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Cancer epigenomics

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https://www.readbyqxmd.com/read/28211524/epigenetic-and-genetic-dissections-of-uv-induced-global-gene-dysregulation-in-skin-cells-through-multi-omics-analyses
#1
Yao Shen, Milda Stanislauskas, Gen Li, Deyou Zheng, Liang Liu
To elucidate the complex molecular mechanisms underlying the adverse effects UV radiation (UVR) on skin homeostasis, we performed multi-omics studies to characterize UV-induced genetic and epigenetic changes. Human keratinocytes from a single donor treated with or without UVR were analyzed by RNA-seq, exome-seq, and H3K27ac ChIP-seq at 4 h and 72 h following UVR. Compared to the relatively moderate mutagenic effects of UVR, acute UV exposure induced substantial epigenomic and transcriptomic alterations, illuminating a previously underappreciated role of epigenomic and transcriptomic instability in skin pathogenesis...
February 17, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28199197/childhood-cancers-and-systems-medicine
#2
William L Stone, Kathryn J Klopfenstein, M J Hajianpour, Marcela I Popescu, Cathleen M Cook, Koymangalath Krishnan
Despite major advances in treatment, pediatric cancers in the 5-16 age group remain the most common cause of disease death, and one out of eight children with cancer will not survive. Among children that do survive, some 60% suffer from late effects such as cancer recurrence and increased risk of obesity. This paper will provide a broad overview of pediatric oncology in the context of systems medicine. Systems medicine utilizes an integrative approach that relies on patient information gained from omics technology...
March 1, 2017: Frontiers in Bioscience (Landmark Edition)
https://www.readbyqxmd.com/read/28188828/role-of-mirnas-in-human-cancer-metastasis-implications-for-therapeutic-intervention
#3
REVIEW
Mohammad Alam Jafri, Mohammed Hussein Al-Qahtani, Jerry William Shay
Metastasis is the spread and growth of localized cancer to new locations in the body and is considered the main cause of cancer-related deaths. Metastatic cancer cells display distinct genomic and epigenomic profiles and almost universally an aggressive pathophysiology. A better understanding of the molecular mechanisms and regulation of metastasis, including how metastatic tumors grow and survive in the nascent niche and the interactions of the emergent metastatic cancer cells within the local microenvironment may provide tools to design strategies to restrict metastatic dissemination...
February 8, 2017: Seminars in Cancer Biology
https://www.readbyqxmd.com/read/28187286/endogenous-dna-damage-as-a-source-of-genomic-instability-in-cancer
#4
REVIEW
Anthony Tubbs, André Nussenzweig
Genome instability, defined as higher than normal rates of mutation, is a double-edged sword. As a source of genetic diversity and natural selection, mutations are beneficial for evolution. On the other hand, genomic instability can have catastrophic consequences for age-related diseases such as cancer. Mutations arise either from inactivation of DNA repair pathways or in a repair-competent background due to genotoxic stress from celluar processes such as transcription and replication that overwhelm high-fidelity DNA repair...
February 9, 2017: Cell
https://www.readbyqxmd.com/read/28184298/recent-advances-in-understanding-assessing-toxicity-to-the-epigenome
#5
REVIEW
Kevin Sweder
The ability of non-genotoxic agents to induce cancer has been documented and clearly requires a reassessment of testing for environmental and human safety. Drug safety testing has historically relied on test batteries designed to detect DNA damage leading to mutation and cancer. The standard genetic toxicology testing battery has been a reliable tool set to identify small molecules/chemicals as hazards that could lead to genetic changes in organisms and induction of cancer. While pharmaceutical companies and regulatory agencies have extensively used the standard battery, it is not suitable for compounds that may induce epigenetic changes...
2017: F1000Research
https://www.readbyqxmd.com/read/28169291/hotspots-of-aberrant-enhancer-activity-punctuate-the-colorectal-cancer-epigenome
#6
Andrea J Cohen, Alina Saiakhova, Olivia Corradin, Jennifer M Luppino, Katreya Lovrenert, Cynthia F Bartels, James J Morrow, Stephen C Mack, Gursimran Dhillon, Lydia Beard, Lois Myeroff, Matthew F Kalady, Joseph Willis, James E Bradner, Ruth A Keri, Nathan A Berger, Shondra M Pruett-Miller, Sanford D Markowitz, Peter C Scacheri
In addition to mutations in genes, aberrant enhancer element activity at non-coding regions of the genome is a key driver of tumorigenesis. Here, we perform epigenomic enhancer profiling of a cohort of more than forty genetically diverse human colorectal cancer (CRC) specimens. Using normal colonic crypt epithelium as a comparator, we identify enhancers with recurrently gained or lost activity across CRC specimens. Of the enhancers highly recurrently activated in CRC, most are constituents of super enhancers, are occupied by AP-1 and cohesin complex members, and originate from primed chromatin...
February 7, 2017: Nature Communications
https://www.readbyqxmd.com/read/28167613/epigenomic-inactivation-of-rasgaps-activates-ras-signaling-in-a-subset-of-luminal-b-breast-cancers
#7
Rosalie Sears, Joe W Gray
Invasion and metastasis of a subset of aggressive luminal B breast cancers is driven by the concomitant inactivation of the RasGAPs DAB2IP and RASAL2. Inactivation of both proteins increases RAS activity and drives invasion, whereas inactivation of DAB2IP specifically promotes NF-κB-mediated epithelial-mesenchymal transition. Cancer Discov; 7(2); 131-3. ©2017 AACRSee related article by Olsen et al., p. 202.
February 2017: Cancer Discovery
https://www.readbyqxmd.com/read/28167242/epigenome-wide-dna-methylation-profiling-identifies-differential-methylation-biomarkers-in-high-grade-bladder-cancer
#8
Ekaterina Olkhov-Mitsel, Andrea J Savio, Ken J Kron, Vaijayanti V Pethe, Thomas Hermanns, Neil E Fleshner, Bas W van Rhijn, Theodorus H van der Kwast, Alexandre R Zlotta, Bharati Bapat
Epigenetic changes, including CpG island hypermethylation, occur frequently in bladder cancer (BC) and may be exploited for BC detection and distinction between high-grade (HG) and low-grade (LG) disease. Genome-wide methylation analysis was performed using Agilent Human CpG Island Microarrays to determine epigenetic differences between LG and HG cases. Pathway enrichment analysis and functional annotation determined that the most frequently methylated pathways in HG BC were enriched for anterior/posterior pattern specification, embryonic skeletal system development, neuron fate commitment, DNA binding, and transcription factor activity...
February 3, 2017: Translational Oncology
https://www.readbyqxmd.com/read/28157211/platelet-activating-factor-induced-expression-of-p21-is-correlated-with-histone-acetylation
#9
Elisabetta Damiani, Nahum Puebla-Osorio, Bree M Lege, Jingwei Liu, Sattva S Neelapu, Stephen E Ullrich
Ultraviolet (UV)-irradiated keratinocytes secrete the lipid mediator of inflammation, platelet-activating factor (PAF). PAF plays an essential role in UV-induced immune suppression and skin cancer induction. Dermal mast cell migration from the skin to the draining lymph nodes plays a prominent role in activating systemic immune suppression. UV-induced PAF activates mast cell migration by up-regulating mast cell CXCR4 surface expression. Recent findings indicate that PAF up-regulates CXCR4 expression via histone acetylation...
February 3, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28155687/subtype-specific-cpg-island-shore-methylation-and-mutation-patterns-in-30-breast-cancer-cell-lines
#10
Heejoon Chae, Sangseon Lee, Kenneth P Nephew, Sun Kim
BACKGROUND: Aberrant epigenetic modifications, including DNA methylation, are key regulators of gene activity in tumorigenesis. Breast cancer is a heterogeneous disease, and large-scale analyses indicate that tumor from normal and benign tissues, as well as molecular subtypes of breast cancer, can be distinguished based on their distinct genomic, transcriptomic, and epigenomic profiles. In this study, we used affinity-based methylation sequencing data in 30 breast cancer cell lines representing functionally distinct cancer subtypes to investigate methylation and mutation patterns at the whole genome level...
December 23, 2016: BMC Systems Biology
https://www.readbyqxmd.com/read/28155630/lndriver-identifying-driver-genes-by-integrating-mutation-and-expression-data-based-on-gene-gene-interaction-network
#11
Pi-Jing Wei, Di Zhang, Junfeng Xia, Chun-Hou Zheng
BACKGROUND: Cancer is a complex disease which is characterized by the accumulation of genetic alterations during the patient's lifetime. With the development of the next-generation sequencing technology, multiple omics data, such as cancer genomic, epigenomic and transcriptomic data etc., can be measured from each individual. Correspondingly, one of the key challenges is to pinpoint functional driver mutations or pathways, which contributes to tumorigenesis, from millions of functional neutral passenger mutations...
December 23, 2016: BMC Bioinformatics
https://www.readbyqxmd.com/read/28148257/epigenetics-in-cancer-stem-cells
#12
REVIEW
Tan Boon Toh, Jhin Jieh Lim, Edward Kai-Hua Chow
Compelling evidence have demonstrated that bulk tumors can arise from a unique subset of cells commonly termed "cancer stem cells" that has been proposed to be a strong driving force of tumorigenesis and a key mechanism of therapeutic resistance. Recent advances in epigenomics have illuminated key mechanisms by which epigenetic regulation contribute to cancer progression. In this review, we present a discussion of how deregulation of various epigenetic pathways can contribute to cancer initiation and tumorigenesis, particularly with respect to maintenance and survival of cancer stem cells...
February 1, 2017: Molecular Cancer
https://www.readbyqxmd.com/read/28143873/emerging-role-of-micrornas-as-liquid-biopsy-biomarkers-in-gastrointestinal-cancers
#13
Kunitoshi Shigeyasu, Shusuke Toden, Timothy J Zumwalt, Yoshinaga Okugawa, Ajay Goel
Cancer has emerged as a leading cause of mortality worldwide, claiming over 8 million lives annually. Gastrointestinal (GI) cancers account for ~35% of these mortalities. Recent advances in diagnostic and treatment strategies have reduced mortality among GI cancer patients, yet a significant number of patients still develop late-stage cancer, where treatment options are inadequate. Emerging interests in 'liquid biopsies' have encouraged investigators to identify and develop clinically-relevant noninvasive genomic and epigenomic signatures that can be exploited as biomarkers capable of detecting premalignant and early-stage cancers...
January 31, 2017: Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
https://www.readbyqxmd.com/read/28141796/epigenomic-landscape-of-5-hydroxymethylcytosine-reveals-its-transcriptional-regulation-of-lncrnas-in-colorectal-cancer
#14
Hanyang Hu, Maoguo Shu, Lin He, Xueyuan Yu, Xiangyu Liu, Yalin Lu, Yinghong Chen, Xiaoping Miao, Xiaohua Chen
BACKGROUND: DNA methylation at the 5 position of cytosine (5mC) can be converted to 5-hydroxymethylcytosine (5hmC) by the ten-eleven translocation family. The loss of global levels of 5hmC has been regarded as a hallmark in various cancers. 5-hydroxymethylcytosine is distributed at protein-coding gene bodies and promoters; however, the role and distribution of 5hmC at long non-coding RNAs (lncRNAs) is not clear. We investigated the distribution and regulatory roles of 5hmC for lncRNAs in colorectal cancer (CRC)...
January 31, 2017: British Journal of Cancer
https://www.readbyqxmd.com/read/28134926/dna-methylation-heterogeneity-defines-a-disease-spectrum-in-ewing-sarcoma
#15
Nathan C Sheffield, Gaelle Pierron, Johanna Klughammer, Paul Datlinger, Andreas Schönegger, Michael Schuster, Johanna Hadler, Didier Surdez, Delphine Guillemot, Eve Lapouble, Paul Freneaux, Jacqueline Champigneulle, Raymonde Bouvier, Diana Walder, Ingeborg M Ambros, Caroline Hutter, Eva Sorz, Ana T Amaral, Enrique de Álava, Katharina Schallmoser, Dirk Strunk, Beate Rinner, Bernadette Liegl-Atzwanger, Berthold Huppertz, Andreas Leithner, Gonzague de Pinieux, Philippe Terrier, Valérie Laurence, Jean Michon, Ruth Ladenstein, Wolfgang Holter, Reinhard Windhager, Uta Dirksen, Peter F Ambros, Olivier Delattre, Heinrich Kovar, Christoph Bock, Eleni M Tomazou
Developmental tumors in children and young adults carry few genetic alterations, yet they have diverse clinical presentation. Focusing on Ewing sarcoma, we sought to establish the prevalence and characteristics of epigenetic heterogeneity in genetically homogeneous cancers. We performed genome-scale DNA methylation sequencing for a large cohort of Ewing sarcoma tumors and analyzed epigenetic heterogeneity on three levels: between cancers, between tumors, and within tumors. We observed consistent DNA hypomethylation at enhancers regulated by the disease-defining EWS-FLI1 fusion protein, thus establishing epigenomic enhancer reprogramming as a ubiquitous and characteristic feature of Ewing sarcoma...
January 30, 2017: Nature Medicine
https://www.readbyqxmd.com/read/28129557/decoding-transcriptional-states-in-cancer
#16
REVIEW
Jasper Wouters, Zeynep Kalender Atak, Stein Aerts
Gene regulatory networks determine cellular identity. In cancer, aberrations of gene networks are caused by driver mutations that often affect transcription factors and chromatin modifiers. Nevertheless, gene transcription in cancer follows the same cis-regulatory rules as normal cells, and cancer cells have served as convenient model systems to study transcriptional regulation. Tumours often show regulatory heterogeneity, with subpopulations of cells in different transcriptional states, which has important therapeutic implications...
January 24, 2017: Current Opinion in Genetics & Development
https://www.readbyqxmd.com/read/28129023/probe-the-function-of-histone-lysine-36-methylation-using-histone-h3-lysine-36-to-methionine-mutant-transgene-in-mammalian-cells
#17
Dong Fang, Haiyun Gan, Heping Wang, Hui Zhou, Zhiguo Zhang
Chondroblastoma is a cartilaginous tumor that typically arises under 25 years of age (80%). Recent studies have identified a somatic and heterozygous mutation at the H3F3B gene in over 90% chondroblastoma cases, leading to a lysine 36 to methionine replacement (H3.3K36M). In human cells, H3F3B gene is one of two genes that encode identical H3.3 proteins. It is not known how H3.3K36M mutant proteins promote tumorigenesis. We and others have shown that, the levels of H3K36 di- and tri-methylation (H3K36me2/me3) are reduced dramatically in chondroblastomas and chondrocytes bearing the H3...
January 27, 2017: Cell Cycle
https://www.readbyqxmd.com/read/28118844/single-cell-epigenomic-variability-reveals-functional-cancer-heterogeneity
#18
Ulrike M Litzenburger, Jason D Buenrostro, Beijing Wu, Ying Shen, Nathan C Sheffield, Arwa Kathiria, William J Greenleaf, Howard Y Chang
BACKGROUND: Cell-to-cell heterogeneity is a major driver of cancer evolution, progression, and emergence of drug resistance. Epigenomic variation at the single-cell level can rapidly create cancer heterogeneity but is difficult to detect and assess functionally. RESULTS: We develop a strategy to bridge the gap between measurement and function in single-cell epigenomics. Using single-cell chromatin accessibility and RNA-seq data in K562 leukemic cells, we identify the cell surface marker CD24 as co-varying with chromatin accessibility changes linked to GATA transcription factors in single cells...
January 24, 2017: Genome Biology
https://www.readbyqxmd.com/read/28115643/zno-nanoparticles-induced-reactive-oxygen-species-promotes-multimodal-cyto-and-epigenetic-toxicity
#19
Samrat Roy Choudhury, Josue Ordaz, Chiao-Ling Lo, Nur P Damayanti, Feng Zhou, Joseph Irudayaraj
In this study we evaluated and correlated the cytotoxic effects of zinc oxide nanoparticles (ZnO-NPs) to epigenetic modifications, using human embryonic kidney (HEK-293) cells as a model system. Imaging of singlet and total reactive oxygen species (ROS) in ZnO-NPs treated live cells was performed followed by the evaluation of its effects on cytoskeletal, mitochondrial, and nuclear integrity, and on the expression of ROS responsive genes. Next, we determined the global and locus specific changes in DNA-methylation at the three genomic repeat sequences namely global LINE-1, subtelomeric D4Z4 and pericentromeric NBL2, and at the promoter of selected ROS responsive genes (AOX1, HMOX1, NCF2, SOD3)...
January 22, 2017: Toxicological Sciences: An Official Journal of the Society of Toxicology
https://www.readbyqxmd.com/read/28115635/body-hypomethylated-human-genes-harbor-extensive-intragenic-transcriptional-activity-and-are-prone-to-cancer-associated-dysregulation
#20
Isabel Mendizabal, Jia Zeng, Thomas E Keller, Soojin V Yi
Genomic DNA methylation maps (methylomes) encode genetic and environmental effects as stable chemical modifications of DNA. Variations in DNA methylation, especially in regulatory regions such as promoters and enhancers, are known to affect numerous downstream processes. In contrast, most transcription units (gene bodies) in the human genome are thought to be heavily methylated. However, epigenetic reprogramming in cancer often involves gene body hypomethylation with consequences on gene expression. In this study, we focus on the relatively unexplored phenomenon that some gene bodies are devoid of DNA methylation under normal conditions...
January 23, 2017: Nucleic Acids Research
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