'; ?> 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, 17 Feb 2020 06:57:33 EST Mon, 17 Feb 2020 06:57:33 EST jirtle@radonc.duke.edu james001@jirtle.com Revealing eukaryotic histone-modifying mechanisms through bacterial infection. Dong W, Hamon MA
Semin Immunopathol (Feb 2020)

In the long co-evolution of host-pathogen interaction, bacteria have developed sophisticated strategies to manipulate host cell mechanisms and reprogram host transcription. Targeting chromatin, mainly through post-translational modification (PTM) of histone proteins, is one strategy that has been revealed over the last decade. Indeed, histone modifications play a crucial role in regulating transcription during cell type and stimulus specific responses, making them good targets during infection. Therefore, the study of host-pathogen interactions provides breakthroughs in understanding virulence mechanisms, but also in host cell mechanisms. Although chromatin is regulated by DNA methylation, noncoding RNAs, and post-translational modifications of histones, most studies have concentrated on bacteria-induced histone modifications, which will be the focus of this review. We will discuss the different mechanisms used by bacteria to induce histone PTMs, whether it is through direct targeting of pathogen effector enzymes, or indirectly through modulation of cellular signaling cascade. We will summarize the concepts we learned in cell biology from exploring bacteria-triggered histone modifications, by focusing on the signaling cascades modified by bacteria, bacterial mimics of eukaryotic enzymes, and the novel histone marks imposed upon infection.]]>
Wed, 31 Dec 1969 19:00:00 EST
Multi-omics analysis at epigenomics and transcriptomics levels reveals prognostic subtypes of lung squamous cell carcinoma. Xu Y, She Y, Li Y, Li H, Jia Z, Jiang G, Liang L, Duan L
Biomed Pharmacother (Feb 2020)

In this study, we identified prognostic biomarkers for lung squamous cell carcinoma (LUSC) by integrating multiple sets of DNA copy number variants (CNV) and methylation variant (MET) data, and performing qPCR and immunohistochemical identification. We examined the expression of CNV and MET in 368 LUSC patients. Gene expression associated with DNA copy number or DNA methylation was identified and four LUSC gene subtypes were defined based on these correlations. The prognosis overall survival (OS) of the iC1 subtype was significantly lower than that in the iC2 and iC4 subtypes. We assessed the immune scores of each subtype and found that the six immune cell scores of the iC3 subtype were significantly higher than the other subtypes (p < 0.01). Three genes associated with prognosis, NFE2L2, ASAH2, and RIMBP2, were identified by comparing the expression of CNV and MET in subtypes. Analysis of mutational differences between subtypes revealed a group of genes with significant mutations between the iC1 and iC4 subtypes. The number of mutations in the NFE2L2 gene in LUSC was significantly higher than that in other genes, and the gene was prognostic. The number of mutations was significantly higher in the best iC4 subtype than the iC1 subtype with the worst prognosis; the other two genes, ASAH2 and RIMBP2, were only found in the worst prognosis of the iC1 subtype. This comprehensive multi-omics analysis of genomics, epigenomics, and transcriptomics data provides new insights into the molecular mechanisms of LUSC and may be helpful in identifying biomolecular markers for early disease diagnosis.]]>
Wed, 31 Dec 1969 19:00:00 EST
Pan-cancer clinical and molecular analysis of racial disparities. Lara OD, Wang Y, Asare A, Xu T, Chiu HS, Liu Y, Hu W, Sumazin P, Uppal S, Zhang L, Rauh-Hain JA, Sood AK
Cancer (Feb 2020)

Racial disparities in cancer outcomes are increasingly recognized, but comprehensive analyses, including molecular studies, are limited. The objective of the current study was to perform a pan-cancer clinical and epigenetic molecular analysis of outcomes in African American (AA) and European American (EA) patients.]]>
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 (Feb 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
Histone ChIP-Seq identifies differential enhancer usage during chondrogenesis as critical for defining cell-type specificity. Cheung K, Barter MJ, Falk J, Proctor CJ, Reynard LN, Young DA
FASEB J (Feb 2020)

Epigenetic mechanisms are known to regulate gene expression during chondrogenesis. In this study, we have characterized the epigenome during the in vitro differentiation of human mesenchymal stem cells (hMSCs) into chondrocytes. Chromatin immunoprecipitation followed by next-generation sequencing (ChIP-seq) was used to assess a range of N-terminal posttranscriptional modifications (marks) to histone H3 lysines (H3K4me3, H3K4me1, H3K27ac, H3K27me3, and H3K36me3) in both hMSCs and differentiated chondrocytes. Chromatin states were characterized using histone ChIP-seq and cis-regulatory elements were identified in chondrocytes. Chondrocyte enhancers were associated with chondrogenesis-related gene ontology (GO) terms. In silico analysis and integration of DNA methylation data with chondrogenesis chromatin states revealed that enhancers marked by histone marks H3K4me1 and H3K27ac were de-methylated during in vitro chondrogenesis. Similarity analysis between hMSC and chondrocyte chromatin states defined in this study with epigenomes of cell-types defined by the Roadmap Epigenomics project revealed that enhancers are more distinct between cell-types compared to other chromatin states. Motif analysis revealed that the transcription factor SOX9 is enriched in chondrocyte enhancers. Luciferase reporter assays confirmed that chondrocyte enhancers characterized in this study exhibited enhancer activity which may be modulated by DNA methylation and SOX9 overexpression. Altogether, these integrated data illustrate the cross-talk between different epigenetic mechanisms during chondrocyte differentiation.]]>
Wed, 31 Dec 1969 19:00:00 EST
Precision cardiovascular medicine: artificial intelligence and epigenetics for the pathogenesis and prediction of coarctation in neonates. Bahado-Singh RO, Vishweswaraiah S, Aydas B, Yilmaz A, Saiyed NM, Mishra NK, Guda C, Radhakrishna U
J Matern Fetal Neonatal Med (Feb 2020)

Advances in omics and computational Artificial Intelligence (AI) have been said to be key to meeting the objectives of precision cardiovascular medicine. The focus of precision medicine includes a better assessment of disease risk and understanding of disease mechanisms. Our objective was to determine whether significant epigenetic changes occur in isolated, non-syndromic CoA. Further, we evaluated the AI analysis of DNA methylation for the prediction of CoA. Genome-wide DNA methylation analysis of newborn blood DNA was performed in 24 isolated, non-syndromic CoA cases and 16 controls using the Illumina HumanMethylation450 BeadChip arrays. Cytosine nucleotide (CpG) methylation changes in CoA in each of 450,000 CpG loci were determined. Ingenuity pathway analysis (IPA) was performed to identify molecular and disease pathways that were epigenetically dysregulated. Using methylation data, six artificial intelligence (AI) platforms including deep learning (DL) was used for CoA detection. We identified significant (FDR -value ≤ .05) methylation changes in 65 different CpG sites located in 75 genes in CoA subjects. DL achieved an AUC (95% CI) = 0.97 (0.80-1) with 95% sensitivity and 98% specificity. Gene ontology (GO) analysis yielded epigenetic alterations in important cardiovascular developmental genes and biological processes: abnormal morphology of cardiovascular system, left ventricular dysfunction, heart conduction disorder, thrombus formation, and coronary artery disease. In an exploratory study we report the use of AI and epigenomics to achieve important objectives of precision cardiovascular medicine. Accurate prediction of CoA was achieved using a newborn blood spot. Further, we provided evidence of a significant epigenetic etiology in isolated CoA development.]]>
Wed, 31 Dec 1969 19:00:00 EST
In vitro development of IVF-derived bovine embryos following cytoplasmic microinjection for the episomal expression of the IGF2 gene. Campagnolo K, Ongaratto FL, de Freitas CR, Bello CAP, Willhelm BR, de Mattos K, Rodrigues JLR, Bertolini M
Reprod Domest Anim (Feb 2020)

Important genomic imprinting changes usually occur following the in vitro production (IVP) of bovine embryos, especially in the imprinting pattern of components of the IGF system. This study aimed to evaluate the effects of a transient episomal overexpression of the IGF2 gene in bovine IVP embryos following embryo cytoplasmic microinjection (CMI) at the 1-cell stage on embryo survival, early and late developmental kinetics and morphological quality up to Day 7 of development. Selected cumulus-oocyte complexes (COCs) were matured and fertilized in vitro and subsequently segregated into six experimental groups: non-CMI control group, and five CMI groups at increasing doses (0, 10, 20, 40, 80 ng/μL) of a GFP vector built for the episomal expression of bovine IGF2. Zygote CMI was effective in delivering the expression vector into the ooplasm, irrespective of the groups, with 58% of positive GFP fluorescence in Day-7 blastocysts. Considering developmental rates and late embryo kinetics, the 10-ng/μL CMI vector dose promoted a lower blastocyst rate (10.4%), but for blastocysts at more advanced stages of development (93.0% blastocysts and expanded blastocysts), and higher number of cells (116.0 ± 3.0) than non-CMI controls (23.3%, 75.0% and 75.0 ± 6.8 were obtained, respectively). In conclusion, CMI at the 1-cell stage did not compromise subsequent in vitro development of surviving embryos, with the 10-ng/μL group demonstrating a possible growth-promoting effect of the IGF2 gene on embryo development, from the 1-cell to the blastocyst stage.]]>
Wed, 31 Dec 1969 19:00:00 EST
The impact of epigenetics on cardiovascular disease. Prasher D, Greenway SC, Singh RB
Biochem Cell Biol (Feb 2020)

Mortality and morbidity from cardiovascular diseases (CVDs) represents a huge burden to society. It is recognized that environmental factors and individual lifestyles play important roles in disease susceptibility, but the link between these external risk factors and our genetics has been unclear. However, the discovery of sequence-independent heritable DNA changes (epigenetics) have helped us to explain the link between genes and the environment. Multiple diverse epigenetic processes, including DNA methylation, histone modification, and the expression of non-coding RNA molecules affect the expression of genes that produce important changes in cellular differentiation and function, influencing the health and adaptability of the organism. CVDs such as congenital heart disease, cardiomyopathy, heart failure, cardiac fibrosis, hypertension, and atherosclerosis are now being viewed as much more complex and dynamic disorders. The role of epigenetics in these and other CVDs is currently under intense scrutiny, and we can expect important insights to emerge, including novel biomarkers and new approaches to enable precision medicine. This review summarizes the recent advances in our understanding of the role of epigenetics in CVD.]]>
Wed, 31 Dec 1969 19:00:00 EST
Resiliency of equid H19 imprint to somatic cell reprogramming by oocyte nuclear transfer and genetically induced pluripotency†. Poirier M, Smith OE, Therrien J, Rigoglio NN, Miglino MA, Silva LA, Meirelles FV, Smith LC
Biol Reprod (Feb 2020)

Cell reprogramming by somatic cell nuclear transfer and in induced pluripotent stem cells is associated with epigenetic modifications that are often incompatible with embryonic development and differentiation. For instance, aberrant DNA methylation patterns of the differentially methylated region and biallelic expression of H19-/IGF2-imprinted gene locus have been associated with abnormal growth of fetuses and placenta in several mammalian species. However, cloned horses are born with normal sizes and with no apparent placental anomalies, suggesting that H19/IGF2 imprinting may be epigenetically stable after reprogramming in this species. In light of this, we aimed at characterizing the equid H19 gene to determine whether imprinting is altered in somatic cell nuclear transfer (SCNT)-derived conceptuses and induced pluripotent stem cell (iPSC) lines using the mule hybrid model. A CpG-rich region containing five CTCF binding sites was identified upstream of the equine H19 gene and analyzed by bisulfite sequencing. Coupled with parent-specific and global H19 transcript analysis, we found that the imprinted H19 remains monoallelic and that on average the methylation levels of both parental differentially methylated regions in embryonic and extra-embryonic SCNT tissues and iPSC lines remained unaltered after reprogramming. Together, these results show that, compared to other species, equid somatic cells are more resilient to epigenetic alterations to the H19-imprinted locus during SCNT and iPSC reprogramming.]]>
Wed, 31 Dec 1969 19:00:00 EST
A method for identifying allele-specific hydroxymethylation. Yamada Y, Sasaki S
Epigenetics (Mar 2020)

We previously identified sequence-dependent allele-specific methylation (sd-ASM) in adult human peripheral blood leukocytes, in which ASM occurs in cis depending on adjacent polymorphic sequences. A number of groups have identified sd-ASM sites in the human and mouse genomes, illustrating the prevalence of sd-ASM in mammalian genomes. In addition, sd-ASM can lead to sequence-dependent allele-specific expression of neighbouring genes. Imprinted genes also often exhibit parent-of-origin-dependent allele-specific methylation (pd-ASM), which causes parent-of-origin-dependent allele-specific expression. However, whether most of the already known sd-ASM and pd-ASM sites are methylated or hydroxymethylated remains unclear due to technical restrictions. Accordingly, a novel method that enables examination of allelic methylation and hydroxymethylation status and also overcomes the drawbacks of conventional methods is needed. Such a method could also be used to elucidate the mechanisms underlying polymorphism-associated inter-individual differences in disease susceptibility and the mechanism of genomic imprinting. Here, we developed a simple method to determine allelic hydroxymethylation status and identified novel sequence- and parent-of-origin-dependent allele-specific hydroxymethylation sites. Correlation analyses of TF binding sequences and methylation or hydroxymethylation between three mouse strains revealed the involvement of in strain-specific methylation and hydroxymethylation in exon 7 of .]]>
Wed, 31 Dec 1969 19:00:00 EST
Multi-omics analysis based on integrated genomics, epigenomics and transcriptomics in pancreatic cancer. Kong L, Liu P, Zheng M, Xue B, Liang K, Tan X
Epigenomics (Feb 2020)

Integrated analysis of genomics, epigenomics, transcriptomics and clinical information contributes to identify specific molecular subgroups and find novel biomarkers for pancreatic cancer. The DNA copy number variation, the simple nucleotide variation, methylation and mRNA data of pancreatic cancer patients were obtained from The Cancer Genome Atlas (TCGA). Four molecular subgroups (iC1, iC2, iC3 and iC4) of pancreatic cancer were identified by integrating analysis. The iC1 subgroup harbors better prognosis, higher immune score, lesser DNA copy number variation mutations and better genomic stability compared with iC2, iC3 and iC4 subgroups. Three new genes (, and ) correlated with prognosis were identified. Integrated multi-omics analysis provides fresh insight into molecular classification of pancreatic cancer, which may help discover new prognostic biomarkers and reveal the underlying mechanism of pancreatic cancer.]]>
Wed, 31 Dec 1969 19:00:00 EST
Multiplatform Molecular Profiling Reveals Epigenomic Intratumor Heterogeneity in Ependymoma. Liu SJ, Magill ST, Vasudevan HN, Hilz S, Villanueva-Meyer JE, Lastella S, Daggubati V, Spatz J, Choudhury A, Orr BA, Demaree B, Seo K, Ferris SP, Abate AR, Oberheim Bush NA, Bollen AW, McDermott MW, Costello JF, Raleigh DR
Cell Rep (Feb 2020)

Ependymomas exist within distinct genetic subgroups, but the molecular diversity within individual ependymomas is unknown. We perform multiplatform molecular profiling of 6 spatially distinct samples from an ependymoma with C11orf95-RELA fusion. DNA methylation and RNA sequencing distinguish clusters of samples according to neuronal development gene expression programs that could also be delineated by differences in magnetic resonance blood perfusion. Exome sequencing and phylogenetic analysis reveal epigenomic intratumor heterogeneity and suggest that chromosomal structural alterations may precede accumulation of single-nucleotide variants during ependymoma tumorigenesis. In sum, these findings shed light on the oncogenesis and intratumor heterogeneity of ependymoma.]]>
Wed, 31 Dec 1969 19:00:00 EST
The role of environmental stress and DNA methylation in the longitudinal course of bipolar disorder. Comes AL, Czamara D, Adorjan K, Anderson-Schmidt H, Andlauer TFM, Budde M, Gade K, Hake M, Kalman JL, Papiol S, Reich-Erkelenz D, Klöhn-Saghatolislam F, Schaupp SK, Schulte EC, Senner F, Juckel G, Schmauß M, Zimmermann J, Reimer J, Reininghaus E, Anghelescu IG, Konrad C, Thiel A, Figge C, von Hagen M, Koller M, Dietrich DE, Stierl S, Scherk H, Witt SH, Sivalingam S, Degenhardt F, Forstner AJ, Rietschel M, Nöthen MM, Wiltfang J, Falkai P, Schulze TG, Heilbronner U
Int J Bipolar Disord (Feb 2020)

Stressful life events influence the course of affective disorders, however, the mechanisms by which they bring about phenotypic change are not entirely known.]]>
Wed, 31 Dec 1969 19:00:00 EST
Imprinted Maternally Expressed microRNAs Antagonize Paternally Driven Gene Programs in Neurons. Whipple AJ, Breton-Provencher V, Jacobs HN, Chitta UK, Sur M, Sharp PA
Mol Cell (Feb 2020)

Imprinted genes with parental-biased allelic expression are frequently co-regulated and enriched in common biological pathways. Here, we functionally characterize a large cluster of microRNAs (miRNAs) expressed from the maternally inherited allele ("maternally expressed") to explore the molecular and cellular consequences of imprinted miRNA activity. Using an induced neuron (iN) culture system, we show that maternally expressed miRNAs from the miR-379/410 cluster direct the RNA-induced silencing complex (RISC) to transcriptional and developmental regulators, including paternally expressed transcripts like Plagl1. Maternal deletion of this imprinted miRNA cluster resulted in increased protein levels of several targets and upregulation of a broader transcriptional program regulating synaptic transmission and neuronal function. A subset of the transcriptional changes resulting from miR-379/410 deletion can be attributed to de-repression of Plagl1. These data suggest maternally expressed miRNAs antagonize paternally driven gene programs in neurons.]]>
Wed, 31 Dec 1969 19:00:00 EST
Synthetic Analyses of Single-Cell Transcriptomes from Multiple Brain Organoids and Fetal Brain. Tanaka Y, Cakir B, Xiang Y, Sullivan GJ, Park IH
Cell Rep (Feb 2020)

Human brain organoid systems offer unprecedented opportunities to investigate both neurodevelopmental and neurological disease. Single-cell-based transcriptomics or epigenomics have dissected the cellular and molecular heterogeneity in the brain organoids, revealing a complex organization. Similar but distinct protocols from different labs have been applied to generate brain organoids, providing a large resource to perform a comparative analysis of brain developmental processes. Here, we take a systematic approach to compare the single-cell transcriptomes of various human cortical brain organoids together with fetal brain to define the identity of specific cell types and differentiation routes in each method. Importantly, we identify unique developmental programs in each protocol compared to fetal brain, which will be a critical benchmark for the utility of human brain organoids in the future.]]>
Wed, 31 Dec 1969 19:00:00 EST
Mutational processes of distinct POLE exonuclease domain mutants drive an enrichment of a specific TP53 mutation in colorectal cancer. Fang H, Barbour JA, Poulos RC, Katainen R, Aaltonen LA, Wong JWH
PLoS Genet (Feb 2020)

Cancer genomes with mutations in the exonuclease domain of Polymerase Epsilon (POLE) present with an extraordinarily high somatic mutation burden. In vitro studies have shown that distinct POLE mutants exhibit different polymerase activity. Yet, genome-wide mutation patterns and driver mutation formation arising from different POLE mutants remains unclear. Here, we curated somatic mutation calls from 7,345 colorectal cancer samples from published studies and publicly available databases. These include 44 POLE mutant samples including 9 with whole genome sequencing data available. The POLE mutant samples were categorized based on the specific POLE mutation present. Mutation spectrum, associations of somatic mutations with epigenomics features and co-occurrence with specific driver mutations were examined across different POLE mutants. We found that different POLE mutants exhibit distinct mutation spectrum with significantly higher relative frequency of C>T mutations in POLE V411L mutants. Our analysis showed that this increase frequency in C>T mutations is not dependent on DNA methylation and not associated with other genomic features and is thus specifically due to DNA sequence context alone. Notably, we found strong association of the TP53 R213* mutation specifically with POLE P286R mutants. This truncation mutation occurs within the TT[C>T]GA context. For C>T mutations, this sequence context is significantly more likely to be mutated in POLE P286R mutants compared with other POLE exonuclease domain mutants. This study refines our understanding of DNA polymerase fidelity and underscores genome-wide mutation spectrum and specific cancer driver mutation formation observed in POLE mutant cancers.]]>
Wed, 31 Dec 1969 19:00:00 EST
Activin A and BMP4 Signaling Expands Potency of Mouse Embryonic Stem Cells in Serum-Free Media. Wu B, Li L, Li B, Gao J, Chen Y, Wei M, Yang Z, Zhang B, Li S, Li K, Wang C, Surani MA, Li X, Tang F, Bao S
Stem Cell Reports (Feb 2020)

Inhibitors of Mek1/2 and Gsk3β, known as 2i, and, together with leukemia inhibitory factor, enhance the derivation of embryonic stem cells (ESCs) and promote ground-state pluripotency (2i/L-ESCs). However, recent reports show that prolonged Mek1/2 suppression impairs developmental potential of ESCs, and is rescued by serum (S/L-ESCs). Here, we show that culturing ESCs in Activin A and BMP4, and in the absence of MEK1/2 inhibitor (ABC/L medium), establishes advanced stem cells derived from ESCs (esASCs). We demonstrate that esASCs contributed to germline lineages, full-term chimeras and generated esASC-derived mice by tetraploid complementation. We show that, in contrast to 2i/L-ESCs, esASCs display distinct molecular signatures and a stable hypermethylated epigenome, which is reversible and similar to serum-cultured ESCs. Importantly, we also derived novel ASCs (blASCs) from blastocysts in ABC/L medium. Our results provide insights into the derivation of novel ESCs with DNA hypermethylation from blastocysts in chemically defined medium.]]>
Wed, 31 Dec 1969 19:00:00 EST
Introducing a panel for early detection of lung adenocarcinoma by using data integration of genomics, epigenomics, transcriptomics and proteomics. Haghjoo N, Moeini A, Masoudi-Nejad A
Exp Mol Pathol (Feb 2020)

Lung Adenocarcinoma is one of the most leading causes of death worldwide. Early detection of this cancer could enhance the survival chance of patients and even lead to better and more effective treatment. One of the approaches to find out more about biological malfunctions is using "omics" data. Among diverse computational procedures, data integration is becoming a striking tool to deal with complicated diseases such as cancer, considering the defective and informative nature of each kind of "omics" data. Data integration as relates to lung adenocarcinoma can lead to finding molecular biomarkers that could solve early-stage detection and progression prediction alongside other screening technologies like low-dose spiral computed tomography. In the present study, we hypothesized that genes with multiple variations are essential to provoke lung adenocarcinoma and one may use them to predict tumor formation or even cancer development. We integrated the genomic, epigenomic, transcriptomic and proteomic data. Consequently, five genes were introduced and validated by different analyses including classification of patients and survival analysis. Furthermore, we constructed a bipartite mRNA-miRNA network to identify a set of miRNAs for further experimental analyses. Finally, a sensitive and specific diagnostic panel comprising CDKN2A, CX3CR1, COX4I2, SLC15A2 and TFRC genes were identified for early detection of Lung Adenocarcinoma.]]>
Wed, 31 Dec 1969 19:00:00 EST
Childhood asthma in the new omics era: challenges and perspectives. Golebski K, Kabesch M, Melén E, Potočnik U, van Drunen CM, Reinarts S, Maitland-van der Zee AH, Vijverberg SJH,  
Curr Opin Allergy Clin Immunol (Feb 2020)

Childhood asthma is a heterogeneous inflammatory disease comprising different phenotypes and endotypes and, particularly in its severe forms, has a large impact on the quality-of-life of patients and caregivers. The application of advanced omics technologies provides useful insights into underlying asthma endotypes and may provide potential clinical biomarkers to guide treatment and move towards a precision medicine approach.]]>
Wed, 31 Dec 1969 19:00:00 EST
Cancer cell niche factors secreted from cancer-associated fibroblast by loss of H3K27me3. Maeda M, Takeshima H, Iida N, Hattori N, Yamashita S, Moro H, Yasukawa Y, Nishiyama K, Hashimoto T, Sekine S, Ishii G, Ochiai A, Fukagawa T, Katai H, Sakai Y, Ushijima T
Gut (02 2020)

Cancer-associated fibroblasts (CAFs), a major component of cancer stroma, can confer aggressive properties to cancer cells by secreting multiple factors. Their phenotypes are stably maintained, but the mechanisms are not fully understood. We aimed to show the critical role of epigenetic changes in CAFs in maintaining their tumour-promoting capacity and to show the validity of the epigenomic approach in identifying therapeutic targets from CAFs to starve cancer cells.]]>
Wed, 31 Dec 1969 19:00:00 EST