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Journal articles on the topic 'CpG-Island-Methylation'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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1

Wong, David J., Scott A. Foster, Denise A. Galloway, and Brian J. Reid. "Progressive Region-Specific De Novo Methylation of the p16 CpG Island in Primary Human Mammary Epithelial Cell Strains during Escape from M0 Growth Arrest." Molecular and Cellular Biology 19, no. 8 (1999): 5642–51. http://dx.doi.org/10.1128/mcb.19.8.5642.

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ABSTRACT CpG island methylation plays an important role in normal cellular processes, such as genomic imprinting and X-chromosome inactivation, as well as in abnormal processes, such as neoplasia. However, the dynamics of de novo CpG island methylation, during which a CpG island is converted from an unmethylated, active state to a densely methylated, inactive state, are largely unknown. It is unclear whether the development of de novo CpG island methylation is a progressive process, in which a subset of CpG sites are initially methylated with a subsequent increase in methylation density, or a

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Feltus, F. A., E. K. Lee, J. F. Costello, C. Plass, and P. M. Vertino. "Predicting aberrant CpG island methylation." Proceedings of the National Academy of Sciences 100, no. 21 (2003): 12253–58. http://dx.doi.org/10.1073/pnas.2037852100.

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Cameron, Elizabeth E., Stephen B. Baylin, and James G. Herman. "p15INK4BCpG Island Methylation in Primary Acute Leukemia Is Heterogeneous and Suggests Density as a Critical Factor for Transcriptional Silencing." Blood 94, no. 7 (1999): 2445–51. http://dx.doi.org/10.1182/blood.v94.7.2445.419k19_2445_2451.

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The promoter region of the cyclin-dependent kinase inhibitorp15INK4Bcontains a CpG island that is hypermethylated in many hematologic malignancies. To explore the relationship between patterns of methylation and gene transcription, we used bisulfite genomic sequencing to obtain a detailed analysis of methylation in acute leukemia, leukemia cell lines, and normal lymphocytes. The entire CpG island region of p15 was largely devoid of methylation in normal lymphocytes, but methylation of varying density was found in primary acute leukemia. Methylation density was generally conserved between the a

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4

Vertino, P. M., R. W. Yen, J. Gao, and S. B. Baylin. "De novo methylation of CpG island sequences in human fibroblasts overexpressing DNA (cytosine-5-)-methyltransferase." Molecular and Cellular Biology 16, no. 8 (1996): 4555–65. http://dx.doi.org/10.1128/mcb.16.8.4555.

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Recent studies showing a correlation between the levels of DNA (cytosine-5-)-methyltransferase (DNA MTase) enzyme activity and tumorigenicity have implicated this enzyme in the carcinogenic process. Moreover, hypermethylation of CpG island-containing promoters is associated with the inactivation of genes important to tumor initiation and progression. One proposed role for DNA MTase in tumorigenesis is therefore a direct role in the de novo methylation of these otherwise unmethylated CpG islands. In this study, we sought to determine whether increased levels of DNA MTase could directly affect C

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Shikauchi, Yuko, Akio Saiura, Takahiko Kubo, et al. "SALL3 Interacts with DNMT3A and Shows the Ability To Inhibit CpG Island Methylation in Hepatocellular Carcinoma." Molecular and Cellular Biology 29, no. 7 (2009): 1944–58. http://dx.doi.org/10.1128/mcb.00840-08.

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ABSTRACT The mechanisms of aberrant CpG island methylation in oncogenesis are not fully characterized. In particular, little is known about the mechanisms of inhibition of CpG island methylation. Here we show that sal-like 3 (SALL3) is a novel inhibitory factor for DNA methyltransferase 3 alpha (DNMT3A). SALL3 binds to DNMT3A by a direct interaction between the double zinc finger motif of SALL3 and the PWWP domain of DNMT3A. SALL3 expression reduces DNMT3A-mediated CpG island methylation in cell culture and in vitro. CpG island methylation is enhanced in SALL3-depleted cells. Consistently, DNM

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Patel, S. A., D. M. Graunke, and R. O. Pieper. "Aberrant silencing of the CpG island-containing human O6-methylguanine DNA methyltransferase gene is associated with the loss of nucleosome-like positioning." Molecular and Cellular Biology 17, no. 10 (1997): 5813–22. http://dx.doi.org/10.1128/mcb.17.10.5813.

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Tumor-associated aberrant silencing of CpG island-containing genes has been correlated with increased cytosine methylation, a "closed" chromatin structure, and exclusion of transcription factor binding in the CpG island/promoter regions of affected genes. Given the lack of understanding of what constitutes a closed chromatin structure in CpG islands, however, it has been difficult to assess the relationship among cytosine methylation, chromatin structure, and inappropriate gene silencing. In this study, nuclease accessibility analysis was used to more clearly define the chromatin structure in

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Rashid, Asif, Lanlan Shen, Jeffrey S. Morris, Jean-Pierre J. Issa, and Stanley R. Hamilton. "CpG Island Methylation in Colorectal Adenomas." American Journal of Pathology 159, no. 3 (2001): 1129–35. http://dx.doi.org/10.1016/s0002-9440(10)61789-0.

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8

Jeon, Yong Tark, Jae Weon Kim, and Soon Beom Kang. "CpG island methylation and gynecolgic malignancy." Korean Journal of Gynecologic Oncology 16, no. 1 (2005): 1. http://dx.doi.org/10.3802/kjgo.2005.16.1.1.

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9

Mitchell, C. M., T. Zakar, S. D. Sykes, K. G. Pringle, and E. R. Lumbers. "141. METHYLATION OF GENES OF THE RENIN ANGIOTENSIN SYSTEM (RAS) IN EARLY HUMAN AMNION." Reproduction, Fertility and Development 22, no. 9 (2010): 59. http://dx.doi.org/10.1071/srb10abs141.

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The renin angiotensin system (RAS) genes angiotensin converting enzyme (ACE), angiotensin II type 1 receptor (AGTR1) and prorenin receptor (ATP6AP2) have CpG islands at their promoters, so these genes may be regulated by CpG island methylation as may the expression of two proteases implicated in prorenin activation (cathepsin D {CTSD} and kallikrein 1 {KLK1}). We measured CpG island methylation of 3 RAS genes and of CTSD and KLK1 in amnion using the Methyl-Profiler assay (SA Biosciences), which discriminates methyl-CpG density between hypermethylated, intermediately methylated and unmethylated

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Gebhard, Claudia, Mohammed Sadeh, Dagmar Glatz, et al. "Profiling of Aberrant DNA Methylation In AML Reveals Subclasses of CpG Islands with Epigenetic or Genetic Association." Blood 116, no. 21 (2010): 2498. http://dx.doi.org/10.1182/blood.v116.21.2498.2498.

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Abstract Abstract 2498 CpG islands show frequent and often disease-specific epigenetic alterations during malignant transformation, however, the underlying mechanisms are poorly understood. We used methyl-CpG immunoprecipitation (MCIp) to generate comparative DNA methylation profiles of 30 patients with acute myeloid leukemia for human CpG islands across the genome. DNA methylation profiles across 23.000 CpG islands revealed highly heterogeneous methylation patterns in AML with over 6000 CpG islands showing aberrant de novo methylation in AML. Based on these profiles we selected a subset of 38

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Zheng, Xu, and Cao. "A Long Polymorphic GT Microsatellite within a Gene Promoter Mediates Non-Imprinted Allele-Specific DNA Methylation of a CpG Island in a Goldfish Inter-Strain Hybrid." International Journal of Molecular Sciences 20, no. 16 (2019): 3923. http://dx.doi.org/10.3390/ijms20163923.

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It is now widely accepted that allele-specific DNA methylation (ASM) commonly occurs at non-imprinted loci. Most of the non-imprinted ASM regions observed both within and outside of the CpG island show a strong correlation with DNA polymorphisms. However, what polymorphic cis-acting elements mediate non-imprinted ASM of the CpG island remains unclear. In this study, we investigated the impact of polymorphic GT microsatellites within the gene promoter on non-imprinted ASM of the local CpG island in goldfish. We generated various goldfish heterozygotes, in which the length of GT microsatellites

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Qu, Ying, Andreas Lennartsson, Verena I. Gaidzik, et al. "Genome-Wide DNA Methylation Analysis Shows Enrichment of Differential Methylation in “Open Seas” and Enhancers and Reveals Hypomethylation in DNMT3A Mutated Cytogenetically Normal AML (CN-AML)." Blood 120, no. 21 (2012): 653. http://dx.doi.org/10.1182/blood.v120.21.653.653.

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Abstract Abstract 653 DNA methylation is involved in multiple biologic processes including normal cell differentiation and tumorigenesis. In AML, methylation patterns have been shown to differ significantly from normal hematopoietic cells. Most studies of DNA methylation in AML have previously focused on CpG islands within the promoter of genes, representing only a very small proportion of the DNA methylome. In this study, we performed genome-wide methylation analysis of 62 AML patients with CN-AML and CD34 positive cells from healthy controls by Illumina HumanMethylation450K Array covering 45

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Kim, Hyoung-Pyo, and Warren J. Leonard. "CREB/ATF-dependent T cell receptor–induced FoxP3 gene expression: a role for DNA methylation." Journal of Experimental Medicine 204, no. 7 (2007): 1543–51. http://dx.doi.org/10.1084/jem.20070109.

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Regulatory T cells (T reg cells) are a population of CD4+ T cells that limit immune responses. FoxP3 is a master control transcription factor for development and function of these cells, but its regulation is poorly understood. We have identified a T cell receptor–responsive enhancer in the FoxP3 first intron that is dependent on a cyclic-AMP response element binding protein (CREB)/activating transcription factor (ATF) site overlapping a CpG island. Methylation of this island inversely correlates with CREB binding and FoxP3 expression. Interestingly, transforming growth factor-β, which induces

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Brakensiek, Kai, Luzie U. Wingen, Florian Länger, Hans Kreipe, and Ulrich Lehmann. "Quantitative High-Resolution CpG Island Mapping with Pyrosequencing™ Reveals Disease-Specific Methylation Patterns of the CDKN2B Gene in Myelodysplastic Syndrome and Myeloid Leukemia." Clinical Chemistry 53, no. 1 (2007): 17–23. http://dx.doi.org/10.1373/clinchem.2007.072629.

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Abstract Background: Gene silencing through aberrant CpG island methylation is the most extensively analyzed epigenetic event in human tumorigenesis and has huge diagnostic and prognostic potential. Methylation patterns are often very heterogeneous, however, presenting a serious challenge for the development of methylation assays for diagnostic purposes. Methods: We used Pyrosequencing™ technology to determine the methylation status of 68 CpG sites in the CpG island of the CDKN2B gene [cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4)], frequently hypermethylated in myeloid malignancie

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Chan, Annie On-On, Jean-Pierre J. Issa, Jeffrey S. Morris, Stanley R. Hamilton, and Asif Rashid. "Concordant CpG Island Methylation in Hyperplastic Polyposis." American Journal of Pathology 160, no. 2 (2002): 529–36. http://dx.doi.org/10.1016/s0002-9440(10)64872-9.

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Sidaway, Peter. "CpG island methylation indicates inferior survival outcomes." Nature Reviews Clinical Oncology 13, no. 8 (2016): 465. http://dx.doi.org/10.1038/nrclinonc.2016.107.

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Kim, Baek-Hee, Nam-Yun Cho, Minhee Choi, Sun Lee, Ja June Jang, and Gyeong Hoon Kang. "Methylation Profiles of Multiple CpG Island Loci in Extrahepatic Cholangiocarcinoma Versus Those of Intrahepatic Cholangiocarcinomas." Archives of Pathology & Laboratory Medicine 131, no. 6 (2007): 923–30. http://dx.doi.org/10.5858/2007-131-923-mpomci.

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Abstract Context.—CpG island hypermethylation is attracting attention because of its importance as a tumor marker and its potential mechanism for the development of human cancers. Extrahepatic cholangiocarcinoma has been poorly investigated with respect to CpG island hypermethylation, and the number of genes known to be methylated in extrahepatic cholangiocarcinomas is fewer than 20. Objective.—To generate methylation profiles of 24 CpG island loci in extrahepatic cholangiocarcinomas, to correlate methylation findings with clinicopathologic findings, and to compare these findings with those of

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18

Zhao, Haiyu, Sihuan Zhang, Xianfeng Wu, et al. "DNA methylation pattern of the goat <i>PITX1</i> gene and its effects on milk performance." Archives Animal Breeding 62, no. 1 (2019): 59–68. http://dx.doi.org/10.5194/aab-62-59-2019.

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Abstract. Paired-like homeodomain transcription factor 1 (PITX1) is a pivotal gene in the hypothalamic–pituitary–adrenal axis, which is a well-known pathway affecting lactation performance. The aim of this study was to analyze the DNA methylation profile of the PITX1 gene and its relevance to milk performance in Xinong Saanen dairy goats; thus, potential epigenetic markers of lactation performance were identified. A total of 267 goat blood samples were divided into “low” and “high” groups according to two milk traits: the average milk yield (AMY) and the average milk density (AMD). One CpG isl

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Yin, Hong, and K. L. Blanchard. "DNA methylation represses the expression of the human erythropoietin gene by two different mechanisms." Blood 95, no. 1 (2000): 111–19. http://dx.doi.org/10.1182/blood.v95.1.111.

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Abstract The human erythropoietin gene is expressed predominantly in the kidney and liver in response to hypoxia. Although the signaling cascade for hypoxia is present in many different cell types, the expression of erythropoietin is restricted to only a few tissues. The authors show that the promoter and 5′-untranslated region (5′-UTR) of the erythropoietin gene comprise a CpG island and that methylation of the CpG island correlates inversely with expression. Methylation represses the expression of the erythropoietin gene in 2 ways: high-density methylation of the 5′-UTR recruits a methyl-CpG

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Yin, Hong, and K. L. Blanchard. "DNA methylation represses the expression of the human erythropoietin gene by two different mechanisms." Blood 95, no. 1 (2000): 111–19. http://dx.doi.org/10.1182/blood.v95.1.111.001k20_111_119.

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The human erythropoietin gene is expressed predominantly in the kidney and liver in response to hypoxia. Although the signaling cascade for hypoxia is present in many different cell types, the expression of erythropoietin is restricted to only a few tissues. The authors show that the promoter and 5′-untranslated region (5′-UTR) of the erythropoietin gene comprise a CpG island and that methylation of the CpG island correlates inversely with expression. Methylation represses the expression of the erythropoietin gene in 2 ways: high-density methylation of the 5′-UTR recruits a methyl-CpG binding

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Izzi, Benedetta, Mariaelena Pistoni, Katrien Cludts, et al. "Allele-specific DNA methylation reinforces PEAR1 enhancer activity." Blood 128, no. 7 (2016): 1003–12. http://dx.doi.org/10.1182/blood-2015-11-682153.

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Key Points Rs12041331 is the first functional CpG-SNP related to platelet function whose regulatory mechanism depends on DNA methylation. Rs12041331 marks allele-specific methylation at the CpG island encompassing the first untranslated exon during megakaryopoiesis.

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Kapatai, Georgia, Stephen O. Nyangoma, Hannah M. Martin, and Pamela R. Kearns. "DNA Methylation in Resistant Paediatric Acute Lymphoblastic Leukaemia." Blood 112, no. 11 (2008): 1185. http://dx.doi.org/10.1182/blood.v112.11.1185.1185.

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Abstract Aberrant DNA methylation is a frequent phenomenon in paediatric acute lymphoblastic leukaemia (ALL). Increased methylation has been identified as an independent factor of poor prognosis in paediatric ALL patients. This study investigates the evolution of epigenetic changes in resistant and relapsed paediatric ALL to increase our understanding of the mechanisms of treatment failure in these patients. The primary objective is to establish global DNA methylation profile in ALL and whether changes in this profile are associated with chemo-resistance and relapse. We performed a genome-wide

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Shin, So-Hyun, Seog-Yun Park, Jae-Sung Ko, Nayoung Kim, and Gyeong Hoon Kang. "Aberrant CpG Island Hypermethylation in Pediatric Gastric Mucosa in Association With Helicobacter pylori Infection." Archives of Pathology & Laboratory Medicine 135, no. 6 (2011): 759–65. http://dx.doi.org/10.5858/2010-0140-oa.1.

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Abstract Context.—Helicobacter pylori infection is primarily acquired during childhood and persists throughout life in the absence of eradication with antibiotics. Helicobacter pylori infection induces methylation in the promoter CpG island loci in gastric epithelial cells. Thus, aberrant CpG island hypermethylation in gastric epithelial cells likely occurs early in life, although there are no existing data supporting this notion. Objectives.—To identify whether aberrant CpG island hypermethylation occurs in pediatric stomach mucosa in association with H pylori infection and to compare methyla

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Roels, Juliette, Morgan Thénoz, Bronisława Szarzyńska, et al. "Aging of Preleukemic Thymocytes Drives CpG Island Hypermethylation in T-Cell Acute Lymphoblastic Leukemia." Blood 136, Supplement 1 (2020): 28–29. http://dx.doi.org/10.1182/blood-2020-138501.

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During the last decade, aberrant DNA methylation has been identified as a hallmark of human cancer and several studies have highlighted the potential of DNA methylation as a clinically or diagnostically relevant biomarker. In comparison to their normal healthy counterparts, cancer cells generally display DNA hypermethylation at specific CpG islands, but the actual mechanism that drives this so-called CpG island methylator phenotype (CIMP) remains poorly understood. To profile the DNA methylation landscape of human T-cell acute lymphoblastic leukemia (T-ALL), we analyzed 109 T-ALLs together wit

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Chan, Annie, and Asif Rashid. "CpG Island Methylation in Precursors of Gastrointestinal Malignancies." Current Molecular Medicine 6, no. 4 (2006): 401–8. http://dx.doi.org/10.2174/156652406777435417.

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Feltus, F. Alex, Eva K. Lee, Joseph F. Costello, Christoph Plass, and Paula M. Vertino. "DNA motifs associated with aberrant CpG island methylation." Genomics 87, no. 5 (2006): 572–79. http://dx.doi.org/10.1016/j.ygeno.2005.12.016.

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Sato, Norihiro, Noriyoshi Fukushima, Ralph H. Hruban, and Michael Goggins. "CpG island methylation profile of pancreatic intraepithelial neoplasia." Modern Pathology 21, no. 3 (2007): 238–44. http://dx.doi.org/10.1038/modpathol.3800991.

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Seeliger, Barbara, Stefan Wilop, Rainhardt Osieka, Oliver Galm, and Edgar Jost. "CpG island methylation patterns in chronic lymphocytic leukemia." Leukemia & Lymphoma 50, no. 3 (2009): 419–26. http://dx.doi.org/10.1080/10428190902756594.

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Moulin, A. P., G. Clement, F. T. Bosman, L. Zografos, and J. Benhattar. "Methylation of CpG island promoters in uveal melanoma." British Journal of Ophthalmology 92, no. 2 (2008): 281–85. http://dx.doi.org/10.1136/bjo.2007.127035.

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Sahm, F., U. Lass, C. Herold-Mende, A. von Deimling, C. Hartmann, and W. Mueller. "Analysis ofCIC-associated CpG island methylation in oligoastrocytoma." Neuropathology and Applied Neurobiology 39, no. 7 (2013): 831–36. http://dx.doi.org/10.1111/nan.12045.

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Rideout, W. M., P. Eversole-Cire, C. H. Spruck, et al. "Progressive increases in the methylation status and heterochromatinization of the myoD CpG island during oncogenic transformation." Molecular and Cellular Biology 14, no. 9 (1994): 6143–52. http://dx.doi.org/10.1128/mcb.14.9.6143.

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Alterations in DNA methylation patterns are one of the earliest and most common events in tumorigenesis. Overall levels of genomic methylation often decrease during transformation, but localized regions of increased methylation have been observed in the same tumors. We have examined changes in the methylation status of the muscle determination gene myoD, which contains a CpG island, as a function of oncogenic transformation. This CpG island underwent de novo methylation during immortalization of 10T1/2 cells, and progressively more sites became methylated during the subsequent transformation o

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Rideout, W. M., P. Eversole-Cire, C. H. Spruck, et al. "Progressive increases in the methylation status and heterochromatinization of the myoD CpG island during oncogenic transformation." Molecular and Cellular Biology 14, no. 9 (1994): 6143–52. http://dx.doi.org/10.1128/mcb.14.9.6143-6152.1994.

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Alterations in DNA methylation patterns are one of the earliest and most common events in tumorigenesis. Overall levels of genomic methylation often decrease during transformation, but localized regions of increased methylation have been observed in the same tumors. We have examined changes in the methylation status of the muscle determination gene myoD, which contains a CpG island, as a function of oncogenic transformation. This CpG island underwent de novo methylation during immortalization of 10T1/2 cells, and progressively more sites became methylated during the subsequent transformation o

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Hatzimichael, Eleftheria, Aggeliki Dasoula, George Dranitsaris, et al. "BIK (Bcl2-Interacting Killer) CpG Methylation Status in Multiple Myeloma Patients: a Potential Predictor of Relapsed/Refractory Disease." Blood 114, no. 22 (2009): 2397. http://dx.doi.org/10.1182/blood.v114.22.2397.2397.

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Abstract Abstract 2397 Poster Board II-374 Background-Aim: BIK (bcl2-interacting killer) is the founding member of the BH3-only family proapoptotic proteins and is implicated in the selection of B cells in humans. The expression of BIK in cancer is prevented by chromosomal deletions or by epigenetic silencing. On the other hand, BIK upregulation is induced by proteasome inhibitors such as bortezomib and MG132. Although it has been shown that BIK is a target of epigenetic silencing in the IL-6 dependent multiple myeloma cell line KAS-6/1, no studies exist regarding the CpG methylation status of

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Tahara, Sayumi, Tomomitsu Tahara, Noriyuki Horiguchi, et al. "Lower LINE-1 methylation is associated with promoter hypermethylation and distinct molecular features in gastric cancer." Epigenomics 11, no. 15 (2019): 1651–59. http://dx.doi.org/10.2217/epi-2019-0091.

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Aim: To investigate the associations between LINE1 methylation, an indicator for genome-wide hypomethylation, molecular and clinicopathological characteristics of gastric cancer (GC) patients. Patients & methods: LINE1 methylation statuses were examined in paired cancerous, non-neoplastic mucosa from 217 GC and gastric mucosa from separate group of 224 noncancer patients. CpG island methylator phenotype, TP53 and KRAS mutation, MLH1 methylation status and promoter hypermethylation of GC related and H. pylori-related genes were examined. Results: Lower LINE1 methylation was observed in prim

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Du, Xin, Leng Han, An-Yuan Guo, and Zhongming Zhao. "Features of Methylation and Gene Expression in the Promoter-Associated CpG Islands Using Human Methylome Data." Comparative and Functional Genomics 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/598987.

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CpG islands are typically located in the 5′end of genes and considered as gene markers because they play important roles in gene regulation via epigenetic change. In this study, we compared the features of CpG islands identified by several major algorithms by setting the parameter cutoff values in order to obtain a similar number of CpG islands in a genome. This approach allows us to systematically compare the methylation and gene expression patterns in the identified CpG islands. We found that Takai and Jones’ algorithm tends to identify longer CpG islands but with weaker CpG island features

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Rietze, Allison H., Yvette P. Conley, Dianxu Ren, et al. "DNA Methylation of Endoglin Pathway Genes in Pregnant Women With and Without Preeclampsia." Epigenetics Insights 13 (January 2020): 251686572095968. http://dx.doi.org/10.1177/2516865720959682.

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Objective: We compared blood-based DNA methylation levels of endoglin ( ENG) and transforming growth factor beta receptor 2 ( TGFβR2) gene promoter regions between women with clinically-overt preeclampsia and women with uncomplicated, normotensive pregnancies. Methods: We used EpiTect Methyl II PCR Assays to evaluate DNA methylation of CpG islands located in promoter regions of ENG (CpG Island 114642) and TGFβR2 (CpG Island 110111). Preeclampsia was diagnosed based on blood pressure, protein, and uric acid criteria. N = 21 nulliparous preeclampsia case participants were 1:1 frequency matched t

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Bender, Christina M., Mark L. Gonzalgo, Felicidad A. Gonzales, Carvell T. Nguyen, Keith D. Robertson, and Peter A. Jones. "Roles of Cell Division and Gene Transcription in the Methylation of CpG Islands." Molecular and Cellular Biology 19, no. 10 (1999): 6690–98. http://dx.doi.org/10.1128/mcb.19.10.6690.

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ABSTRACT De novo methylation of CpG islands within the promoters of eukaryotic genes is often associated with their transcriptional repression, yet the methylation of CpG islands located downstream of promoters does not block transcription. We investigated the kinetics of mRNA induction, demethylation, and remethylation of the p16promoter and second-exon CpG islands in T24 cells after 5-aza-2′-deoxycytidine (5-Aza-CdR) treatment to explore the relationship between CpG island methylation and gene transcription. The rates of remethylation of both CpG islands were associated with time but not wit

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Macleod, Donald, Robin R. Ali та Adrian Bird. "An Alternative Promoter in the Mouse Major Histocompatibility Complex Class II I-Aβ Gene: Implications for the Origin of CpG Islands". Molecular and Cellular Biology 18, № 8 (1998): 4433–43. http://dx.doi.org/10.1128/mcb.18.8.4433.

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ABSTRACT Nonmethylated CpG islands are generally located at the 5′ ends of genes, but a CpG island in the mouse major histocompatibility complex class II I-Aβ gene is remote from the promoter and covers exon 2. We have found that this CpG island includes a novel intronic promoter that is active in embryonic and germ cells. The resulting transcript potentially encodes a severely truncated protein which would lack the signal peptide and external β1 domains. The functional significance of the internal CpG island may be to facilitate gene conversion, thereby sustaining the high level of polymorphi

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Esteller, Manel. "ABERRANT DNA METHYLATION AS A CANCER-INDUCING MECHANISM." Annual Review of Pharmacology and Toxicology 45, no. 1 (2005): 629–56. http://dx.doi.org/10.1146/annurev.pharmtox.45.120403.095832.

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Aberrant DNA methylation is the most common molecular lesion of the cancer cell. Neither gene mutations (nucleotide changes, deletions, recombinations) nor cytogenetic abnormalities are as common in human tumors as DNA methylation alterations. The most studied change of DNA methylation in neoplasms is the silencing of tumor suppressor genes by CpG island promoter hypermethylation, which targets genes such as p16INK4a, BRCA1, and hMLH1. There is a profile of CpG island hypermethylation according to the tumor type, and genes silent by methylation represent all cellular pathways. The introduction

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Sandler, Anna, Jonathan Anderson, Ariane Balaram, et al. "Decitabine treatment demethylates vast majority of high-confidence differentially methylated regions in HCT-116 colorectal cancer cells." F1000Research 9 (August 4, 2020): 886. http://dx.doi.org/10.12688/f1000research.20442.1.

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Background: Gene silencing by CpG island hypermethylation often plays a role in colorectal cancer (CRC) progression. Certain regions of the genome, called high confidence differentially-methylated regions (DMRs), are consistently hypermethylated across numerous patient samples. Methods: In this study, we used bioinformatics and bisulfite PCR sequencing of HCT-116 cells to investigate methylation levels at DMRs in the promoters of six genes: DKK3, EN1, MiR34b, SDC2, SPG20, and TLX1. We then investigated whether the anti-cancer drug decitabine, had a demethylating effect at these promoter region

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AL-Eitan, Laith N., Mansour A. Alghamdi, Amneh H. Tarkhan, and Firas A. Al-Qarqaz. "Genome-Wide CpG Island Methylation Profiles of Cutaneous Skin with and without HPV Infection." International Journal of Molecular Sciences 20, no. 19 (2019): 4822. http://dx.doi.org/10.3390/ijms20194822.

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HPV infection is one of the most commonly transmitted diseases among the global population. While it can be asymptomatic, non-genital HPV infection often gives rise to cutaneous warts, which are benign growths arising from the epidermal layer of the skin. This study aimed to produce a global analysis of the ways in which cutaneous wart formation affected the CpG island methylome. The Infinium MethylationEPIC BeadChip microarray was utilized in order to quantitatively interrogate CpG island methylation in genomic DNA extracted from 24 paired wart and normal skin samples. Differential methylatio

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Strunnikova, Maria, Undraga Schagdarsurengin, Astrid Kehlen, James C. Garbe, Martha R. Stampfer, and Reinhard Dammann. "Chromatin Inactivation Precedes De Novo DNA Methylation during the Progressive Epigenetic Silencing of the RASSF1A Promoter." Molecular and Cellular Biology 25, no. 10 (2005): 3923–33. http://dx.doi.org/10.1128/mcb.25.10.3923-3933.2005.

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ABSTRACT Epigenetic inactivation of the RASSF1A tumor suppressor by CpG island methylation was frequently detected in cancer. However, the mechanisms of this aberrant DNA methylation are unknown. In the RASSF1A promoter, we characterized four Sp1 sites, which are frequently methylated in cancer. We examined the functional relationship between DNA methylation, histone modification, Sp1 binding, and RASSF1A expression in proliferating human mammary epithelial cells. With increasing passages, the transcription of RASSF1A was dramatically silenced. This inactivation was associated with deacetylati

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Stumpel, Dominique J. P. M., Pauline Schneider, Eddy H. J. van Roon, et al. "Distinct Methylation Patterns among Infants with MLL Rearranged Acute Lymphoblastic Leukemia." Blood 110, no. 11 (2007): 2794. http://dx.doi.org/10.1182/blood.v110.11.2794.2794.

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Abstract Acute Lymphoblastic Leukemia (ALL) in infants (i.e. children <1 year of age) is characterized by a high incidence of rearrangements of the MLL gene (∼80%) which is associated with a poor prognosis. The most frequent MLL rearrangements in infant ALL are translocations t(4;11), t(11;19) and t(9;11). Recently, gene expression profiling has established MLL rearranged leukemia as a unique type of leukemia (denoted MLL), that is clearly distinguishable from other ALL subtypes. Currently, these gene expression profiles are slowly revealing important genetic properties underlying this aggr

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Hornstra, I. K., and T. P. Yang. "High-resolution methylation analysis of the human hypoxanthine phosphoribosyltransferase gene 5' region on the active and inactive X chromosomes: correlation with binding sites for transcription factors." Molecular and Cellular Biology 14, no. 2 (1994): 1419–30. http://dx.doi.org/10.1128/mcb.14.2.1419.

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DNA methylation within GC-rich promoters of constitutively expressed X-linked genes is correlated with transcriptional silencing on the inactive X chromosome in female mammals. For most X-linked genes, X chromosome inactivation results in transcriptionally active and inactive alleles occupying each female nucleus. To examine mechanisms responsible for maintaining this unique system of differential gene expression, we have analyzed the methylation of individual cytosine residues in the 5' CpG island of the human hypoxanthine phosphoribosyltransferase (HPRT) gene on the active and inactive X chr

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Hornstra, I. K., and T. P. Yang. "High-resolution methylation analysis of the human hypoxanthine phosphoribosyltransferase gene 5' region on the active and inactive X chromosomes: correlation with binding sites for transcription factors." Molecular and Cellular Biology 14, no. 2 (1994): 1419–30. http://dx.doi.org/10.1128/mcb.14.2.1419-1430.1994.

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DNA methylation within GC-rich promoters of constitutively expressed X-linked genes is correlated with transcriptional silencing on the inactive X chromosome in female mammals. For most X-linked genes, X chromosome inactivation results in transcriptionally active and inactive alleles occupying each female nucleus. To examine mechanisms responsible for maintaining this unique system of differential gene expression, we have analyzed the methylation of individual cytosine residues in the 5' CpG island of the human hypoxanthine phosphoribosyltransferase (HPRT) gene on the active and inactive X chr

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Barnett, Addison, Anas Saeed Bamashmos, Hong Li, et al. "PATH-62. QUANTITATIVE ANALYSIS OF SEX-ASSOCIATED MGMT METHYLATION IN NEWLY DIAGNOSED GLIOBLASTOMA." Neuro-Oncology 21, Supplement_6 (2019): vi157. http://dx.doi.org/10.1093/neuonc/noz175.657.

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Abstract INTRO/OBJECTIVE Glioblastoma (GBM) and MGMT have been reported to have sexual dimorphism. In multiple studies, including our own population-based cohort analysis, females had higher rates of MGMT methylation and improved methylation-associated progression-free and overall survival outcomes compared to males. MGMT methylation is assessed as a mean of five cysteine-phosphate-guanine (CpG1-5) islands (CpG methylation is highly inversely correlated with MGMT RNA expression). The primary objective of this study was to investigate differences in mean and individual CpG methylation by sex. M

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Saied, Marwa, Sabah Khaled, Thomas Down, et al. "Genome Wide Study of DNA Methylation In AML." Blood 116, no. 21 (2010): 3618. http://dx.doi.org/10.1182/blood.v116.21.3618.3618.

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Abstract Abstract 3618 DNA methylation is the most stable epigenetic modification and has a major role in cancer initiation and progression. The two main aims for this research were, firstly, to use the genome wide analysis of DNA methylation to better understand the development of acute myeloid leukemia (AML). The second aim was to detect differentially methylated genes/regions between certain subtypes of AML and normal bone marrow (NBM). We used the methylated DNA immunoprecipitation technique followed by high-throughput sequencing by Illumina Genome Analyser II (MeDIP -seq) for 9 AML sample

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CHAN, A., J. ISSA, J. MORRIS, S. HAMILTTON, and A. RASHID. "CpG Island methylation and the pathogenesis of hyperplastic polyposis." Gastroenterology 120, no. 5 (2001): A292. http://dx.doi.org/10.1016/s0016-5085(01)81449-9.

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Vaughn, Cecily P., Andrew R. Wilson, and Wade S. Samowitz. "Quantitative evaluation of CpG island methylation in hyperplastic polyps." Modern Pathology 23, no. 1 (2009): 151–56. http://dx.doi.org/10.1038/modpathol.2009.150.

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Chan, Annie O., Jean-Pierre J. Issa, Jeffrey S. Morris, Stanley R. Hamiltton, and Asif Rashid. "CpG Island methylation and the pathogenesis of hyperplastic polyposis." Gastroenterology 120, no. 5 (2001): A292. http://dx.doi.org/10.1016/s0016-5085(08)81449-7.

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