'; ?> geneimprint : Hot off the Press http://www.geneimprint.com/site/hot-off-the-press Daily listing of the most recent articles in epigenetics and imprinting, collected from the PubMed database. en-us Mon, 27 Jun 2022 13:17:32 EDT Mon, 27 Jun 2022 13:17:32 EDT jirtle@radonc.duke.edu james001@jirtle.com Epigenetic promoter alterations in GI tumour immune-editing and resistance to immune checkpoint inhibition. Sundar R, Huang KK, Kumar V, Ramnarayanan K, Demircioglu D, Her Z, Ong X, Bin Adam Isa ZF, Xing M, Tan AL, Tai DWM, Choo SP, Zhai W, Lim JQ, Das Thakur M, Molinero L, Cha E, Fasso M, Niger M, Pietrantonio F, Lee J, Jeyasekharan AD, Qamra A, Patnala R, Fabritius A, De Simone M, Yeong J, Ng CCY, Rha SY, Narita Y, Muro K, Guo YA, Skanderup AJ, So JBY, Yong WP, Chen Q, Göke J, Tan P
Gut (Jul 2022)

Epigenomic alterations in cancer interact with the immune microenvironment to dictate tumour evolution and therapeutic response. We aimed to study the regulation of the tumour immune microenvironment through epigenetic alternate promoter use in gastric cancer and to expand our findings to other gastrointestinal tumours.]]>
Wed, 31 Dec 1969 19:00:00 EST
Current and emerging molecular and epigenetic disease entities in acute myeloid leukemia and a critical assessment of their therapeutic modalities. Zhao X, Liu HQ, Wang LN, Yang L, Liu XL
Semin Cancer Biol (08 2022)

Acute myeloid leukemia (AML) is the most frequently diagnosed acute leukemia, and its incidence increases with age. Although the etiology of AML remains unknown, exposure to genotoxic agents or some prior hematologic disorders could lead to the development of this condition. The pathogenesis of AML involves the development of malignant transformation of hematopoietic stem cells that undergo successive genomic alterations, ultimately giving rise to a full-blown disease. From the disease biology perspective, AML is considered to be extremely complex with significant genetic, epigenetic, and phenotypic variations. Molecular and cytogenetic alterations in AML include mutations in those subsets of genes that are involved in normal cell proliferation, maturation and survival, thus posing significant challenge to targeting these pathways without attendant toxicity. In addition, multiple malignant cells co-exist in the majority of AML patients. Individual subclones are characterized by unique genetic and epigenetic abnormalities, which contribute to the differences in their response to treatment. As a result, despite a dramatic progress in our understanding of the pathobiology of AML, not much has changed in therapeutic approaches to treat AML in the past four decades. Dose and regimen modifications with improved supportive care have contributed to improved outcomes by reducing toxicity-related side effects. Several drug candidates are currently being developed, including targeted small-molecule inhibitors, cytotoxic chemotherapies, monoclonal antibodies and epigenetic drugs. This review summarizes the current state of affairs in the pathobiological and therapeutic aspects of AML.]]>
Wed, 31 Dec 1969 19:00:00 EST
Role of epigenetics in carcinogenesis: Recent advancements in anticancer therapy. Hussain S, Tulsyan S, Dar SA, Sisodiya S, Abiha U, Kumar R, Mishra BN, Haque S
Semin Cancer Biol (08 2022)

The role of epigenetics in the etiology of cancer progression is being emphasized for the past two decades to check the impact of chromatin modifiers and remodelers. Histone modifications, DNA methylation, chromatin remodeling, nucleosome positioning, regulation by non-coding RNAs and precisely microRNAs are influential epigenetic marks in the field of progressive cancer sub-types. Furthermore, constant epigenetic changes due to hyper or hypomethylation could efficiently serve as effective biomarkers of cancer diagnosis and therapeutic development. Ongoing research in the field of epigenetics has resulted in the resolutory role of various epigenetic markers and their inhibition using specific inhibitors to arrest their key cellular functions in in-vitro and pre-clinical studies. Although, the mechanism of epigenetics in cancer largely remains unexplored. Nevertheless, various advancements in the field of epigenetics have been made through transcriptome analysis and in-vitro genome targeting technologies to unravel the applicability of epigenetic markers for future cancer therapeutics and management. Therefore, this review emphasizes on recent advances in epigenetic landscapes that could be targeted/explored using novel approaches as personalized treatment modalities for cancer containment.]]>
Wed, 31 Dec 1969 19:00:00 EST
Generation of a human iPSC line CIBi011-A from amniocytes of a healthy fetus. Shi Y, Wu S, Yang B, Yu B, Yan Y, Yang J, Chu M, Hu X
Stem Cell Res (Jul 2022)

Human induced pluripotent stem cells (iPSC) resemble human embryonic stem cells with potential to differentiate into cells of all adult tissues. Nonetheless human iPSCs may have an epigenetic memory of their donor tissue origin, are easier to differentiate to those lineages, and their potential to other cell fates can be controlled. We generated a human iPSC line CIBi011-A from amniocytes of a healthy fetus. CIBi011-A serves as a useful source to investigate the epigenetic memory of iPSCs. As an iPSC line from a healthy donor, this line can also serve as a potential cell source from which to develop stem cell-based cell therapies.]]>
Wed, 31 Dec 1969 19:00:00 EST
Epigenetic signature associated with thyroid cancer progression and metastasis. Zhang H, Duan HL, Wang S, Liu Y, Ding GN, Lin RX
Semin Cancer Biol (08 2022)

Thyroid cancer is not among the top cancers in terms of diagnosis or mortality but it still ranks fifth among the cancers diagnosed in women. Infact, women are more likely to be diagnosed with thyroid cancer than the males. The burden of thyroid cancer has dramatically increased in last two decades in China and, in the United States, it is the most diagnosed cancer in young adults under the age of twenty-nine. All these factors make it worthwhile to fully understand the pathogenesis of thyroid cancer. Towards this end, microRNAs (miRNAs) have constantly emerged as the non-coding RNAs of interest in various thyroid cancer subtypes on which there have been numerous investigations over the last decade and half. This comprehensive review takes a look at the current knowledge on the topic with cataloging of miRNAs known so far, particularly related to their utility as epigenetic signatures of thyroid cancer progression and metastasis. Such information could be of immense use for the eventual development of miRNAs as therapeutic targets or even therapeutic agents for thyroid cancer therapy.]]>
Wed, 31 Dec 1969 19:00:00 EST
Epigenetic and breast cancer therapy: Promising diagnostic and therapeutic applications. Sher G, Salman NA, Khan AQ, Prabhu KS, Raza A, Kulinski M, Dermime S, Haris M, Junejo K, Uddin S
Semin Cancer Biol (08 2022)

The global burden of breast cancer (BC) is increasing significantly. This trend is caused by several factors such as late diagnosis, limited treatment options for certain BC subtypes, drug resistance which all lead to poor clinical outcomes. Recent research has reported the role of epigenetic alterations in the mechanism of BC pathogenesis and its hallmarks include drug resistance and stemness features. The understanding of these modifications and their significance in the management of BC carcinogenesis is challenging and requires further attention. Nevertheless, it promises to provide novel insight needed for utilizing these alterations as potential diagnostic, prognostic markers, predict treatment efficacy, as well as therapeutic agents. This highlights the importance of continuing research development to further advance the existing knowledge on epigenetics and BC carcinogenesis to overcome the current challenges. Hence, this review aims to shed light and discuss the current state of epigenetics research in the diagnosis and management of BC.]]>
Wed, 31 Dec 1969 19:00:00 EST
Epigenetic reprogramming during prostate cancer progression: A perspective from development. Goel S, Bhatia V, Biswas T, Ateeq B
Semin Cancer Biol (08 2022)

Conrad Waddington's theory of epigenetic landscape epitomize the process of cell fate and cellular decision-making during development. Wherein the epigenetic code maintains patterns of gene expression in pluripotent and differentiated cellular states during embryonic development and differentiation. Over the years disruption or reprogramming of the epigenetic landscape has been extensively studied in the course of cancer progression. Cellular dedifferentiation being a key hallmark of cancer allow us to take cues from the biological processes involving epigenetic reprogramming in development such as the cellular differentiation and morphogenesis. Here, we discuss the role of epigenetic landscape and its modifiers in cell-fate determination, differentiation and prostate cancer progression. Lately, the emergence of RNA-modifications has also furthered our understanding of epigenetics in cancer. The overview of the epigenetic code regulating androgen signalling, and progression to aggressive neuroendocrine stage of PCa reinforces its gene regulatory functions during the development of prostate gland as well as cancer progression. Additionally, we also highlight the clinical implications of cancer cell epigenome, and discuss the recent advancements in the therapeutic strategies targeting the advanced stage disease.]]>
Wed, 31 Dec 1969 19:00:00 EST
Epigenetics of type 2 diabetes mellitus and weight change - a tool for precision medicine? Ling C, Bacos K, Rönn T
Nat Rev Endocrinol (Jul 2022)

Pioneering studies performed over the past few decades demonstrate links between epigenetics and type 2 diabetes mellitus (T2DM), the metabolic disorder with the most rapidly increasing prevalence in the world. Importantly, these studies identified epigenetic modifications, including altered DNA methylation, in pancreatic islets, adipose tissue, skeletal muscle and the liver from individuals with T2DM. As non-genetic factors that affect the risk of T2DM, such as obesity, unhealthy diet, physical inactivity, ageing and the intrauterine environment, have been associated with epigenetic modifications in healthy individuals, epigenetics probably also contributes to T2DM development. In addition, genetic factors associated with T2DM and obesity affect the epigenome in human tissues. Notably, causal mediation analyses found DNA methylation to be a potential mediator of genetic associations with metabolic traits and disease. In the past few years, translational studies have identified blood-based epigenetic markers that might be further developed and used for precision medicine to help patients with T2DM receive optimal therapy and to identify patients at risk of complications. This Review focuses on epigenetic mechanisms in the development of T2DM and the regulation of body weight in humans, with a special focus on precision medicine.]]>
Wed, 31 Dec 1969 19:00:00 EST
CRISPR/Cas mediated epigenome editing for cancer therapy. Ansari I, Chaturvedi A, Chitkara D, Singh S
Semin Cancer Biol (08 2022)

The understanding of the relationship between epigenetic alterations, their effects on gene expression and the knowledge that these epigenetic alterations are reversible, have opened up new therapeutic pathways for treating various diseases, including cancer. This has led the research for a better understanding of the mechanism and pathways of carcinogenesis and provided the opportunity to develop the therapeutic approaches by targeting such pathways. Epi-drugs, DNA methyl transferase (DNMT) inhibitors and histone deacetylase (HDAC) inhibitors are the best examples of epigenetic therapies with clinical applicability. Moreover, precise genome editing technologies such as CRISPR/Cas has proven their efficacy in epigenome editing, including the alteration of epigenetic markers, such as DNA methylation or histone modification. The main disadvantage with DNA gene editing technologies is off-target DNA sequence alteration, which is not an issue with epigenetic editing. It is known that cancer is linked with epigenetic alteration, and thus CRISPR/Cas system shows potential for cancer therapy via epigenome editing. This review outlines the epigenetic therapeutic approach for cancer therapy using CRISPR/Cas, from the basic understanding of cancer epigenetics to potential applications of CRISPR/Cas in treating cancer.]]>
Wed, 31 Dec 1969 19:00:00 EST
In-utero exposure to indoor air pollution or tobacco smoke and cognitive development in a South African birth cohort study. Christensen GM, Rowcliffe C, Chen J, Vanker A, Koen N, Jones MJ, Gladish N, Hoffman N, Donald KA, Wedderburn CJ, Kobor MS, Zar HJ, Stein DJ, Hüls A
Sci Total Environ (Aug 2022)

There is increasing evidence indicating that air pollution exposure is associated with neuronal damage. Since pregnancy is a critical window of vulnerability, air pollution exposure during this period could have adverse effects on neurodevelopment. This study aims 1) to analyze associations of prenatal exposure to indoor air pollution (particulate matter with diameters ≤10 μm, PM) and tobacco smoke with neurodevelopment and 2) to determine whether these associations are mediated by deviations of epigenetic gestational age from chronological gestational age (ΔGA).]]>
Wed, 31 Dec 1969 19:00:00 EST
Targeting epigenetic regulatory machinery to overcome cancer therapy resistance. Guo L, Lee YT, Zhou Y, Huang Y
Semin Cancer Biol (08 2022)

Drug resistance, either intrinsic or acquired, represents a major hurdle to achieving optimal therapeutic outcomes during cancer treatment. In addition to acquisition of resistance-conferring genetic mutations, accumulating evidence suggests an intimate involvement of the epigenetic machinery in this process as well. Recent studies have revealed that epigenetic reprogramming, such as altered expression or relocation of DNA/histone modulators accompanied with chromatin structure remodeling, can lead to transcriptional plasticity in tumor cells, thereby driving their transformation towards a persistent state. These "persisters" represent a pool of slow-growing cells that can either re-expand when treatment is discontinued or acquire permanent resistance. Targeting epigenetic reprogramming or plasticity represents a new strategy to prevent the emergence of drug-refractory populations and to enable more consistent clinical responses. With the growing numbers of drugs or drug candidates developed to target epigenetic regulators, more and more epigenetic therapies are under preclinical evaluation, early clinical trials or approved by FDA as single agent or in combination with existing antitumor drugs. In this review, we highlight latest discoveries in the mechanistic understanding of epigenetically-induced drug resistance. In parallel, we discuss the potential of combining epigenetic drugs with existing anticancer regimens as a promising strategy for overcoming cancer drug resistance.]]>
Wed, 31 Dec 1969 19:00:00 EST
Dietary molecules and experimental evidence of epigenetic influence in cancer chemoprevention: An insight. Ullah MF, Usmani S, Shah A, Abuduhier FM
Semin Cancer Biol (08 2022)

The world-wide rate of incidence of cancer disease has been only modestly contested by the past and current preventive and interventional strategies. Hence, the global effort towards novel ideas to contain the disease still continues. Constituents of human diets have in recent years emerged as key regulators of carcinogenesis, with studies reporting their inhibitory potential against all the three stages vis-a-vis initiation, promotion and progression. Unlike drugs which usually act on single targets, these dietary factors have an advantage of multi-targeted effects and pleiotropic action mechanisms, which are effective against cancer that manifest as a micro-evolutionary and multi-factorial disease. Since most of the cellular targets have been identified and their consumption considered relatively safe, these diet-derived agents often appear as molecules of interest in repurposing strategies. Currently, many of these molecules are being investigated for their ability to influence the aberrant alterations in cell's epigenome for epigenetic therapy against cancer. Targeting the epigenetic regulators is a new paradigm in cancer chemoprevention which acts to reverse the warped-up epigenetic alterations in a cancer cell, thereby directing it towards a normal phenotype. In this review, we discuss the significance of dietary factors and natural products as chemopreventive agents. Further, we corroborate the experimental evidence from existing literature, reflecting the ability of a series of such molecules to act as epigenetic modifiers in cancer cells, by interfering with molecular events that map the epigenetic imprints such as DNA methylation, histone acetylation and non-coding RNA mediated gene regulation.]]>
Wed, 31 Dec 1969 19:00:00 EST
Epigenetics of glioblastoma multiforme: From molecular mechanisms to therapeutic approaches. Uddin MS, Mamun AA, Alghamdi BS, Tewari D, Jeandet P, Sarwar MS, Ashraf GM
Semin Cancer Biol (08 2022)

Glioblastoma multiforme (GBM) is the most common form of brain cancer and one of the most aggressive cancers found in humans. Most of the signs and symptoms of GBM can be mild and slowly aggravated, although other symptoms might demonstrate it as an acute ailment. However, the precise mechanisms of the development of GBM remain unknown. Due to the improvement of molecular pathology, current researches have reported that glioma progression is strongly connected with different types of epigenetic phenomena, such as histone modifications, DNA methylation, chromatin remodeling, and aberrant microRNA. Furthermore, the genes and the proteins that control these alterations have become novel targets for treating glioma because of the reversibility of epigenetic modifications. In some cases, gene mutations including P16, TP53, and EGFR, have been observed in GBM. In contrast, monosomies, including removals of chromosome 10, particularly q23 and q25-26, are considered the standard markers for determining the development and aggressiveness of GBM. Recently, amid the epigenetic therapies, histone deacetylase inhibitors (HDACIs) and DNA methyltransferase inhibitors have been used for treating tumors, either single or combined. Specifically, HDACIs are served as a good choice and deliver a novel pathway to treat GBM. In this review, we focus on the epigenetics of GBM and the consequence of its mutations. We also highlight various treatment approaches, namely gene editing, epigenetic drugs, and microRNAs to combat GBM.]]>
Wed, 31 Dec 1969 19:00:00 EST
Novel multilocus imprinting disturbances in a child with expressive language delay and intellectual disability. Tayeh MK, DeVaul J, LeSueur K, Yang C, Bedoyan JK, Thomas P, Hannibal MC, Innis JW
Am J Med Genet A (Jul 2022)

Multilocus imprinting disturbances (MLID) have been associated with up to 12% of patients with Beckwith-Wiedemann syndrome, Silver-Russell syndrome, and pseudohypoparathyroidism type 1B (PHP1B). Single-gene defects affecting components of the subcortical maternal complex (SCMC) have been reported in cases with multilocus hypomethylation defects. We present a patient with speech and language impairment with mild Angelman syndrome (AS) features who demonstrates maternal hypomethylation at 15q11.2 (SNRPN) as well as 11p15.5 (KCNQ1OT1) imprinted loci, but normal methylation at 6q24.2 (PLAGL1), 7p12.1 (GRB10), 7q32.2 (MEST), 11p15.5 (H19), 14q32.2 (MEG3), 19q13.43 (PEG3), and 20q13.32 (GNAS and GNAS-AS1). The proband also has no copy number nor sequence variants within the AS imprinting center or in UBE3A. Maternal targeted next generation sequencing did not identify any pathogenic variants in ZPF57, NLRP2, NLRP5, NLRP7, KHDC3L, PADI6, TLE6, OOEP, UHRF1 or ZAR1. The presence of very delayed, yet functional speech, behavioral difficulties, EEG abnormalities but without clinical seizures, and normocephaly are consistent with the 15q11.2 hypomethylation defect observed in this patient. To our knowledge, this is the first report of MLID in a patient with mild, likely mosaic, Angelman syndrome.]]>
Wed, 31 Dec 1969 19:00:00 EST
Causes, effects, and clinical implications of perturbed patterns within the cancer epigenome. Oleksiewicz U, Machnik M
Semin Cancer Biol (08 2022)

Somatic mutations accumulating over a patient's lifetime are well-defined causative factors that fuel carcinogenesis. It is now clear, however, that epigenomic signature is also largely perturbed in many malignancies. These alterations support the transcriptional program crucial for the acquisition and maintenance of cancer hallmarks. Epigenetic instability may arise due to the genetic mutations or transcriptional deregulation of the proteins implicated in epigenetic signaling. Moreover, external stimulation and physiological aging may also participate in this phenomenon. The epigenomic signature is frequently associated with a cell of origin, as well as with tumor stage and differentiation, which all reflect its high heterogeneity across and within various tumors. Here, we will overview the current understanding of the causes and effects of the altered and heterogeneous epigenomic landscape in cancer. We will focus mainly on DNA methylation and post-translational histone modifications as the key regulatory epigenetic signaling marks. In addition, we will describe how this knowledge is translated into the clinic. We will particularly concentrate on the applicability of epigenetic alterations as biomarkers for improved diagnosis, prognosis, and prediction. Finally, we will also review current developments regarding epi-drug usage in clinical and experimental settings.]]>
Wed, 31 Dec 1969 19:00:00 EST
Modeling Susceptibility to Cardiotoxicity in Cancer Therapy Using Human iPSC-Derived Cardiac Cells and Systems Biology. Mullen M, Wen Tan WL, Rhee JW, Wu JC
Heart Fail Clin (Jul 2022)

The development of human-induced pluripotent stem cell-derived cardiac cell types has created a new paradigm in assessing drug-induced cardiotoxicity. Advances in genomics and epigenomics have also implicated several genomic loci and biological pathways that may contribute to susceptibility to cancer therapies. In this review, we first provide a brief overview of the cardiotoxicity associated with chemotherapy. We then provide a detailed summary of systems biology approaches being applied to elucidate potential molecular mechanisms involved in cardiotoxicity. Finally, we discuss combining systems biology approaches with iPSC technology to help discover molecular mechanisms associated with cardiotoxicity.]]>
Wed, 31 Dec 1969 19:00:00 EST
Use of DNA methylation profiling in translational oncology. Ortiz-Barahona V, Joshi RS, Esteller M
Semin Cancer Biol (08 2022)

DNA methylation is a highly regulated process that has a critical role in human development and homeostatic control of the cell. The number of genes affected by anomalous DNA methylation in cancer-associated pathways is swiftly accelerating and with the advancement of molecular technologies, new layers of complexity are opening up and refining our strategies to combat cancer. DNA methylation profiling is an essential facet to understanding malignant transformation and is becoming an increasingly important tool for cancer diagnosis, prognosis and therapy monitoring. In this review, the role of DNA methylation in normal cellular function is discussed, as well as how epigenetic aberrations override normal cellular cues that lead to tumor initiation and propagation. The review also focuses on the latest advancements in DNA methylation profiling as a biomarker for early cancer detection, predicting patient clinical outcomes and responses to treatment and provides new insights into epigenetic-based therapy in clinical oncology.]]>
Wed, 31 Dec 1969 19:00:00 EST
Multigenerational epigenetic inheritance: Transmitting information across generations. Burton NO, Greer EL
Semin Cell Dev Biol (Jul 2022)

Inherited epigenetic information has been observed to regulate a variety of complex organismal phenotypes across diverse taxa of life. This continually expanding body of literature suggests that epigenetic inheritance plays a significant, and potentially fundamental, role in inheritance. Despite the important role these types of effects play in biology, the molecular mediators of this non-genetic transmission of information are just now beginning to be deciphered. Here we provide an intellectual framework for interpreting these findings and how they can interact with each other. We also define the different types of mechanisms that have been found to mediate epigenetic inheritance and to regulate whether epigenetic information persists for one or many generations. The field of epigenetic inheritance is entering an exciting phase, in which we are beginning to understand the mechanisms by which non-genetic information is transmitted to, and deciphered by, subsequent generations to maintain essential environmental information without permanently altering the genetic code. A more complete understanding of how and when epigenetic inheritance occurs will advance our understanding of numerous different aspects of biology ranging from how organisms cope with changing environments to human pathologies influenced by a parent's environment.]]>
Wed, 31 Dec 1969 19:00:00 EST
Progress and promises of epigenetic drugs and epigenetic diets in cancer prevention and therapy: A clinical update. Mondal P, Natesh J, Penta D, Meeran SM
Semin Cancer Biol (08 2022)

Epigenetic modifications are heritable yet reversible, essential for normal physiological functions and biological development. Aberrant epigenetic modifications, including DNA methylation, histone modification, and non-coding RNA (ncRNA)-mediated gene regulation play a crucial role in cancer progression. In cellular reprogramming, irregular epigenomic modulations alter cell signaling pathways and the expression of tumor suppressor genes and oncogenes, resulting in cancer growth and metastasis. Therefore, alteration of epigenetic-status in cancer cells can be used as a potential target for cancer therapy. Several synthetic epigenetic inhibitors (epi-drugs) and natural epigenetic modulatory bioactives (epi-diets) have been shown to have the potential to alter the aberrant epigenetic status and inhibit cancer progression. Further, the use of combinatorial approaches with epigenetic drugs and diets has brought promising outcomes in cancer prevention and therapy. In this article, we have summarized the epigenetic modulatory activities of epi-drugs, epi-diets, and their combination against various cancers. We have also compiled the preclinical and clinical status of these epigenetic modulators in different cancers.]]>
Wed, 31 Dec 1969 19:00:00 EST
Multi-locus DNA methylation analysis of imprinted genes in cattle from somatic cell nuclear transfer. Mangiavacchi PM, Caldas-Bussiere MC, Mendonça MDS, Rumpf R, Lemos Júnior PES, Alves CS, Carneiro WDS, Dias AJB, Rios ÃFL
Theriogenology (Jul 2022)

Multi-locus methylation defects (MLMDs) in imprinted loci have been reported in Beckwith-Wiedemann Syndrome (BWS). Large offspring syndrome (LOS), a phenotypic subgroup of abnormal offspring syndrome (AOS), is considered a molecular and phenotypic model for BWS. Both LOS and BWS have presented epigenetic defects in some common imprinted loci. In this study, methylation-specific restriction digestion assay - quantitative PCR was used to analyze the DNA methylation pattern in differentially methylated regions (DMRs) of the H19 (H19-DMR), KCNQ1OT1 (KvDMR1) and PEG1/MEST (PEG1-DMR) genes in bovine clone tissues from calves that did not survive after birth. Individual and tissue-specific changes in DNA methylation levels in the bovine KvDMR1, H19-DMR, and PEG1-DMR were observed. In contrast to what has been reported in the literature on BWS and AOS/LOS, the KvDMR1 showed gain (GOM) and loss (LOM) of DNA methylation. LOM and GOM events were found in the DMRs studied in animals produced by the same nucleus donor cell line. This is the first report of epimutations in the PEG1-DMR and GOM at the KvDMR1 found in bovine clones. The findings showed that epigenetic modification in imprinted loci in cloned cattle occurred in a multi-locus pattern similar to that seen in human imprinting disorders. Other multi-locus analyzes must be done to elucidate the MLMD pattern in AOS in bovine clones.]]>
Wed, 31 Dec 1969 19:00:00 EST