'; ?> 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 Thu, 03 Jul 2025 07:55:55 EDT Thu, 03 Jul 2025 07:55:55 EDT jirtle@radonc.duke.edu james001@jirtle.com MDR1 DNA glycosylase regulates the expression of genomically imprinted genes and Helitrons. Higgins K, Gent J, Anderson S
Plant J (Jul 2025)

Targeted demethylation by DNA glycosylases (DNGs) results in differential methylation between parental alleles in the endosperm, which drives imprinted expression. Here, we performed RNA sequencing on endosperm derived from DNG mutant mdr1 and wild-type (WT) endosperm. Consistent with the role of DNA methylation in gene silencing, we find 108 genes and 96 TEs differentially expressed (DE) transcripts that lost expression in the hypermethylated mdr1 mutant. Compared with other endosperm transcripts, the mdr1 targets are enriched for TEs (particularly Helitrons), and DE genes are depleted for both core genes and GO term assignments, suggesting that the majority of DE transcripts are TEs and pseudo-genes. By comparing DE genes to imprinting calls from prior studies, we find that the majority of DE genes have maternally biased expression, and approximately half of all maternally expressed genes (MEGs) are DE in this study. In contrast, no paternally expressed genes (PEGs) are DE. DNG-dependent imprinted genes are distinguished by maternal demethylation and expression primarily in the endosperm, so we also performed Enzymatic Methyl-seq on hybrids to identify maternal demethylation and utilized a W22 gene expression atlas to identify genes expressed primarily in the endosperm. Overall, approximately ⅔ of all MEGs show evidence of regulation by DNGs. Taken together, this study solidifies the role of MDR1 in the regulation of maternally expressed, imprinted genes and TEs and identifies subsets of genes with DNG-independent imprinting regulation.]]> Wed, 31 Dec 1969 19:00:00 EST Genomic and epigenomic insight into giga-chromosome architecture and adaptive evolution of royal lily (Lilium regale). Sun J, Wang X, Wang K, Meng D, Mu Y, Zhang L, Wang J, Yao G, Guo L
Nat Commun (Jul 2025)

Lilies are popular ornamental and medicinal plants with gigantic genomes. Due to the challenge of assembling complex giga-genomes, our understanding of the genetic architecture, epigenetic regulation and evolution of large-genome plants such as lily remains limited. Here, we report a high-quality chromosome-level 35.6 Gb reference genome of royal lily (Lilium regale), a parent of many modern lily cultivars, using PacBio HiFi and Hi-C sequencing data. We show that genome expansion of L. regale is mainly caused by extensive proliferation of transposable elements resulting in long intergenic and intronic regions, along with whole-genome duplications and tandem repeats. L. regale genome is repeat-rich (80.06%) encoding abundant large genes (>10 Kb) with long introns that account for ~90% length of 67,862 genes encoded. Phylogenomics reveals significant gene family expansion related to defense response and biosynthesis of terpenoids, reflecting its adaptation strategy. Through multiomic analysis, we reveal how transposable element activity and epigenetic regulations may impact transcription, alternative splicing, and three-dimensional organization, which contribute to its adaptive evolution. Collectively, this significantly improved lily genome assembly and annotation will serve as an essential resource for research on lily genetics, breeding, conservation biology, and angiosperm genome evolution.]]> Wed, 31 Dec 1969 19:00:00 EST The myoblast methylome: multiple types of associations with chromatin and transcription. Sen S, Lacey M, Baribault C, Ponnaluri VKC, Esteve PO, Ehrlich KC, Meletta M, Pradhan S, Ehrlich M
Epigenetics (Dec 2025)

Epigenetic changes are implicated in development, repair, and physiology of postnatal skeletal muscle (SkM). We generated methylomes for human myoblasts (SkM progenitor cells) and determined myoblast differentially methylated regions (DMRs) for comparison to the epigenomics and transcriptomics of diverse cell types. Analyses were from global genomic and single-gene perspectives and included reporter gene assays. One atypical finding was the association of promoter-adjacent hypermethylation in myoblasts with transcription turn-on, but at downmodulated levels, for certain genes (., and ). In contrast, brain-specific was in repressed chromatin and silent in most cell types but linked to hypermethylated DMRs specifically in myoblasts. The -linked DMRs might be needed because of the overlapping or nearby binding of myogenic differentiation protein 1 (MYOD). We found genome-wide overlap of DMRs with MYOD or CCCTC-binding factor (CTCF) binding sites in myoblasts that is consistent with the importance of MYOD, as well as CTCF, in organizing myoblast transcription-enhancing chromatin interactions. We also observed some gene upregulation correlated with a special association of regional DNA hypomethylation with H3K36me3, H3K27ac, and H3K4me1 enrichment. Our study highlights unusual relationships between epigenetics and gene expression that illustrate the interplay between DNA methylation and chromatin epigenetics in the regulation of transcription.]]> Wed, 31 Dec 1969 19:00:00 EST Tissular chromatin-state cartography based on double-barcoded DNA arrays that capture unloaded PA-Tn5 transposase. Mendoza-Ferri MG, Lozachmeur G, Duvina M, Perret L, Merciris D, Gigout A, Mendoza-Parra MA
Genome Res (Jul 2025)

Recent developments in spatial omics are revolutionizing our understanding of tissue structure organization and their deregulation in disease. Here, we present a strategy for capturing chromatin histone modification signatures across tissue sections by taking advantage of a double-barcoded DNA arrays design compatible with in situ Protein A-transposase Tn5 tagmentation. This approach has been validated in presence of fresh-frozen mouse brain tissues but also in decalcified formalin-fixed paraffin-embedded (FFPE) mouse paw samples, in which either the histone modification H3K4 trimethylation or H3K27 acetylation has been used as proxy for interrogating active promoter signatures. Furthermore, because combinatorial enrichment of multiple histone modifications was shown to code for various states of gene transcriptional status (active, bivalent, repressed), we have integrated several histone modifications generated from consecutive mouse embryo sections to reveal changes in chromatin states across the tissue. Overall, this spatial epigenomic technology combined with the use of a spatial chromatin-state analytical strategy paves the way for future epigenetics studies for addressing tissue architecture complexity.]]> Wed, 31 Dec 1969 19:00:00 EST Differential methylation patterns in cord blood associated with prenatal exposure to neighborhood crime: an epigenome-wide association study and regional analysis. Martin CL, Chen J, D'Alessio AS, Ward-Caviness CK, Ye A, Lodge EK, Ghastine L, Dhingra R, Jima DD, Murphy SK, Hoyo C
Epigenetics (Dec 2025)

Exposure to prenatal social stressors during pregnancy is associated with adverse birth outcomes and has been linked to epigenetic changes in DNA methylation (DNAm); however, less understood is the effect of neighborhood-level stressors like crime during pregnancy on offspring DNAm. Using data from the Newborn Epigenetic Study, we conducted epigenome-wide and regional analyses of the association between exposure to neighborhood crime and DNAm in offspring cord blood using Illumina's HumanMethylation450k BeadChip among 185 mother-offspring pairs. Prenatal exposure to neighborhood crime at the census block group level was mapped to participants' residential addresses during the gestational window from the date of last menstrual period to delivery. Models for the epigenome-wide and regional analyses were adjusted for maternal age, race/ethnicity, education, smoking, cell-type composition, and offspring sex. Genetic influence and gene expression enrichment were assessed using methylation quantitative trait loci (mQTLs) and expression quantitative trait methylation (eQTMs) analyses. Functional enrichment was determined using Gene Ontology and KEGG databases. We did not find evidence of epigenome-wide associations between prenatal neighborhood crime exposure and DNAm; however, we identified nine differentially methylated regions (DMRs) comprising 51 CpG sites associated with neighborhood crime. CpG sites within significant differentially methylated regions were associated with mQTLs at birth and eQTMs upon further examination. KEGG analysis identified a significant Th1 and Th2 cell differentiation pathway. Our results suggest potential links between prenatal neighborhood crime exposure and offspring DNAm; however, additional research is needed in larger cohorts across wider geographic areas to confirm our results.]]> Wed, 31 Dec 1969 19:00:00 EST Comprehensive pan-cancer analysis of NLRs family as prognostic and immunity markers based on multi-omics data. Wen X, Cui M, Zhang J, Huang H
Discov Oncol (Jul 2025)

Members of the NOD-like receptors(NLRs)gene family members involved in inflammasome formation have been implicated in cancer initiation, development, progression, angiogenesis, and invasion. This study comprehensively investigated the role of NLRs in cancer through multi-omics analysis, which is of great necessity for a deeper understanding of the pathogenesis of cancer, improvement of cancer prognosis assessment, promotion of drug development, and advancement of precision medicine.]]> Wed, 31 Dec 1969 19:00:00 EST use capsules, transporters, mobile genetic elements, and other evolutionary adaptations to survive antibiotics exposure in the absence of resistance genes. Mmatli M, Mbelle NM, Fourie B, Osei Sekyere J
Virulence (Dec 2025)

Whole-genome sequencing, transcriptomic profiling, and epigenomic analyses were performed. Phenotypic assays were used to evaluate the effects of various inhibitors on antibiotic susceptibility, while bioinformatic pipelines were used to characterize resistance determinants, virulence factors, and mobile genetic elements (MGEs).]]> Wed, 31 Dec 1969 19:00:00 EST Comprehensive functional annotation of ESR1-driven enhancers in breast cancer reveals hierarchical activity independent of genomic and epigenomic contexts. Zekri Y, Gregoricchio S, Yapıcı E, Huang CF, Morova T, Altıntaş UB, Korkmaz G, Lack NA, Zwart W
Genome Res (Jul 2025)

Estrogen receptor 1 (ESR1; also known as ERα, encoded by gene) is the driving transcription factor in breast cancer development and progression. ESR1 genomic action is thought to operate under tight epigenetic control, with its chromatin binding and subsequent transcriptional output heavily reliant on the pioneer transcription factor FOXA1, which renders chromatin accessible for ESR1 binding. However, the exact contribution of the epigenome to selective enhancer activation by ESR1 remains to be fully elucidated. To address this, we employ a massively parallel reporter assay to profile 7576 individual ESR1 binding sites for hormone responsiveness. Only a minority of ESR1-occupied enhancers exhibit hormone-induced activity. These findings are confirmed by genomic data in situ, indicating that enhancer activation within a chromatinized context is robustly captured in a plasmid-based reporter assay. In silico integration of our findings with publicly available functional genomics data sets from breast cancer cell lines and tumor samples reveal distinct transcription complex compositions, 3D genome contexts, and regulatory dynamics associated with different classes of ESR1 binding sites. Overall, our results establish a comprehensive framework to highlight and elucidate the molecular basis underlying ESR1 genomic heterogeneity and its contribution to breast cancer biology and clinical outcomes.]]> Wed, 31 Dec 1969 19:00:00 EST Host-microbe multi-omics and succinotype profiling have prognostic value for future relapse in patients with inflammatory bowel disease. O'Sullivan J, Patel S, Leventhal GE, Fitzgerald RS, Laserna-Mendieta EJ, Huseyin CE, Konstantinidou N, Rutherford E, Lavelle A, Dabbagh K, DeSantis TZ, Shanahan F, Temko A, Iwai S, Claesson MJ
Gut Microbes (Dec 2025)

Crohn's disease (CD) and ulcerative colitis (UC) are chronic relapsing inflammatory bowel disorders (IBD), the pathogenesis of which is uncertain but includes genetic susceptibility factors, immune-mediated tissue injury and environmental influences, most of which appear to act via the gut microbiome. We hypothesized that host-microbe alterations could be used to prognostically stratify patients experiencing relapses up to four years after endoscopy. We therefore examined multiple omics data, including published and new datasets, generated from paired inflamed and non-inflamed mucosal biopsies from 142 patients with IBD (54 CD; 88 UC) and from 34 control (non-diseased) biopsies. The relapse-predictive potential of 16S rRNA gene and transcript amplicons (standing and active microbiota) were investigated along with host transcriptomics, epigenomics and genetics. While standard single-omics analysis could not distinguish between patients who relapsed and those that remained in remission within four years of colonoscopy, we did find an association between the number of flares and a patient's succinotype. Our multi-omics machine learning approach was also able to predict relapse when combining features from the microbiome and human host. Therefore multi-omics, rather than single omics, better predicts relapse within 4 years of colonoscopy, while a patient's succinotype is associated with a higher frequency of relapses.]]> Wed, 31 Dec 1969 19:00:00 EST and are human placenta-specific imprinted genes associated with germline-inherited maternal DNA methylation. Daskeviciute D, Sainty B, Chappell-Maor L, Bone C, Russell S, Iglesias-Platas I, Arnaud P, Monteagudo-Sánchez A, Greenberg MVC, Chen K, Manerao-Azua A, Perez de Nanclares G, Lartey J, Monk D
Epigenetics (Dec 2025)

Genomic imprinting is the parent-of-origin specific monoallelic expression of genes that result from complex epigenetic interactions. It is often achieved by monoallelic 5-methylcytosine, resulting in the formation of differentially methylated regions (DMRs). These show a bias towards oocyte-derived methylation and survive reprogramming in the pre-implantation embryo. Imprinting is widespread in the human placenta. We have recently performed whole-genome screens for novel imprinted placenta-specific germline DMRs (gDMRs) by comparing methylomes of gametes, blastocysts and various somatic tissues, including placenta. We observe that, unlike conventional imprinting, for which methylation at gDMRs is observed in all tissues, placenta-specific imprinting is associated with transient gDMRs, present only in the pre-implantation embryo and extra-embryonic lineages. To expand the list of imprinted genes subject to placenta-specific imprinting, we reinvestigated our list of candidate loci and characterized two novel imprinted genes, and , both of which display polymorphic imprinting. Interrogation of placenta single-cell RNA-seq datasets, as well as cell-type methylation profiles, revealed complex cell-type specificity. We further interrogated their methylation and expression in placental samples from complicated pregnancies, but failed to identify differences between intrauterine growth restricted or pre-eclamptic samples and controls, suggesting they are not involved in these conditions.]]> Wed, 31 Dec 1969 19:00:00 EST Multigenerational exposure to DEHP drives dysregulation of imprinted gene Snurf to impair decidualization. Tan L, Gao R, Su Y, Zhang Y, Geng Y, Liu Q, Ma Y, Chen X, Li F, He J
J Hazard Mater (Aug 2025)

Phthalate-induced female reproductive health issues, particularly those related to di (2-ethylhexyl) phthalate (DEHP), are growing global concerns. Although most studies have focused on single-generation exposure, studies on prolonged DEHP exposure across multiple generations are limited. This study assessed the effects of multigenerational DEHP exposure on endometrial decidualization, which is crucial for embryo implantation. The results showed that sustained DEHP exposure over three generations exacerbated decidualization injury and led to adverse pregnancy outcomes. RNA sequencing revealed upregulation of the imprinted gene Snurf in the decidua, with changes that may not depend on alterations in DNA methylation. Knockdown of Snurf significantly alleviated in vitro decidualization deficiency induced by mono(2-ethylhexyl) phthalate (MEHP), the biologically active metabolite of DEHP. Proteomic analysis and the AlphaFold 3 algorithm indicated that Stn1 is a downstream target of Snurf, with silencing Stn1 resensitizing Snurf-knockdown stromal cells to MEHP. Human decidual stromal cells (hDSCs) from healthy participants showed sensitivity to MEHP, with the inhibition of decidualization. Epidemiological data from the 2017-2018 National Health and Nutrition Examination Survey (NHANES) indicated a positive association between DEHP exposure and female infertility. This study highlighted the cumulative toxic effects of multigenerational DEHP exposure on female reproduction and revealed the contribution of imprinted genes.]]> Wed, 31 Dec 1969 19:00:00 EST Spatial profiling of chromatin accessibility in formalin-fixed paraffin-embedded tissues. Guo P, Chen Y, Mao L, Cardilla A, Lee CN, Cui Y, Jin D, Hua Y, Xu X, Deng Y
Nat Commun (Jul 2025)

Formalin-fixed paraffin-embedded (FFPE) samples represent a vast, untapped resource for epigenomic research, yet molecular tools for deep analysis of these specimens remain limited. We introduce spatial FFPE-ATAC-seq, an approach for in situ profiling chromatin accessibility within archived tissues. This approach overcomes formalin-induced crosslinking challenges, allowing high-resolution mapping of chromatin landscapes while preserving tissue architecture. Applying spatial FFPE-ATAC-seq to mouse and human tissues, including brain and thymus, reveals intricate spatial organization and distinct cell types in alignment with tissue morphology. Integration with single-cell RNA sequencing validates the precision of our chromatin profiles in identifying key cell types and regulatory elements. We further apply this method to human melanoma, comprehensively characterizing chromatin accessibility across both tumor and non-tumor regions. This method significantly expands the toolkit for epigenomic research, unlocking the potential of an extensive collection of archived FFPE samples for studying gene regulation and disease mechanisms with spatial context.]]> Wed, 31 Dec 1969 19:00:00 EST Fertile androgenetic mice generated by targeted epigenetic editing of imprinting control regions. Wei Y, Yue T, Wang Y, Yang Y
Proc Natl Acad Sci U S A (Jul 2025)

Each new mammalian life begins with the fusion of an oocyte and a sperm to produce a fertilized egg containing two sets of genomes, one from the mother and one from the father. Androgenesis, a way for producing offspring solely from male genetic material, is limited in mammals, presumably due to barriers arising from genomic imprinting, an epigenetic mechanism leading to monoallelic gene expression. Here, we report adult mammalian offspring derived from the genetic material of two sperm cells. These mice, which we refer to as androgenetic mice, were produced via targeted DNA methylation editing of seven imprinting control regions (ICRs) through CRISPR-based epigenome engineering. Two sperm cells were injected into an enucleated oocyte to form putatively diploid embryos. Allele-specific epigenetic editing was achieved by injecting guide RNAs with protospacer adjacent motif (PAM) sequences designed to match one allele but not the other. The birth of androgenetic mice that were able to develop to adulthood demonstrates that mammalian androgenesis is achievable by targeted epigenetic remodeling of a few defined ICRs.]]> Wed, 31 Dec 1969 19:00:00 EST Multi-omics analyses of the complex interplay between genetic variants, DNA methylation, and gene expression in COVID-19. Chen G, DeRoo L, Goodney G, Doumatey AP, Zhou J, Adeyemo AA, Rotimi CN, Gaye A
Am J Physiol Heart Circ Physiol (Jul 2025)

SARS-CoV-2, which drove the 2019 COVID-19 pandemic, continues to engender inquiries into the role of host genetic factors in disease susceptibility. Despite the identification of over 1,000 genes potentially associated with SARS-CoV-2 and COVID-19, the mechanisms connecting genetic variants to phenotype remain elusive. To shed light on these mechanisms, we undertook an integrated analysis, merging data from whole-genome association analyses of COVID-19 with methylome and transcriptomic. Study includes African American adults from the GENE-FORECAST study, encompassing 371 individuals with whole genome sequencing (WGS), 203 with DNA methylation, and 321 with RNA sequencing (RNA-Seq) of blood. 53.3% of participants reported COVID-19. Significant loci associated with COVID-19 were examined within the framework of methylation quantitative trait loci (mQTL) which located near the gene-of-original (-mQTL) and expression quantitative trait loci (eQTL) which located near the gene-of-origin (-eQTL), enabling analysis to assess mediators between genetic variants and COVID-19 status. Our analysis identified four intronic variants and confirmed a missense variant, rs1052067, in associated with COVID-19. Causal mediation analysis revealed that the combination of genetic variants within , epigenomics, and transcriptomics mapped four pathways influencing COVID-19 status. These pathways include: rs9659072 -> DNAm at chr1:156285845 (annotated to ) -> ENSG00000198715:13 (annotated to ); rs12083543 -> DNAm at chr1:155951748 () -> ENSG00000198715:13 (); rs1052067 -> DNAm at chr1:155951748 ()-> ENSG00000198715:13 (); rs1543294 -> ENSG00000198715:13 () -> DNAm at chr1:156077518 (). Through integrated multi-omics analyses, we identified genetic variants whose effects on COVID-19 susceptibility are mediated by changes in DNA methylation and mRNA expression. These findings offer insights into potential mechanistic pathways that merit further exploration.]]> Wed, 31 Dec 1969 19:00:00 EST Understanding the molecular basis of Sjögren's disease using omic technologies. Gómez-Gómez A, Aterido A, Li T, Guillén Y, Martínez S, Julià A, Marsal S, Andreu JL
Rheumatology (Oxford) (Jul 2025)

Primary Sjögren's Disease (SjD) is a chronic autoimmune disease (AD) that primarily affects the exocrine glands, particularly lacrimal and salivary glands, presenting extra glandular manifestations in a significant number of patients. Although it is a prevalent and globally widespread disease, its pathogenesis has not been fully elucidated. Recently, high-throughput omics technologies are providing unprecedented insights into the molecular landscape of various ADs, including SjD. These technical advances are prepared to decipher new aspects of its pathogenesis and to eventually enable the development of more effective treatment strategies. This review explores recent developments in genetics, transcriptomics, epigenomics, proteomics, and metagenomics in SjD, highlighting the potential of integrating multiple omics datasets to identify better drug targets and useful biomarkers for precision medicine.]]> Wed, 31 Dec 1969 19:00:00 EST Personalized medicine for cardiovascular diseases: how next generation epigenetic technologies can contribute? Dogan M, Philibert R
Epigenomics (Jul 2025)

Advances in DNA methylation and artificial intelligence have led to new methods for assessing risk and diagnosing coronary heart disease (CHD), the leading cause of death. However, whether these technologies can also be harnessed to generate new pharmacotherapeutic agents or monitor the effectiveness of new or existing CHD therapies is unknown. In this perspective, we review the development of cardiac assessment technologies and the challenges that these older approaches attempted to address. We next describe Precision Epigenetic methods and describe their strengths and limitations, as well as the conceptual framework through which these tools operate. Finally, we discuss their potential application to the development and evaluation of new therapies for CHD and how Precision Epigenetic tools compare to existing testing modalities for CHD. We conclude that the future is bright for the use of Precision Epigenetic methods in cardiovascular medicine and suggest that their routine use could lead to faster, less expensive and more effective healthcare.]]> Wed, 31 Dec 1969 19:00:00 EST Comparative analysis of statistical and deep learning-based multi-omics integration for breast cancer subtype classification. Omran MM, Emam M, Gamaleldin M, Abushady AM, Elattar MA, El-Hadidi M
J Transl Med (Jul 2025)

Breast cancer (BC) is a critical cause of cancer-related death globally. The heterogeneity of BC subtypes poses challenges in understanding molecular mechanisms, early diagnosis, and disease management. Recent studies suggest that integrating multi-omics layers can significantly enhance BC subtype identification. However, evaluating different multi-omics integration methods for BC subtyping remains ambiguous.]]> Wed, 31 Dec 1969 19:00:00 EST NSD1 mutation status determines metabolic inhibitor sensitivity in head and neck squamous cell carcinomas by regulating mitochondrial respiration. Tang S, Wang Q, Wang Z, Cai L, Pan D, Li J, Chen Q, Zhou Y, Shen YQ
J Pathol (Jul 2025)

Head and neck squamous cell carcinomas (HNSCCs) are the most common malignant tumors in the head and neck region, characterized by a high recurrence rate and early metastasis. Despite advances in treatment, patient outcomes and prognosis remain poor, highlighting the urgent need for new therapeutic strategies. Recent research has increasingly focused on targeting glucose metabolism as a therapeutic strategy for cancer, revealing multiple promising targets and potential drugs. However, the metabolic heterogeneity among tumors leads to variable sensitivity to metabolic inhibitors in different patients, limiting their clinical utility. In this study, we employed bioinformatics analysis, cell experiments, animal models, and multi-omics approaches to reveal differences in glucose metabolism phenotypes among HNSCC patients and elucidated the underlying molecular mechanisms driving these differences. Our findings showed that NSD1 mutation status affects the glucose metabolism phenotype in HNSCC, with NSD1 wild-type HNSCC exhibiting higher mitochondrial respiration and NSD1 mutant HNSCC showing weaker mitochondrial respiration but enhanced glycolysis. We further demonstrated that NSD1 regulates mitochondrial respiration in HNSCC via epigenetic modulation of the TGFB2/PPARGC1A signaling axis. Additionally, we found that NSD1 wild-type HNSCC is more sensitive to mitochondrial respiration inhibitors, whereas NSD1 mutant HNSCC shows increased sensitivity to glycolysis inhibitors. In summary, we found that NSD1 can epigenetically regulate the TGFB2/PPARGC1A axis to modulate mitochondrial respiration and sensitivity to metabolic inhibitors in HNSCC. These findings suggest a novel strategy for selecting metabolic inhibitors for HNSCC based on the NSD1 gene status of patients. © 2025 The Pathological Society of Great Britain and Ireland.]]> Wed, 31 Dec 1969 19:00:00 EST Multi-dimensional annotation of porcine variants using genomic and epigenomic features in pigs. Yin H, Yang L, Zhao Q, Yao W, Teng J, Gao Y, Xu Z, Lin Q, Diao S, Liu X, Zhao F, Zhou Z, Wang Q, Li J, Zhang Z, Zhou H, Groenen MAM, Madsen O, Bai L, Guan D, Fang L, Li K
BMC Biol (Jul 2025)

Investigating the functional impact of genomic variants is essential to uncover the molecular mechanisms behind complex traits. This study compiled a comprehensive dataset of 1,817 whole-genome sequences from diverse pig breeds and populations, capturing the global pig genetic diversity.]]> Wed, 31 Dec 1969 19:00:00 EST Advances and applications of multiomics technologies in precision diagnosis and treatment for gastric cancer. Shen K, Hu C, Zhang Y, Cheng X, Xu Z, Pan S
Biochim Biophys Acta Rev Cancer (Jul 2025)

Gastric cancer (GC), one of the most prevalent malignancies worldwide, is distinguished by extensive genetic and phenotypic heterogeneity, posing persistent challenges to conventional diagnostic and therapeutic strategies. The significant global burden of GC highlights an urgent need to unravel its complex underlying mechanisms, discover novel diagnostic and prognostic biomarkers, and develop more effective therapeutic interventions. In this context, this review comprehensively examines the transformative roles of cutting-edge technologies, including radiomics, pathomics, genomics, transcriptomics, epigenomics, proteomics, and metabolomics, in advancing precision diagnosis and treatment for GC. Multiomics data analysis not only deepens our understanding of GC pathogenesis and molecular subtypes but also identifies promising biomarkers, facilitating the creation of tailored therapeutic approaches. Additionally, integrating multiomics approaches holds immense potential for elucidating drug resistance mechanisms, predicting patient outcomes, and uncovering novel therapeutic targets, thereby laying a robust foundation for precision medicine in the comprehensive management of GC.]]> Wed, 31 Dec 1969 19:00:00 EST