Me2)R3, H3(Me2)R8, H4(Me2)R3) plays a critical role in B cell transformation, correlates with increased tumor cell proliferation and survival. PRMT5 expression is enh

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3

Arumugam, Paritha, Fabrizia Urbinati, Chinavenmeni S. Velu, H. Leighton Grimes, and Punam Malik. "The 3′ End of the Chicken Hypersensitive Site-4 Insulator Has Properties Similar to the 5′ Insulator Core and Is Necessary in Conjunction with the Core for Full Insulator Activity." Blood 112, no. 11 (2008): 817. http://dx.doi.org/10.1182/blood.v112.11.817.817.

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Abstract Genetic correction of hematologic defects is currently impeded by inefficient vector technology. We find that vectors that insulate the correcting transgene from position effects and genotoxicity compromise viral titers. Here we present an improved vector system which utilizes a modified insulator element, without sacrificing viral titers. Specifically, our genetic and epigenetic analysis of the 1.2kb chicken β-globin hypersensitive site-4 (cHS4) insulator reveal heretofore unknown activities in regions of the chicken β-globin insulator element outside the canonical and well studied 2

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4

Watanabe, Toshiki. "Adult T-cell leukemia: molecular basis for clonal expansion and transformation of HTLV-1–infected T cells." Blood 129, no. 9 (2017): 1071–81. http://dx.doi.org/10.1182/blood-2016-09-692574.

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Abstract Adult T-cell leukemia (ATL) is an aggressive T-cell malignancy caused by human T-cell leukemia virus type 1 (HTLV-1) that develops through a multistep carcinogenesis process involving 5 or more genetic events. We provide a comprehensive overview of recently uncovered information on the molecular basis of leukemogenesis in ATL. Broadly, the landscape of genetic abnormalities in ATL that include alterations highly enriched in genes for T-cell receptor–NF-κB signaling such as PLCG1, PRKCB, and CARD11 and gain-of function mutations in CCR4 and CCR7. Conversely, the epigenetic landscape of

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Chung, Jihyun, Vrajesh Karkhanis, Said Sif та Robert A. Baiocchi. "Protein Arginine Methyltransferase 5 Supports MYC, Survivin and Cyclin D1 Activity in Aggressive Lymphomas By Regulating the WNT/β-Catenin Pathway". Blood 124, № 21 (2014): 58. http://dx.doi.org/10.1182/blood.v124.21.58.58.

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Abstract Introduction: Aggressive histologic subtypes of lymphoma such as mantle cell (MCL) and activated B cell (ABC) are considered incurable and affected patients often have a short median survival despite multimodal therapy. It is well established that altered expression of oncogenes and epigenetic dysregulation of tumor suppressor and regulatory genes promote cellular transformation of normal B cells into malignant lymphoma. Hypermethylation of histone proteins (H3R8 and H4R3) by the protein arginine methyltransferase 5 (PRMT5) enzyme has been documented in multiple cancer types and has b

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6

Meng, Fanli, Kathrin Stamms, Romina Bennewitz, et al. "Targeted histone demethylation improves somatic cell reprogramming into cloned blastocysts but not postimplantation bovine concepti†." Biology of Reproduction 103, no. 1 (2020): 114–25. http://dx.doi.org/10.1093/biolre/ioaa053.

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Abstract Correct reprogramming of epigenetic marks in the donor nucleus is a prerequisite for successful cloning by somatic cell transfer (SCT). In several mammalian species, repressive histone (H) lysine (K) trimethylation (me3) marks, in particular H3K9me3, form a major barrier to somatic cell reprogramming into pluripotency and totipotency. We engineered bovine embryonic fibroblasts (BEFs) for the doxycycline-inducible expression of a biologically active, truncated form of murine Kdm4b, a demethylase that removes H3K9me3 and H3K36me3 marks. Upon inducing Kdm4b, H3K9me3 and H3K36me3 levels w

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7

Chung, JI Hyun, Shelby Sloan, Peggy Scherle, et al. "PRMT5 Is a Key Epigenetic Regulator That Promotes Transcriptional Activation in Mantle Cell Lymphoma By Regulating the Lysine Methyltransferase SETD7 and MLL1 Activity." Blood 134, Supplement_1 (2019): 2777. http://dx.doi.org/10.1182/blood-2019-131020.

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Introduction: Post-translational histone modifications directly modify chromatin structure to influence a wide variety of cellular events including gene expression, DNA replication and repair, and cell cycle control. While histone lysine methylation can confer either transcriptionally active or repressive states, the symmetric dimethylation of arginine residues on histone tails is generally associated with transcriptional repression. Overexpression and dysregulation of PRMT5, the major type II protein arginine methyltransferase, has been shown to drive cellular proliferation and survival of mu

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8

Lichtenberg, Jens, Elisabeth F. Heuston, Cheryl A. Keller, Ross C. Hardison, and David M. Bodine. "Comparison of Expression and Epigenetic Profiles in Human and Mouse Erythropoiesis and Megakaryopoiesis Using a Systems Biology Model." Blood 126, no. 23 (2015): 2383. http://dx.doi.org/10.1182/blood.v126.23.2383.2383.

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Abstract To date numerous datasets of gene expression and epigenetic profiles for mouse and human hematopoietic cells have been generated. While individual data sets for a particular cell type have been correlated, no approach exists to harness all expression and epigenetic profiles for the different types of hematopoietic cells. Our goal is to develop a systems biology platform to compare epigenetic profiles of hematopoietic cells towards a better understanding of epigenetic mechanisms governing hematopoiesis. To provide the necessary foundation to support systematic studies of hematopoiesis,

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Fiskus, Warren, Rekha Rao, Ramesh Balusu, et al. "Efficacy of Combined Epigenetic Targeting of Histone Methyltransferase EZH2 and Histone deacetylases Against Human Mantle Cell Lymphoma Cells." Blood 116, no. 21 (2010): 2488. http://dx.doi.org/10.1182/blood.v116.21.2488.2488.

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Abstract Abstract 2488 Lysine specific histone methylation and deacetylation are chromatin modifications that, along with DNA methylation, are involved in the epigenetic silencing of tumor suppressor genes (TSGs). This silencing is mediated by multi-protein complexes PRC (polycomb repressive complexes) 1 and 2. Of the three core protein components of PRC2, i.e., EZH2, SUZ12 and EED, EZH2 has the SET domain with its intrinsic histone methyltransferase activity, which induces the trimethylation (Me3) of lysine (K) 27 on histone (H) 3-a repressive histone modification mediating gene repression. T

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10

Gambacorta, Valentina, Daniela Gnani, Laura Zito, et al. "Integrated Epigenetic Profiling Identifies EZH2 As a Therapeutic Target to Re-Establish Immune Recognition of Leukemia Relapses with Loss of HLA Class II Expression." Blood 134, Supplement_1 (2019): 514. http://dx.doi.org/10.1182/blood-2019-127395.

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Background It is becoming increasingly recognized that evasion from immune control represents one of the main drivers of acute myeloid leukemia (AML) relapse after allogeneic hematopoietic cell transplantation (allo-HCT). In particular, alterations in the antigen processing and presentation machinery represent one of the most effective strategies enacted by tumor cells to avoid recognition from T cells. Whereas it is now well recognized that genomic loss of HLA is frequently at the basis of post-transplantation relapse, it was only recently reported that up to 40% of AML relapses display trans

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Szpurka, Hadrian, Anna M. Jankowska, Bartlomiej Przychodzen, et al. "UTX Mutations and Epigenetic Changes In MDS/MPN and Related Myeloid Malignancies." Blood 116, no. 21 (2010): 121. http://dx.doi.org/10.1182/blood.v116.21.121.121.

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Abstract Abstract 121 Balanced and unbalanced chromosomal lesions and genetic mutations are hallmarks of myeloid malignancies. In addition, aberrant methylation of CpG islands, leading to epigenetic silencing appears to play a significant role in tumor suppressor gene inactivation and malignant progression. While various mechanisms of chromosomal instability have been identified, the pathogenesis of epigenetic instability remains unexplored. ASXL1, EZH2 and TET2 mutations, found in myeloid disorders provide a potential link between genetic and epigenetic events. UTX is a histone H3K27 demethyl

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Burda, Pavel, Nikola Curik, Nina Dusilkova, et al. "Erythroid Transcription Factor GATA-1 Binds and Represses PU.1 Gene – Candidate Mechanism Of Epigenetic Repression Of PU.1 and Inefficient Erythropoiesis In MDS." Blood 122, no. 21 (2013): 1558. http://dx.doi.org/10.1182/blood.v122.21.1558.1558.

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Abstract Introduction Myelodysplastic syndrome (MDS) is often manifested by anemia due to ineffective erythropoiesis. Upon transformation to MDS/AML the uniform population of leukemic blasts overgrow dysplastic bone marrow. Hematopoiesis is regulated by transcription factors GATA-1 and PU.1 that interact and mutually inhibit each other in progenitor cells to guide multilineage commitment and subsequent lineage differentiation. Expression of PU.1 is controlled by several transcription factors including PU.1 itself at distal URE enhancer. It has been well established that underexpression of PU.1

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13

Payton, Jacqueline E., Olivia I. Koues, Rodney Kowalewski, et al. "Defining the Malignant Epigenome in Non-Hodgkin Lymphoma." Blood 120, no. 21 (2012): 524. http://dx.doi.org/10.1182/blood.v120.21.524.524.

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Abstract Abstract 524 Understanding epigenetic mechanisms of gene regulation will provide an unprecedented opportunity for therapeutic intervention in cancer because, unlike genetic lesions, pathogenic changes to the epigenome are reversible. Non-Hodgkin Lymphoma (NHL), which strikes 70,000 Americans annually, is characterized by deregulated expression of large gene cohorts that mediate unchecked cell growth, the molecular basis of which remains poorly understood. Recently, recurrent somatic mutations were identified in chromatin modifier genes (EZH2, MLL2, EP300) in ∼30% of NHL, suggesting th

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Woo, Andrew J., Jonghwan Kim, Jian Xu, Hui Huang, and Alan Cantor. "Role of the Krüppel-Type Zinc Finger Transcription Factor ZBP-89 In Human Globin Gene Regulation and Erythroid Development." Blood 116, no. 21 (2010): 2067. http://dx.doi.org/10.1182/blood.v116.21.2067.2067.

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Abstract Abstract 2067 The molecular mechanisms underlying developmental globin gene regulation remain incompletely understood. Prior studies have identified key cis-regulatory elements within the beta globin locus that contain core regions of closely spaced functional binding sites for GATA, NF-E2p45/maf and GT/GC box binding transcription factors. We recently identified the GT/GC-box binding transcription factor ZBP-89 as a novel GATA-1 interacting partner, and showed that it is involved in erythroid development in mice (Woo et al. 2008. Mol. Cell Bio. 28:2675-2689). Brand et al. independent

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15

Karkhanis, Vrajesh, Olivier Elemento, Maurizio Di Liberto, Selina Chen-Kiang, Said Sif, and Robert A. Baiocchi. "Protein Arginine Methyltransferase 5 Directly Targets and Epigenetically Silences microRNAs miR33b and miR96 to Support Constitutive Cyclin D1 Activity in Non-Hodgkin’s Lymphoma." Blood 124, no. 21 (2014): 60. http://dx.doi.org/10.1182/blood.v124.21.60.60.

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Abstract Epigenetic regulation mediated by arginine-specific methyltransferases enzymes play a central role in tumorigenesis, and enhanced expression of the type II protein arginine methyltransferase PRMT5 has been associated with increased cell proliferation and survival. We have previously demonstrated that PRMT5 is over expressed in mantle cell lymphoma (MCL) and supports constitutive CYCLIN D1/CDK4/6 activity leading to inactivation of the RB/E2F pathway. PRMT5 is also a driver of PRC2 epigenetic activity and promotes activation of b-CATENIN target genes MYC and SURVIVIN (Chung et al ASH,

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Chung, Jihyun, Vrajesh Karkhanis, Sif Said та Robert A. Baiocchi. "Protein Arginine Methyltransferase 5 Regulates WNT/β-Catenin Target Gene Expression in at Multiple Levels". Blood 128, № 22 (2016): 4106. http://dx.doi.org/10.1182/blood.v128.22.4106.4106.

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Abstract Introduction: It is well established that altered expression of oncogenes and epigenetic dysregulation of tumor suppressor and regulatory genes promotes lymphomagenesis. Over-expression of the type II protein arginine methyltransferase (PRMT5) enzyme has been associated with increased cell proliferation and survival in both solid and blood cancers. We have reported that PRMT5 is essential for EBV-driven B cell transformation and that it regulates the EZH2, EED and SUZ12, components of the Polycomb-repressive complex 2 (PRC2) complex via transcriptional silencing of RBL2and hyper-phosp

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Vaitkus, Kestis, Vinzon Ibanez, Maria Armila Ruiz та ін. "The LSD1 Inhibitor RN-1 Increases γ-Globin Expression in Baboons By Targeting an Early Event Responsible for γ-Globin Repression". Blood 132, Supplement 1 (2018): 1054. http://dx.doi.org/10.1182/blood-2018-99-113539.

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Abstract The HbF to HbA developmental globin switch is recapitulated during adult erythroid differentiation and involves the acquisition of repressive epigenetic marks at the γ-globin promoter catalyzed by "druggable" enzymes such as histone deacetylases (HDACs), DNA methyltransferase (DNMT1), LSD1 (KDM1A), and G9A (EHMT2) that are functional components of multiprotein co-repressors recruited to the γ-globin gene promoter by the trans-acting repressors TR2/TR4, BCL11A, and ZBTB7A. A logical approach to increase HbF that has been successfully pursued by our laboratory is to intervene with the e

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Bapat, Sharmila A., Victor Jin, Nicholas Berry, et al. "Multivalent epigenetic marks confer microenvironment-responsive epigenetic plasticity to ovarian cancer cells." Epigenetics 5, no. 8 (2010): 716–29. http://dx.doi.org/10.4161/epi.5.8.13014.

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19

Hu, Xin, Xingguo Li, River Ybarra, et al. "LSD1-Mediated Epigenetic Modification Is Important for TAL1 Function." Blood 112, no. 11 (2008): 4757. http://dx.doi.org/10.1182/blood.v112.11.4757.4757.

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Abstract TAL1/SCL is critical for normal and abnormal hematopoiesis by regulating hematopoietic stem/progenitor cell growth and differentiation. However, it is still unclear how its transcriptional activities are controlled during hematopoiesis. Here, we undertook the biochemical isolation of TAL1-associated protein complexes in erythroleukemia cells and showed that TAL1 interacts with histone demethylase LSD1 complexes containing LSD1, CoREST, HDAC1 and HDAC2. Interestingly, although TAL1 specifically colocalizes with LSD1 at the target gene promoter p4.2 in undifferentiated MEL cells, the re

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Stanworth, S. J., N. A. Roberts, J. A. Sharpe, J. A. Sloane-Stanley, and W. G. Wood. "Established epigenetic modifications determine the expression of developmentally regulated globin genes in somatic cell hybrids." Molecular and Cellular Biology 15, no. 8 (1995): 3969–78. http://dx.doi.org/10.1128/mcb.15.8.3969.

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Somatic cell hybrids generated from transgenic mouse cells have been used to examine the developmental regulation of human gamma-to-beta-globin gene switching. In hybrids between mouse erythroleukemia (MEL) cells and transgenic erythroblasts taken at various stages of development, there was regulated expression of the human fetal gamma and adult beta genes, reproducing the in vivo pattern prior to fusion. Hybrids formed from embryonic blood cells produced predominantly gamma mRNA, whereas beta gene expression was observed in adult hybrids and a complete range of intermediate patterns was found

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Kint, Sam, Wim Van Criekinge, Linos Vandekerckhove, et al. "Single cell epigenetic visualization assay." Nucleic Acids Research 49, no. 8 (2021): e43-e43. http://dx.doi.org/10.1093/nar/gkab009.

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Abstract Characterization of the epigenetic status of individual cells remains a challenge. Current sequencing approaches have limited coverage, and it is difficult to assign an epigenetic status to the transcription state of individual gene alleles in the same cell. To address these limitations, a targeted microscopy-based epigenetic visualization assay (EVA) was developed for detection and quantification of epigenetic marks at genes of interest in single cells. The assay is based on an in situ biochemical reaction between an antibody-conjugated alkaline phosphatase bound to the epigenetic ma

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Wibowo, Anjar, Claude Becker, Julius Durr, et al. "Partial maintenance of organ-specific epigenetic marks during plant asexual reproduction leads to heritable phenotypic variation." Proceedings of the National Academy of Sciences 115, no. 39 (2018): E9145—E9152. http://dx.doi.org/10.1073/pnas.1805371115.

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Plants differ from animals in their capability to easily regenerate fertile adult individuals from terminally differentiated cells. This unique developmental plasticity is commonly observed in nature, where many species can reproduce asexually through the ectopic initiation of organogenic or embryogenic developmental programs. While organ-specific epigenetic marks are not passed on during sexual reproduction, the fate of epigenetic marks during asexual reproduction and the implications for clonal progeny remain unclear. Here we report that organ-specific epigenetic imprints in Arabidopsis thal

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Ramanouskaya, Tatsiana V., Anastasiya V. Kviatko, and Vasily V. Grinev. "Epigenetic marks on the chromatin are associated with RNA splicing in human leukemia cells." Journal of the Belarusian State University. Biology, no. 2 (July 18, 2019): 70–81. http://dx.doi.org/10.33581/2521-1722-2019-2-70-81.

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In this work we estimated associations between distribution patterns of several epigenetic marks and splicing events on the level of full genome and transcriptome in the cells of two leukemic cell lines containing two different reciprocal chromosome translocations. Significant difference in distribution of epigenetic marks was found, contributing to more opened or more closed chromatin in loci of donor vs acceptor and canonical vs alternative splice sites in expressing genes. Marks of the opened chromatin are significantly more often present in the genomic regions with alternative splicing eve

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Negi, Sandeep S., Eric S. Schafer, Donald Small, and Patrick Brown. "Histone Profiling of Normal B-Precursors and Primary Pre-B Acute Lymphoblastic Leukemia Reveals Distinct Aberrant Histone Codes In MLL-Rearranged Vs. Wild Type MLL Leukemias That Correlate with Differential Expression of Key MLL Target Genes." Blood 116, no. 21 (2010): 2503. http://dx.doi.org/10.1182/blood.v116.21.2503.2503.

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Abstract 2503 Epigenetic regulation of gene transcription is mediated both by methylation of DNA CpG islands and the local configuration of chromatin, which is dynamically regulated by post-translational modifications, or “marks”, of key lysines (K) of histones (especially H3). Some marks are associated with transcriptional repression [trimethylation (me3) of K9 and K27], and some with activation [me3 of K4, dimethylation (me2) of K79 and acetylation (Ac) of K9 and K14]. The MLL gene encodes a protein that functions as a master regulator of target gene expression by methylating H3K4 via its SE

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Patra, Samir Kumar, Moonmoon Deb, and Aditi Patra. "Molecular marks for epigenetic identification of developmental and cancer stem cells." Clinical Epigenetics 2, no. 1 (2010): 27–53. http://dx.doi.org/10.1007/s13148-010-0016-0.

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Uller, Tobias, Sinead English, and Ido Pen. "When is incomplete epigenetic resetting in germ cells favoured by natural selection?" Proceedings of the Royal Society B: Biological Sciences 282, no. 1811 (2015): 20150682. http://dx.doi.org/10.1098/rspb.2015.0682.

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Resetting of epigenetic marks, such as DNA methylation, in germ cells or early embryos is not always complete. Epigenetic states may therefore persist, decay or accumulate across generations. In spite of mounting empirical evidence for incomplete resetting, it is currently poorly understood whether it simply reflects stochastic noise or plays an adaptive role in phenotype determination. Here, we use a simple model to show that incomplete resetting can be adaptive in heterogeneous environments. Transmission of acquired epigenetic states prevents mismatched phenotypes when the environment change

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Cheng, Xiaodong, Hideharu Hashimoto, Yusuf Olatunde Olanrewaju, Samuel Hong, and Xing Zhang. "Generation, Recognition, and Erasure of 5-methylcytosine and its Oxidative Derivatives." Acta Crystallographica Section A Foundations and Advances 70, a1 (2014): C297. http://dx.doi.org/10.1107/s2053273314097022.

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During the development, mammalian germ line cells and brains undergo a series of cellular and molecular events that lead to the erasure and re-establishment of epigenetic programs. It is possible that the active erasure and the re-establishment of 5-methylcytosine (5mC) marks during germ line differentiation and brain development from fetus to young adult involve dynamic changes of 5mC into oxidative marks, and that these modified cytosine residues in DNA are recognized by specific protein readers with distinct roles in the maintenance of epigenetic memory. Here we report our on-going biochemi

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Harandi-Zadeh, Sadaf, Cayla Boycott, Megan Beetch, et al. "Pterostilbene Changes Epigenetic Marks at Enhancer Regions of Oncogenes in Breast Cancer Cells." Antioxidants 10, no. 8 (2021): 1232. http://dx.doi.org/10.3390/antiox10081232.

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Epigenetic aberrations are linked to sporadic breast cancer. Interestingly, certain dietary polyphenols with anti-cancer effects, such as pterostilbene (PTS), have been shown to regulate gene expression by altering epigenetic patterns. Our group has proposed the involvement of DNA methylation and DNA methyltransferase 3B (DNMT3B) as vital players in PTS-mediated suppression of candidate oncogenes and suggested a role of enhancers as target regions. In the present study, we assess a genome-wide impact of PTS on epigenetic marks at enhancers in highly invasive MCF10CA1a breast cancer cells. Foll

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Kamada, Rui, Wenjing Yang, Yubo Zhang, et al. "Interferon stimulation creates chromatin marks and establishes transcriptional memory." Proceedings of the National Academy of Sciences 115, no. 39 (2018): E9162—E9171. http://dx.doi.org/10.1073/pnas.1720930115.

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Epigenetic memory for signal-dependent transcription has remained elusive. So far, the concept of epigenetic memory has been largely limited to cell-autonomous, preprogrammed processes such as development and metabolism. Here we show that IFNβ stimulation creates transcriptional memory in fibroblasts, conferring faster and greater transcription upon restimulation. The memory was inherited through multiple cell divisions and led to improved antiviral protection. Of ∼2,000 IFNβ-stimulated genes (ISGs), about half exhibited memory, which we define as memory ISGs. The rest, designated nonmemory IS

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Ohguchi, Hiroto, Teru Hideshima, Manoj Bhasin, et al. "The KDM3A-KLF2-IRF4 Axis Maintains Myeloma Cell Survival." Blood 126, no. 23 (2015): 3633. http://dx.doi.org/10.1182/blood.v126.23.3633.3633.

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Abstract Histone methylations are tightly regulated by a balance between methyltransferases and demethylases that mediate the addition and removal of these modifications. Importantly, dysregulation of histone methylation is implicated in pathogenesis of cancers, including multiple myeloma (MM). For example, the t(4;14) (p16;q32) is present in 15 - 20% of MM patients and results in overexpression of WHSC1, a histone H3 lysine 36 (H3K36) methyltransferase. On the other hand, approximately 10% of MM patients without the t(4;14) have inactivating mutations in KDM6A, a H3K27 demethylase. KDM3A is a

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Capparelli, Rosanna, and Domenico Iannelli. "Role of Epigenetics in Type 2 Diabetes and Obesity." Biomedicines 9, no. 8 (2021): 977. http://dx.doi.org/10.3390/biomedicines9080977.

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Epigenetic marks the genome by DNA methylation, histone modification or non-coding RNAs. Epigenetic marks instruct cells to respond reversibly to environmental cues and keep the specific gene expression stable throughout life. In this review, we concentrate on DNA methylation, the mechanism often associated with transgenerational persistence and for this reason frequently used in the clinic. A large study that included data from 10,000 blood samples detected 187 methylated sites associated with body mass index (BMI). The same study demonstrates that altered methylation results from obesity (OB

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Sloan, Shelby, Fiona Brown, JI Hyun Chung, et al. "Targeting PRMT5 to Circumvent Acquired Ibrutinib Resistance in Mantle Cell Lymphoma." Blood 134, Supplement_1 (2019): 4065. http://dx.doi.org/10.1182/blood-2019-128998.

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Mantle cell lymphoma (MCL) is an incurable B-cell malignancy characterized by genetic dysregulation of cyclin D1 and activation of signaling pathways driving uncontrolled MCL cell proliferation and survival. Ibrutinib is an FDA-approved irreversible inhibitor of Bruton's tyrosine kinase (BTK), a downstream target of the B-cell receptor (BCR) pathway. While ibrutinib exhibits significant single-agent therapeutic activity in patients with relapsed/refractory MCL, the vast majority of MCL patients on ibrutinib progress with aggressive disease and short survival (3-8 mo). Although ~80% of chronic

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Antony, J., F. Oback, R. Broadhurst, et al. "500. THE MANIPULATION OF THE EPIGENETIC MARK HISTONE 3 LYSINE 9 TRIMETHYLATION IN DONOR CELLS AND ITS EFFECTS ON THE DEVELOPMENT OF CLONED MOUSE EMBRYOS." Reproduction, Fertility and Development 21, no. 9 (2009): 101. http://dx.doi.org/10.1071/srb09abs500.

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To produce live cloned mammals from adult somatic cells the nuclei of these cells must be first reprogrammed from a very restricted, cell lineage-specific gene expression profile to an embryo-like expression pattern, compatible with embryonic development. Although this has been achieved in a number of species the efficiency of cloning remains very low. Inadequate reprogramming of epigenetic marks in the donor cells correlated with aberrant embryonic gene expression profiles has been identified as a key cause of this inefficiency. Some of the most common epigenetic marks are chemical modificati

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Zarakowska, Ewelina, Jolanta Czerwinska, Agnieszka Tupalska, et al. "Oxidation Products of 5-Methylcytosine are Decreased in Senescent Cells and Tissues of Progeroid Mice." Journals of Gerontology: Series A 73, no. 8 (2018): 1003–9. http://dx.doi.org/10.1093/gerona/gly012.

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Abstract 5-Hydroxymethylcytosine and 5-formylcytosine are stable DNA base modifications generated from 5-methylcytosine by the ten-eleven translocation protein family that function as epigenetic markers. 5-Hydroxymethyluracil may also be generated from thymine by ten-eleven translocation enzymes. Here, we asked if these epigenetic changes accumulate in senescent cells, since they are thought to be inversely correlated with proliferation. Testing this in ERCC1-XPF-deficient cells and mice also enabled discovery if these DNA base changes are repaired by nucleotide excision repair. Epigenetic mar

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Robbez-Masson, Luisa, Christopher H. C. Tie, and Helen M. Rowe. "Cancer cells, on your histone marks, get SETDB1, silence retrotransposons, and go!" Journal of Cell Biology 216, no. 11 (2017): 3429–31. http://dx.doi.org/10.1083/jcb.201710068.

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Cancer cells thrive on genetic and epigenetic changes that confer a selective advantage but also need strategies to avoid immune recognition. In this issue, Cuellar et al. (2017. J. Cell Biol. https://doi.org/10.1083/jcb.201612160) find that the histone methyltransferase SETDB1 enables acute myeloid leukemia cells to evade sensing of retrotransposons by innate immune receptors.

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Arnaud, Philippe. "Genomic imprinting in germ cells: imprints are under control." REPRODUCTION 140, no. 3 (2010): 411–23. http://dx.doi.org/10.1530/rep-10-0173.

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The cis-acting regulatory sequences of imprinted gene loci, called imprinting control regions (ICRs), acquire specific imprint marks in germ cells, including DNA methylation. These epigenetic imprints ensure that imprinted genes are expressed exclusively from either the paternal or the maternal allele in offspring. The last few years have witnessed a rapid increase in studies on how and when ICRs become marked by and subsequently maintain such epigenetic modifications. These novel findings are summarised in this review, which focuses on the germline acquisition of DNA methylation imprints and

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de Miranda, Juliana Xavier, Fábia de Oliveira Andrade, Aline de Conti, Maria Lúcia Zaidan Dagli, Fernando Salvador Moreno, and Thomas Prates Ong. "Effects of selenium compounds on proliferation and epigenetic marks of breast cancer cells." Journal of Trace Elements in Medicine and Biology 28, no. 4 (2014): 486–91. http://dx.doi.org/10.1016/j.jtemb.2014.06.017.

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Fessele, Kristen L., and Fay Wright. "Primer in Genetics and Genomics, Article 6: Basics of Epigenetic Control." Biological Research For Nursing 20, no. 1 (2017): 103–10. http://dx.doi.org/10.1177/1099800417742967.

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The epigenome is a collection of chemical compounds that attach to and overlay the DNA sequence to direct gene expression. Epigenetic marks do not alter DNA sequence but instead allow or silence gene activity and the subsequent production of proteins that guide the growth and development of an organism, direct and maintain cell identity, and allow for the production of primordial germ cells (PGCs; ova and spermatozoa). The three main epigenetic marks are (1) histone modification, (2) DNA methylation, and (3) noncoding RNA, and each works in a different way to regulate gene expression. This art

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Rhie, Suhn K., Shannon Schreiner, Heather Witt, et al. "Using 3D epigenomic maps of primary olfactory neuronal cells from living individuals to understand gene regulation." Science Advances 4, no. 12 (2018): eaav8550. http://dx.doi.org/10.1126/sciadv.aav8550.

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As part of PsychENCODE, we developed a three-dimensional (3D) epigenomic map of primary cultured neuronal cells derived from olfactory neuroepithelium (CNON). We mapped topologically associating domains and high-resolution chromatin interactions using Hi-C and identified regulatory elements using chromatin immunoprecipitation and nucleosome positioning assays. Using epigenomic datasets from biopsies of 63 living individuals, we found that epigenetic marks at distal regulatory elements are more variable than marks at proximal regulatory elements. By integrating genotype and metadata, we identif

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Nesvick, Cody, Charles Day, Liang Zhang, Edward Hinchcliffe, and David Daniels. "DIPG-78. REVERTANCE OF THE H3K27M MUTATION RESCUES CHROMATIN MARKS NECESSARY FOR ONCOGENESIS IN DIFFUSE MIDLINE GLIOMA." Neuro-Oncology 22, Supplement_3 (2020): iii302. http://dx.doi.org/10.1093/neuonc/noaa222.120.

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Abstract Diffuse midline glioma (DMG) is a lethal brain tumor that typically occurs in children. Numerous studies have demonstrated the central role of the H3K27M mutation and secondary loss of H3K27 trimethylation (H3K27me3) in DMG tumorigenesis. Understanding how the H3K27M mutation alters the epigenetic landscape of the cell is necessary for revealing molecular targets that are critical to tumorigenesis. To investigate the epigenetic effects of H3K27M mutation in DMG, we developed revertant DMG cell lines with the mutant methionine residue reverted to wildtype (i.e., M27K). Revertant cells

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Pruvost, Mathilde, and Sarah Moyon. "Oligodendroglial Epigenetics, from Lineage Specification to Activity-Dependent Myelination." Life 11, no. 1 (2021): 62. http://dx.doi.org/10.3390/life11010062.

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Oligodendroglial cells are the myelinating cells of the central nervous system. While myelination is crucial to axonal activity and conduction, oligodendrocyte progenitor cells and oligodendrocytes have also been shown to be essential for neuronal support and metabolism. Thus, a tight regulation of oligodendroglial cell specification, proliferation, and myelination is required for correct neuronal connectivity and function. Here, we review the role of epigenetic modifications in oligodendroglial lineage cells. First, we briefly describe the epigenetic modalities of gene regulation, which are k

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Jurkiewicz, Dorota, Elżbieta Ciara, Małgorzata Krajewska-Walasek, and Krystyna Chrzanowska. "DNA methylation as an epigenetic biomarker in imprinting disorders." Postępy Higieny i Medycyny Doświadczalnej 74 (December 7, 2020): 532–40. http://dx.doi.org/10.5604/01.3001.0014.5687.

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Epigenetic modifications control gene expression and enable the same genotype to lead to various phenotypes, thus exhibiting extensive variability in human cells function. DNA methylation is one of the most often investigated epigenetic modifications, playing a key part in genomic imprinting. Genomic imprinting is an epigenetic process by which the male and the female germ cells confer specific marks (imprints). Maternal chromatin marks differ from paternal ones, leading to expression of specific genes from only one allele. Disturbance in imprinting process results in epimutations, which are e

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Zhang, Zhichao, Adeel Manaf, Yanjiao Li, et al. "Histone Methylations Define Neural Stem/Progenitor Cell Subtypes in the Mouse Subventricular Zone." Molecular Neurobiology 57, no. 2 (2019): 997–1008. http://dx.doi.org/10.1007/s12035-019-01777-5.

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Abstract Neural stem/progenitor cells (NSPCs) persist in the mammalian brain throughout life and can be activated in response to the physiological and pathophysiological stimuli. Epigenetic reprogramming of NPSC represents a novel strategy for enhancing the intrinsic potential of the brain to regenerate after brain injury. Therefore, defining the epigenetic features of NSPCs is important for developing epigenetic therapies for targeted reprogramming of NSPCs to rescue neurologic function after injury. In this study, we aimed at defining different subtypes of NSPCs by individual histone methyla

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Zaidi, Sayyed K., Daniel W. Young, Martin Montecino, et al. "Architectural Epigenetics: Mitotic Retention of Mammalian Transcriptional Regulatory Information." Molecular and Cellular Biology 30, no. 20 (2010): 4758–66. http://dx.doi.org/10.1128/mcb.00646-10.

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ABSTRACT Epigenetic regulatory information must be retained during mammalian cell division to sustain phenotype-specific and physiologically responsive gene expression in the progeny cells. Histone modifications, DNA methylation, and RNA-mediated silencing are well-defined epigenetic mechanisms that control the cellular phenotype by regulating gene expression. Recent results suggest that the mitotic retention of nuclease hypersensitivity, selective histone marks, as well as the lineage-specific transcription factor occupancy of promoter elements contribute to the epigenetic control of sustaine

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Motti, Maria Letizia, and Rosaria Meccariello. "Minireview: The Epigenetic Modulation of KISS1 in Reproduction and Cancer." International Journal of Environmental Research and Public Health 16, no. 14 (2019): 2607. http://dx.doi.org/10.3390/ijerph16142607.

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Epigenetics describes how both lifestyle and environment may affect human health through the modulation of genome functions and without any change to the DNA nucleotide sequence. The discovery of several epigenetic mechanisms and the possibility to deliver epigenetic marks in cells, gametes, and biological fluids has opened up new perspectives in the prevention, diagnosis, and treatment of human diseases. In this respect, the depth of knowledge of epigenetic mechanisms is fundamental to preserving health status and to developing targeted interventions. In this minireview, we summarize the epig

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Ozyerli-Goknar, Ezgi, and Tugba Bagci-Onder. "Epigenetic Deregulation of Apoptosis in Cancers." Cancers 13, no. 13 (2021): 3210. http://dx.doi.org/10.3390/cancers13133210.

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Cancer cells possess the ability to evade apoptosis. Genetic alterations through mutations in key genes of the apoptotic signaling pathway represent a major adaptive mechanism of apoptosis evasion. In parallel, epigenetic changes via aberrant modifications of DNA and histones to regulate the expression of pro- and antiapoptotic signal mediators represent a major complementary mechanism in apoptosis regulation and therapy response. Most epigenetic changes are governed by the activity of chromatin modifying enzymes that add, remove, or recognize different marks on histones and DNA. Here, we disc

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Kent, Clement, and Pavan Agrawal. "Regulation of Social Stress and Neural Degeneration by Activity-Regulated Genes and Epigenetic Mechanisms in Dopaminergic Neurons." Molecular Neurobiology 57, no. 11 (2020): 4500–4510. http://dx.doi.org/10.1007/s12035-020-02037-7.

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Abstract Transcriptional and epigenetic regulation of both dopaminergic neurons and their accompanying glial cells is of great interest in the search for therapies for neurodegenerative disorders such as Parkinson’s disease (PD). In this review, we collate transcriptional and epigenetic changes identified in adult Drosophila melanogaster dopaminergic neurons in response to either prolonged social deprivation or social enrichment, and compare them with changes identified in mammalian dopaminergic neurons during normal development, stress, injury, and neurodegeneration. Surprisingly, a small set

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Joglekar, Mugdha V., Vinay M. Joglekar, Sheela V. Joglekar, and Anandwardhan A. Hardikar. "Human fetal pancreatic insulin-producing cells proliferate in vitro." Journal of Endocrinology 201, no. 1 (2009): 27–36. http://dx.doi.org/10.1677/joe-08-0497.

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There have been considerable efforts towards understanding the potential of human pancreatic endocrine cells to proliferate and transition into mesenchymal cell populations. Since rodent studies have demonstrated that mouse insulin-producing cells do not proliferate in vitro, a similar possibility has been considered for human islet endocrine cells. Considering the inherent differences in mouse and human pancreatic islets, we decided to assess the potential of human fetal pancreatic insulin-producing cells to proliferate in vitro. We studied the proliferative potential of human fetal pancreati

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Inoue, Daichi, Takeshi Fujino, and Toshio Kitamura. "ASXL1 as a critical regulator of epigenetic marks and therapeutic potential of mutated cells." Oncotarget 9, no. 81 (2018): 35203–4. http://dx.doi.org/10.18632/oncotarget.26230.

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Shiota, Kunio, Yasushi Kogo, Jun Ohgane, et al. "Epigenetic marks by DNA methylation specific to stem, germ and somatic cells in mice." Genes to Cells 7, no. 9 (2002): 961–69. http://dx.doi.org/10.1046/j.1365-2443.2002.00574.x.

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