'; ?> 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 Sat, 18 Jan 2020 02:29:27 EST Sat, 18 Jan 2020 02:29:27 EST jirtle@radonc.duke.edu james001@jirtle.com DNA methylation analysis of multiple imprinted DMRs in Sotos syndrome reveals IGF2-DMR0 as a DNA methylation-dependent, P0 promoter-specific enhancer. Watanabe H, Higashimoto K, Miyake N, Morita S, Horii T, Kimura M, Suzuki T, Maeda T, Hidaka H, Aoki S, Yatsuki H, Okamoto N, Uemura T, Hatada I, Matsumoto N, Soejima H
FASEB J (Jan 2020)

Haploinsufficiency of NSD1, which dimethylates histone H3 lysine 36 (H3K36), causes Sotos syndrome (SoS), an overgrowth syndrome. DNMT3A and DNMT3B recognizes H3K36 trimethylation (H3K36me3) through PWWP domain to exert de novo DNA methyltransferase activity and establish imprinted differentially methylated regions (DMRs). Since decrease of H3K36me3 and genome-wide DNA hypomethylation in SoS were observed, hypomethylation of imprinted DMRs in SoS was suggested. We explored DNA methylation status of 28 imprinted DMRs in 31 SoS patients with NSD1 defect and found that hypomethylation of IGF2-DMR0 and IG-DMR in a substantial proportion of SoS patients. Luciferase assay revealed that IGF2-DMR0 enhanced transcription from the IGF2 P0 promoter but not the P3 and P4 promoters. Chromatin immunoprecipitation-quantitative PCR (ChIP-qPCR) revealed active enhancer histone modifications at IGF2-DMR0, with high enrichment of H3K4me1 and H3 lysine 27 acetylation (H3K27ac). CRISPR-Cas9 epigenome editing revealed that specifically induced hypomethylation at IGF2-DMR0 increased transcription from the P0 promoter but not the P3 and P4 promoters. NSD1 knockdown suggested that NSD1 targeted IGF2-DMR0; however, IGF2-DMR0 DNA methylation and IGF2 expression were unaltered. This study could elucidate the function of IGF2-DMR0 as a DNA methylation dependent, P0 promoter-specific enhancer. NSD1 may play a role in the establishment or maintenance of IGF2-DMR0 methylation during the postimplantation period.]]>
Wed, 31 Dec 1969 19:00:00 EST
Short AIP1 (ASK1-Interacting Protein-1) Isoform Localizes to the Mitochondria and Promotes Vascular Dysfunction. Li Z, Li L, Zhang H, Zhou HJ, Ji W, Min W
Arterioscler Thromb Vasc Biol (Jan 2020)

Vascular endothelial cells (ECs) normally maintain vascular homeostasis and are regulated by proinflammatory cytokines and reactive oxygen species. A human genome-wide association study identified that (ASK1 [apoptosis signal-regulating kinase 1]-interacting protein-1; also identified as ) gene variants confer susceptibility to cardiovascular disease, but the underlying mechanism is unknown. Approach and Results: We detected a normal AIP1 form (named AIP1A) in the healthy aorta, but a shorter form of AIP1 (named AIP1B) was found in diseased aortae that contained atherosclerotic plaques and graft arteriosclerosis. AIP1B transcription in resting ECs was suppressed through epigenetic inhibition by RIF1 (Rap1 [ras-related protein 1]-interacting factor 1)/H3K9 (histone H3 lysine 9) methyltransferase-mediated H3K9 trimethylation, and this inhibition was released by proinflammatory cytokines. AIP1A, but not AIP1B, was downregulated by proteolytic degradation through a Smurf1 (SMAD [suppressor of mothers against decapentaplegic miscellaneous] ubiquitylation regulatory factor 1)-dependent pathway in ECs under inflammation. Therefore, AIP1B was the major form present during inflammatory conditions. AIP1B, which lacks the N-terminal pleckstrin homology domain of AIP1A, localized to the mitochondria and augmented TNFα (tumor necrosis factor alpha)-induced mitochondrial reactive oxygen species generation and EC activation. AIP1B-ECTG (EC-specific AIP1B transgenic) mice exhibited augmented reactive oxygen species production, EC activation, and neointima formation in vascular remodeling models.]]>
Wed, 31 Dec 1969 19:00:00 EST
Epigenetics/epigenomics and prevention by curcumin of early stages of inflammatory-driven colon cancer. Wu R, Wang L, Yin R, Hudlikar R, Li S, Kuo HD, Peter R, Sargsyan D, Guo Y, Liu X, Kong AT
Mol Carcinog (Feb 2020)

Colorectal cancer (CRC) is associated with significant morbidity and mortality in the US and worldwide. CRC is the second most common cancer-related death in both men and women globally. Chronic inflammation has been identified as one of the major risk factors of CRC. It may drive genetic and epigenetic/epigenomic alterations, such as DNA methylation, histone modification, and non-coding RNA regulation. Current prevention modalities for CRC are limited and some treatment regimens such as use the nonsteroidal anti-inflammatory drug aspirin may have severe side effects, namely gastrointestinal ulceration and bleeding. Therefore, there is an urgent need of developing alternative strategies. Recently, increasing evidence suggests that several dietary cancer chemopreventive phytochemicals possess anti-inflammation and antioxidative stress activities, and may prevent cancers including CRC. Curcumin (CUR) is the yellow pigment that is found in the rhizomes of turmeric (Curcuma longa). Many studies have demonstrated that CUR exhibit strong anticancer, antioxidative stress, and anti-inflammatory activities by regulating signaling pathways, such as nuclear factor erythroid-2-related factor 2, nuclear factor-κB, and epigenetics/epigenomics pathways of histones modifications, and DNA methylation. In this review, we will discuss the latest evidence in epigenetics/epigenomics alterations by CUR in CRC and their potential contribution in the prevention of CRC.]]>
Wed, 31 Dec 1969 19:00:00 EST
The impact of perceived stress on skin ageing. Lee CM, Watson REB, Kleyn CE
J Eur Acad Dermatol Venereol (Jan 2020)

Skin ageing can be divided according to phenotypical features into intrinsic (by the passage of time) and extrinsic (with the addition of the effects of environmental factors). Photoageing is by far the most researched factor of extrinsic ageing but the additional impact of other factors such as cigarette smoking and exposure to air pollution ought to be taken into account. One of the least researched topics in relation to extrinsic skin ageing is the impact of psychological stress. A contemporary review of response of human skin to stress describes the molecular mechanisms of extrinsic skin ageing, but has fallen short of explaining resilience to stress exhibited by people. Mechanisms to regulate gene expression, define cellular identity and promote functionality are responsible for the adaptive response to stressful events. Conversely, maladaptive response of human tissues to chronic stress appears to have an impact on gene regulation. Epigenetics is the study of heritable changes in organisms due to modifications in gene activity and expression, as opposed to the genetic code (DNA genome). Chronic stress appears to be an important factor in determining an individual's vulnerability to ageing and age-related comorbidities via epigenetic modifications. Forerunners in epigenetic research recognized the necessity of a reliable biomarker in order to develop a better understanding of the role of epigenomics in ageing. Genomic DNA methylation patterns (DNAm) appear to be valuable in age prediction but variability in specificity exists across species of mammals, human races and tissues. Neuroscience research appears to be leading the way in epigenomics whilst the lack of a valid and reliable DNAm-associated age predictor compatible with human skin tissue hinders research endeavours for the epigenetics of skin ageing.]]>
Wed, 31 Dec 1969 19:00:00 EST
Epigenetic reprogramming in periodontal disease: Dynamic crosstalk with potential impact in oncogenesis. Barros SP, Fahimipour F, Tarran R, Kim S, Scarel-Caminaga RM, Justice A, North K
Periodontol 2000 (Feb 2020)

Periodontitis is a chronic multifactorial inflammatory disease associated with microbial dysbiosis and characterized by progressive destruction of the periodontal tissues. Such chronic infectious inflammatory disease is recognized as a major public health problem worldwide with measurable impact in systemic health. It has become evident that the periodontal disease phenotypes are not only determined by the microbiome effect, but the extent of the tissue response is also driven by the host genome and epigenome patterns responding to various environmental exposures. More recently there is mounting evidence indicating that epigenetic reprogramming in response to combined intrinsic and environmental exposures, might be particularly relevant due its plasticity and potential application towards precision health. The complex epigenetic crosstalk is reflected in the prognosis and progress of periodontal diseases and may also lead to a favorable landscape for cancer development. This review discusses epigenomics modifications focusing on the role of DNA methylation and pathways linking microbial infection and inflammatory pathways, which are also associated with carcinogenesis. There is a more clear vision whereas 'omics' technologies applied to unveil relevant epigenetic factors could play a significant role in the treatment of periodontal disease in a personalized mode, evidencing that public health approach should coexist with precision individualized treatment.]]>
Wed, 31 Dec 1969 19:00:00 EST
Understanding osteoarthritis pathogenesis: a multiomics system-based approach. Ratneswaran A, Rockel JS, Kapoor M
Curr Opin Rheumatol (Jan 2020)

Osteoarthritis is a heterogeneous, multifactorial condition regulated by complex biological interactions at multiple levels. Comprehensive understanding of these regulatory interactions is required to develop feasible advances to improve patient outcomes. Improvements in technology have made extensive genomic, transcriptomic, epigenomic, proteomic, and metabolomic profiling possible. This review summarizes findings over the past 20 months related to omics technologies in osteoarthritis and examines how using a multiomics approach is necessary for advancing our understanding of osteoarthritis as a disease to improve precision osteoarthritis treatments.]]>
Wed, 31 Dec 1969 19:00:00 EST
Brain Development in School-Age and Adolescent Girls: Effects of Turner Syndrome, Estrogen Therapy, and Genomic Imprinting. O'Donoghue S, Green T, Ross JL, Hallmayer J, Lin X, Jo B, Huffman LC, Hong DS, Reiss AL
Biol Psychiatry (Jan 2020)

The study of Turner syndrome (TS) offers a unique window of opportunity for advancing scientific knowledge of how X chromosome gene imprinting, epigenetic factors, hormonal milieu, and chronologic age affect brain development in females.]]>
Wed, 31 Dec 1969 19:00:00 EST
Detailed analysis of paternal knockout Grb10 mice suggests effects on stability of social behavior, rather than social dominance. Rienecker KDA, Chavasse AT, Moorwood K, Ward A, Isles AR
Genes Brain Behav (Jan 2020)

Imprinted genes are highly expressed in monoaminergic regions of the midbrain and their functions in this area are thought to have an impact on mammalian social behaviors. One such imprinted gene is Grb10, of which the paternal allele is generally recognized as mediating social dominance behavior. However, there has been no detailed study of social dominance in Grb10 mice. Moreover, the original study examined tube-test behavior in isolated mice 10 months of age. Isolation testing favors more territorial and aggressive behaviors, and does not address social dominance strategies employed in group housing contexts. Furthermore, isolation stress impacts midbrain function and dominance related behavior, often through alterations in monoaminergic signaling. Thus, we undertook a systematic study of Grb10 social rank and dominance behavior within the cage group, using a number of convergent behavioral tests. We examined both male and female mice to account for sex differences and tested cohorts aged 2, 6 and 10 months to examine any developments related to age. We found group-housed Grb10 mice do not show evidence of enhanced social dominance, but cages containing Grb10 and wild-type mice lacked the normal correlation between three different measures of social rank. Moreover, a separate study indicated isolation stress induced inconsistent changes in tube test behavior. Taken together, these data suggest future research on Grb10 mice should focus on the stability of social behaviors, rather than dominance per se.]]>
Wed, 31 Dec 1969 19:00:00 EST
Placental effects on the maternal brain revealed by disrupted placental gene expression in mouse hybrids. Arévalo L, Campbell P
Proc Biol Sci (Jan 2020)

The mammalian placenta is both the physical interface between mother and fetus, and the source of endocrine signals that target the maternal hypothalamus, priming females for parturition, lactation and motherhood. Despite the importance of this connection, the effects of altered placental signalling on the maternal brain are insufficiently studied. Here, we show that placental dysfunction alters gene expression in the maternal brain, with the potential to affect maternal behaviour. Using a cross between the house mouse and the Algerian mouse, in which hybrid placental development is abnormal, we sequenced late-gestation placental and maternal medial preoptic area transcriptomes and quantified differential expression and placenta-maternal brain co-expression between normal and hybrid pregnancies. The expression of and was significantly altered in the brains of females exposed to hybrid placentas. Most strikingly, expression patterns of placenta-specific gene families and in the brains of house mouse females carrying hybrid litters matched those of female Algerian mice, the paternal species in the cross. Our results indicate that the paternally derived placental genome can influence the expression of maternal-fetal communication genes, including placental hormones, suggesting an effect of the offspring's father on the mother's brain.]]>
Wed, 31 Dec 1969 19:00:00 EST
Epigenetic Modifications in T Cells: The Role of DNA Methylation in Salt-Sensitive Hypertension. Dasinger JH, Alsheikh AJ, Abais-Battad JM, Pan X, Fehrenbach DJ, Lund H, Roberts ML, Cowley AW, Kidambi S, Kotchen TA, Liu P, Liang M, Mattson DL
Hypertension (Feb 2020)

The SS (Dahl salt sensitive) rat is an established model of hypertension and renal damage that is accompanied with immune system activation in response to a high-salt diet. Investigations into the effects of sodium-independent and dependent components of the diet were shown to affect the disease phenotype with SS/MCW (JrHsdMcwi) rats maintained on a purified diet (AIN-76A) presenting with a more severe phenotype relative to grain-fed SS/CRL (JrHsdMcwiCrl) rats. Since contributions of the immune system, environment, and diet are documented to alter this phenotype, this present study examined the epigenetic profile of T cells isolated from the periphery and the kidney from these colonies. T cells isolated from kidneys of the 2 colonies revealed that transcriptomic and functional differences may contribute to the susceptibility of hypertension and renal damage. In response to high-salt challenge, the methylome of T cells isolated from the kidney of SS/MCW exhibit a significant increase in differentially methylated regions with a preference for hypermethylation compared with the SS/CRL kidney T cells. Circulating T cells exhibited similar methylation profiles between colonies. Utilizing transcriptomic data from T cells isolated from the same animals upon which the DNA methylation analysis was performed, a predominant negative correlation was observed between gene expression and DNA methylation in all groups. Lastly, inhibition of DNA methyltransferases blunted salt-induced hypertension and renal damage in the SS/MCW rats providing a functional role for methylation. This study demonstrated the influence of epigenetic modifications to immune cell function, highlighting the need for further investigations.]]>
Wed, 31 Dec 1969 19:00:00 EST
Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development. Laukoter S, Beattie R, Pauler FM, Amberg N, Nakayama KI, Hippenmeyer S
Nat Commun (Jan 2020)

The cyclin-dependent kinase inhibitor p57 is encoded by the imprinted Cdkn1c locus, exhibits maternal expression, and is essential for cerebral cortex development. How Cdkn1c regulates corticogenesis is however not clear. To this end we employ Mosaic Analysis with Double Markers (MADM) technology to genetically dissect Cdkn1c gene function in corticogenesis at single cell resolution. We find that the previously described growth-inhibitory Cdkn1c function is a non-cell-autonomous one, acting on the whole organism. In contrast we reveal a growth-promoting cell-autonomous Cdkn1c function which at the mechanistic level mediates radial glial progenitor cell and nascent projection neuron survival. Strikingly, the growth-promoting function of Cdkn1c is highly dosage sensitive but not subject to genomic imprinting. Collectively, our results suggest that the Cdkn1c locus regulates cortical development through distinct cell-autonomous and non-cell-autonomous mechanisms. More generally, our study highlights the importance to probe the relative contributions of cell intrinsic gene function and tissue-wide mechanisms to the overall phenotype.]]>
Wed, 31 Dec 1969 19:00:00 EST
Single Cell Omics: From Assay Design to Biomedical Application. Chen W, Li S, Kulkarni AS, Huang L, Cao J, Qian K, Wan J
Biotechnol J (Jan 2020)

Given the existence of cell heterogeneity, single cell analysis is undergoing a rapid expansion for life science and precision medicine. Recent numerous innovations in analytical platforms and instruments have re-energized the field and led to the emergence of single cell omics with high sensitivity, throughput and multiplexity. The omics knowledge builds the bridge between underlying molecular changes and cell behavior, and facilitates a deeper understanding of disease development processes. Here, the authors highlight important achievements of single cell omics mainly including genomics, epigenomics, transcriptomics, proteomics, and metabolomics, and discuss the biomedical applications of single cell omics in stem cells differentiation, immune cells function, nerve cells development and activity, and circulating tumor cells based cancer research.]]>
Wed, 31 Dec 1969 19:00:00 EST
Genome-wide analysis of epigenetic and transcriptional changes associated with heterosis in pigeonpea. Sinha P, Singh VK, Saxena RK, Kale SM, Li Y, Garg V, Tang M, Khan AW, Kim KD, Chitikineni A, Saxena KB, Sameer Kumar CV, Liu X, Xu X, Jackson S, Powell W, Nevo E, Searle IR, Lodha M, Varshney RK
Plant Biotechnol J (Jan 2020)

Hybrids are extensively used in agriculture to deliver an increase in yield, yet the molecular basis of heterosis is not well understood. Global DNA methylation analysis, transcriptome analysis and small RNA profiling were aimed to understand the epigenetic effect of the changes in gene expression level in the two hybrids and their parental lines. Increased DNA methylation was observed in both the hybrids as compared to their parents. This increase DNA methylation in hybrids showed that majority of the 24-nt sRNA clusters had higher expression in hybrids than the parents. Transcriptome analysis revealed that various phytohormones (auxin and salicylic acid) responsive hybrid-MPV DEGs were significantly altered in both the hybrids in comparison to MPV. DEGs associated with plant immunity and growth were overexpressed whereas DEGs associated with basal defense level were repressed. This antagonistic patterns of gene expression might contribute to the greater growth of the hybrids. It was also noticed that some common as well as unique changes in regulatory pathways associated with heterotic growth in both the hybrids. Approximately 70% and 67% of down-regulated hybrid-MPV DEGs were found to be differentially methylated in ICPH 2671 and ICPH 2740 hybrid, respectively. This reflected the association of epigenetic regulation in altered gene expressions. Our findings also revealed that miRNAs might play important roles in hybrid vigor in both the hybrids by regulating their target genes, especially in controlling plant growth and development, defense and stress response pathways. The above finding provides an insight into the molecular mechanism of pigeonpea heterosis.]]>
Wed, 31 Dec 1969 19:00:00 EST
The role of environmental exposures and the epigenome in health and disease. Perera BPU, Faulk C, Svoboda LK, Goodrich JM, Dolinoy DC
Environ Mol Mutagen (Jan 2020)

The genetic material of every organism exists within the context of regulatory networks that govern gene expression, collectively called the epigenome. Epigenetics has taken center stage in the study of diseases such as cancer and diabetes, but its integration into the field of environmental health is still emerging. As the Environmental Mutagenesis and Genomics Society (EMGS) celebrates its 50th Anniversary this year, we have come together to review and summarize the seminal advances in the field of environmental epigenomics. Specifically, we focus on the role epigenetics may play in multigenerational and transgenerational transmission of environmentally induced health effects. We also summarize state of the art techniques for evaluating the epigenome, environmental epigenetic analysis, and the emerging field of epigenome editing. Finally, we evaluate transposon epigenetics as they relate to environmental exposures and explore the role of noncoding RNA as biomarkers of environmental exposures. Although the field has advanced over the past several decades, including being recognized by EMGS with its own Special Interest Group, recently renamed Epigenomics, we are excited about the opportunities for environmental epigenetic science in the next 50 years. Environ. Mol. Mutagen. 61:176-192, 2020. © 2019 Wiley Periodicals, Inc.]]>
Wed, 31 Dec 1969 19:00:00 EST
Using What We Already Have: Uncovering New Drug Repurposing Strategies in Existing Omics Data. Pulley JM, Rhoads JP, Jerome RN, Challa AP, Erreger KB, Joly MM, Lavieri RR, Perry KE, Zaleski NM, Shirey-Rice JK, Aronoff DM
Annu Rev Pharmacol Toxicol (Jan 2020)

The promise of drug repurposing is to accelerate the translation of knowledge to treatment of human disease, bypassing common challenges associated with drug development to be more time- and cost-efficient. Repurposing has an increased chance of success due to the previous validation of drug safety and allows for the incorporation of omics. Hypothesis-generating omics processes inform drug repurposing decision-making methods on drug efficacy and toxicity. This review summarizes drug repurposing strategies and methodologies in the context of the following omics fields: genomics, epigenomics, transcriptomics, proteomics, metabolomics, microbiomics, phenomics, pregomics, and personomics. While each omics field has specific strengths and limitations, incorporating omics into the drug repurposing landscape is integral to its success.]]>
Wed, 31 Dec 1969 19:00:00 EST
The systems medicine of neonatal abstinence syndrome. Stone WL, Wood DL, Justice NA, Shah DS, Olsen ME, Bharti D
Front Biosci (Landmark Ed) (Jan 2020)

This review will focus on a systems medicine approach to neonatal abstinence syndrome (NAS). Systems medicine utilizes information gained from the application of "omics" technology and bioinformatics (1). The omic approaches we will emphasize include genomics, epigenomics, proteomics, and metabolomics. The goals of systems medicine are to provide clinically relevant and objective insights into disease diagnosis, prognosis, and stratification as well as pharmacological strategies and evidence-based individualized clinical guidance. Despite the increasing incidence of NAS and its societal and economic costs, there has been only a very modest emphasis on utilizing a systems medicine approach, and this has been primarily in the areas of genomics and epigenomics. As detailed below, proteomics and metabolomics hold great promise in advancing our knowledge of NAS and its treatment. Metabolomics, in particular, can provide a quantitative assessment of the exposome, which is a comprehensive picture of both internal and external environmental factors affecting health.]]>
Wed, 31 Dec 1969 19:00:00 EST
Targeting epigenetic regulators in the treatment of T-cell lymphoma. Ahmed N, Feldman AL
Expert Rev Hematol (Jan 2020)

: T-cell lymphomas represent a broad group of malignant T-cell neoplasms with marked molecular, clinical, and biologic heterogeneity. Survival rates after conventional chemotherapy regimens are poor for most subtypes and new therapies are needed. Rapidly expanding knowledge in the field of epigenomics and the development of an increasing number of epigenetic modifying agents have created new opportunities for epigenetic therapies for patients with this complex group of diseases.: The present review summarizes current knowledge on epigenetic alterations in T-cell lymphomas, availability and mechanisms of action of epigenetic modifying agents, results of clinical trials of epigenetic therapies in T-cell lymphomas, status of FDA approval, and biomarker approaches to guide therapy. Promising future directions are discussed.: Mutations in epigenetic modifying genes are among the most common genetic alterations in T-cell lymphomas, highlighting the potential for epigenetic therapies to improve management of this group of diseases. Single-agent efficacy is well documented, leading to FDA approval for several indications, but overall response rates and durability of responses remain modest. Critical next steps for the field include optimizing combination therapies that incorporate epigenetic modifying agents and developing predictive biomarkers that help guide patient and drug selection.]]>
Wed, 31 Dec 1969 19:00:00 EST
Genomic imprinting in plants-revisiting existing models. Batista RA, Köhler C
Genes Dev (Jan 2020)

Genomic imprinting is an epigenetic phenomenon leading to parentally biased gene expression. Throughout the years, extensive efforts have been made to characterize the epigenetic marks underlying imprinting in animals and plants. As a result, DNA methylation asymmetries between parental genomes emerged as the primary factor controlling the imprinting status of many genes. Nevertheless, the data accumulated so far suggest that this process cannot solely explain the imprinting of all genes. In this review, we revisit the current models explaining imprinting regulation in plants, and discuss novel regulatory mechanisms that could function independently of parental DNA methylation asymmetries in the establishment of imprinting.]]>
Wed, 31 Dec 1969 19:00:00 EST
Understanding epigenomics based on the rice model. Lu Y, Zhou DX, Zhao Y
Theor Appl Genet (Jan 2020)

The purpose of this paper provides a comprehensive overview of the recent researches on rice epigenomics, including DNA methylation, histone modifications, noncoding RNAs, and three-dimensional genomics. The challenges and perspectives for future research in rice are discussed. Rice as a model plant for epigenomic studies has much progressed current understanding of epigenetics in plants. Recent results on rice epigenome profiling and three-dimensional chromatin structure studies reveal specific features and implication in gene regulation during rice plant development and adaptation to environmental changes. Results on rice chromatin regulator functions shed light on mechanisms of establishment, recognition, and resetting of epigenomic information in plants. Cloning of several rice epialleles associated with important agronomic traits highlights importance of epigenomic variation in rice plant growth, fitness, and yield. In this review, we summarize and analyze recent advances in rice epigenomics and discuss challenges and directions for future research in the field.]]>
Wed, 31 Dec 1969 19:00:00 EST
Advancing neuro-oncology of glial tumors from big data and multidisciplinary studies. Lin CA, Berger MS
J Neurooncol (Jan 2020)

Multidisciplinary studies for glial tumors has produced an enormous amount of information including imaging, histology, and a large cohort of molecular data (i.e. genomics, epigenomics, metabolomics, proteomics, etc.). The big data resources are made possible through open access that offers great potential for new biomarker or therapeutic intervention via deep-learning and/or machine learning for integrated multi-omics analysis. An equally important effort to define the hallmarks of glial tumors will also advance precision neuro-oncology and inform patient-specific therapeutics. This review summarizes past studies regarding tumor classification, hallmarks of cancer, and hypothetical mechanisms. Leveraging on advanced big data approaches and ongoing cross-disciplinary endeavors, this review also discusses how to integrate multiple layers of big data toward the goal of precision medicine.]]>
Wed, 31 Dec 1969 19:00:00 EST