'; ?> 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, 22 Dec 2025 23:48:09 EST Mon, 22 Dec 2025 23:48:09 EST jirtle@radonc.duke.edu james001@jirtle.com Ischemia/Reperfusion Injury and Outcomes in Liver Transplantation Assessed by Omics Technologies: Where Do We Stand? Giraudi PJ, Codotto G, Baccarani U, Baralle F, Gondolesi G, Licastro D, Tiribelli C
Transplantation (Jan 2026)

Liver transplantation faces several biological challenges, including those related to ischemia/reperfusion injury, graft rejection or tolerance, and disease recurrence. These processes significantly impact posttransplant outcomes and highlight the need for a deeper understanding to improve patient care. The progress of omics sciences has been remarkable over the past decades, and omics techniques are widely used in clinical investigations. In this review, we have explored and briefly described investigations using omics technologies (epigenomics, transcriptomics, and proteomics) to better understand the processes affecting liver transplantation. Additionally, we have highlighted recent studies that use cutting-edge omics technologies, including single-cell RNA sequencing, spatial transcriptomics, and multiplex proteomics, often integrated into multiomics approaches, which enable a more detailed and holistic analysis of the produced data, paving the way for the discovery of precise biomarkers for liver transplant monitoring and the development of novel therapies to prevent allograft rejection.]]> Wed, 31 Dec 1969 19:00:00 EST Decoding preterm birth: Non-Invasive biomarkers and personalized multi-omics strategies. Farzizadeh N, Najmi Z, Rosenbaum AJ, Amoozgar M, Hariri A, Aminbeidokhti M, Khosravi A, Zarrabi A
Dev Biol (Jan 2026)

A birth that occurs prior to 37 weeks of gestation is referred to as preterm birth (PTB). PTB is a health concern globally with significant outcomes including neonatal morbidity and mortality. Advancements in multi-omics have revolutionized the understanding of PTB pathogenesis, offering new opportunities for early prediction and risk categorization. This review highlights emerging liquid biomarkers derived from proteomic, metabolomic, genomic, transcriptomic, and epigenomic studies, emphasizing the integrative power of multi-omics approaches. Proteomic analyses have revealed key proteins in maternal and fetal compartments associated with inflammatory and extracellular matrix pathways, while metabolomics have identified lipid and metabolite profiles linked to energy metabolism and fetal development. Genomic and epigenomic studies have uncovered genetic variations and microRNAs involved in uterine contractility and immune modulation, providing novel insights into PTB's molecular underpinnings. Transcriptomic research further underscores the act of long non-coding RNAs (ncRNAs) in regulating gene expression and inflammatory responses. Multi-omics integration, coupled with machine learning models, has demonstrated superior predictive accuracy by synthesizing data across these domains, revealing intricate molecular interactions underlying PTB. Future research should prioritize longitudinal multi-omics studies to capture dynamic biological changes during pregnancy, expanding diverse population cohorts to enhance generalizability. Translating multi-omics insights into clinical practice necessitates collaborative efforts to develop cost-effective, accessible biomarker panels and establish standardized guidelines for implementation. These advancements hold the potential to transform prenatal care through personalized risk assessment and targeted preventive strategies, reducing the global burden of PTB.]]> Wed, 31 Dec 1969 19:00:00 EST CRISPR 2.0: Expanding the genome engineering Toolbox for epigenetics, RNA editing, and molecular diagnostics. Pradhan K, Anoop S
Gene (Feb 2026)

Non-canonical CRISPR systems adaptation has led to genome editing through nucleases, and the development of transcriptional and epigenetic regulation, transcriptome editing, and molecular diagnostics has resulted in a diversified set of tools-CRISPR 2.0. In this review, the author summarizes the mechanisms and recent engineering advances of (i) dCas9-based epigenetic effectors, (ii) RNA-targeting Cas13 systems and engineered RNA editors, (iii) DNA base editors and prime editors, and (iv) CRISPR-powered diagnostic platforms and their translational readiness. There is a critical comparison of the various approaches (e.g., RNAi/ASO versus Cas13-based methods; base editing versus prime editing) along with practical translational considerations such as delivery technologies, safety (off-target/edit windows, mosaicism), and regulatory pathways which are evaluated. Three concise case studies refer to map laboratory evidence to clinical or near-clinical outcomes and the ethical and governance discussion is widened to include global access, intellectual property and equity in deployment. Finally, the authors classify technologies according to their level of readiness - diagnostics and some ex-vivo therapeutic approaches are already in or very close to clinical use, chosen in-vivo editing methods are undergoing early trials, and AI-assisted nuclease design is still mostly theoretical but is getting better fast. This comprehensive viewpoint is intended to help researchers and physicians understand which CRISPR tools are most likely to be translated soon and where more validation is required.]]> Wed, 31 Dec 1969 19:00:00 EST Towards personalized epigenomics: learning shared chromatin landscapes and joint de-noising of histone modification assays. Narendra T, Visonà G, Cardona CJ, Abbott J, Schweikert G
NAR Genom Bioinform (Dec 2025)

Epigenetic mechanisms enable cellular differentiation and the maintenance of distinct cell types. They enable rapid responses to external signals through changes in gene regulation and their registration over longer time spans. Consequently, the chromatin landscape, which is the overall organization and biochemical state of chromatin, exhibits both cell-type and individual specificity and contributes to phenotypic diversity. Genomic distributions of chromatin features are typically measured using chromatin immunoprecipitation sequencing and related methods. However, these measurements are subject to substantial biases introduced by the chromatin landscape itself. Here, we introduce DecoDen, which uses measurements of several different histone modifications, to simultaneously learn shared chromatin landscapes while de-biasing individual measurement tracks. We demonstrate DecoDen's effectiveness on an integrative analysis of histone modification patterns across multiple tissues in personal epigenomes. DecoDen is available at https://github.com/ntanmayee/decoden.]]> Wed, 31 Dec 1969 19:00:00 EST Epigenomics-guided precision oncology: Chromatin variants in prostate tumor evolution. Furlano K, Keshavarzian T, Biernath N, Fendler A, de Santis M, Weischenfeldt J, Lupien M
Int J Cancer (Jan 2026)

Prostate cancer is a common malignancy that in 5%-30% leads to treatment-resistant and highly aggressive disease. Metastasis-potential and treatment-resistance is thought to rely on increased plasticity of the cancer cells-a mechanism whereby cancer cells alter their identity to adapt to changing environments or therapeutic pressures to create cellular heterogeneity. To understand the molecular basis of this plasticity, genomic studies have uncovered genetic variants to capture clonal heterogeneity of primary tumors and metastases. As cellular plasticity is largely driven by non-genetic events, complementary studies in cancer epigenomics are now being conducted to identify chromatin variants. These variants, defined as genomic loci in cancer cells that show changes in chromatin state due to the loss or gain of epigenomic marks, inclusive of histone post-translational modifications, DNA methylation and histone variants, are considered the fundamental units of epigenomic heterogeneity. In prostate cancer chromatin variants hold the promise of guiding the new era of precision oncology. In this review, we explore the role of epigenomic heterogeneity in prostate cancer, focusing on how chromatin variants contribute to tumor evolution and therapy resistance. We therefore discuss their impact on cellular plasticity and stochastic events, highlighting the value of single-cell sequencing and liquid biopsy epigenomic assays to uncover new therapeutic targets and biomarkers. Ultimately, this review aims to support a new era of precision oncology, utilizing insights from epigenomics to improve prostate cancer patient outcomes.]]> Wed, 31 Dec 1969 19:00:00 EST Immunofluorescence Staining and Microscopic Imaging of Plant Nuclei for Epigenetic Modifications. Gandhivel VH, Raju S, Shivaprasad PV
Methods Mol Biol (2026)

Histone posttranslational modifications (PTMs) and DNA methylation are the predominant epigenetic modifications on the chromatin that regulate gene expression. These modifications can be spatially resolved using microscopic examination of the nuclei with the help of commercially available antibodies. Here, we describe a detailed method to obtain intact nuclei from plant tissues and reproducibly immunostain the nuclei for specific chromatin marks and microscopic examination. This method can be readily extended to multiple plant species as the antibodies are raised against conserved epigenetic marks.]]> Wed, 31 Dec 1969 19:00:00 EST A hitchhiker's guide to single-cell epigenomics: Methods and applications for cancer research. Moreno-Gonzalez M, Sierra I, Kind J
Int J Cancer (Jan 2026)

Genetic mutations are well known to influence tumorigenesis, tumor progression, treatment response and relapse, but the role of epigenetic variation in cancer progression is still largely unexplored. The lack of epigenetic understanding in cancer evolution is in part due to the limited availability of methods to examine such a heterogeneous disease. However, in the last decade the development of several single-cell methods to profile diverse chromatin features (chromatin accessibility, histone modifications, DNA methylation, etc.) has propelled the study of cancer epigenomics. In this review, we detail the current landscape of single-omic and multi-omic single-cell methods with a particular focus on the examination of histone modifications. Furthermore, we provide recommendations on both the application of these methods to cancer research and how to perform initial computational analyses. Together, this review serves as a referential framework for incorporating single-cell methods as an important tool for tumor biology.]]> Wed, 31 Dec 1969 19:00:00 EST Integration of omics data in the diagnosis and therapy of glioblastoma. Möller C, Schoof M, Ligon KL, Schüller U
Brain Pathol (Jan 2026)

Since the 2016 update of the WHO Classification of Tumors of the Central Nervous System, omics data have been officially integrated into the diagnostic process for glioblastoma, the most prevalent and aggressive primary malignant brain tumor in adults. This review will examine the current and future integration of omics data in both the diagnosis and therapy of glioblastomas. The current clinical use of omics data primarily focuses on genomics for determining the IDH- and H3-wildtype status of the tumor, and on epigenomics, such as assessing MGMT promoter methylation status as a prognostic and predictive biomarker. However, it can be anticipated that the usage and importance of omics data will likely increase in the future. This work highlights how omics technologies have significantly enhanced our understanding of glioblastoma, particularly of its extensive heterogeneity. This enhanced understanding has not only improved diagnostic accuracy but has also facilitated the identification of new predictive and/or prognostic biomarkers. It is likely that the ongoing integration of omics data will transform many aspects of the diagnostic process, including sample acquisition. Additionally, omics data will be integrated into future glioblastoma treatment procedures, with possible applications ranging from identifying potential therapeutic targets to selecting individual treatment plans. The implications of the ongoing integration of omics data for clinical routine, future classification systems, and trial design are also discussed in this review, outlining the pivotal role omics data play in shaping future glioblastoma diagnosis and treatment.]]> Wed, 31 Dec 1969 19:00:00 EST Genetic and epigenetic insights into systemic lupus erythematosus: linking long non-coding RNA growth arrest-specific transcript 5 and interferon signature. Maghraby GG, El-Menyawi MA, Rehiem HAA, Shaker OG, Habib MM, Elgohary R
J Rheum Dis (Jan 2026)

Interferon (IFN) signaling, and excessive apoptosis have a well-established role in systemic lupus erythematosus (SLE) pathogenesis. Long non-coding RNA (lncRNA) growth arrest-specific transcript 5 (GAS5) has been linked to excessive apoptosis and upregulation of IFN genes. We aimed to investigate the expression of IFN-stimulated genes in SLE patients compared to healthy controls, and to assess their association with lncRNA GAS5 and clinical characteristics of SLE.]]> Wed, 31 Dec 1969 19:00:00 EST A cell type enrichment analysis tool for brain DNA methylation data (CEAM). Müller J, Laroche VT, Imm J, Weymouth L, Harvey J, Reijnders RA, Smith AR, van den Hove D, Lunnon K, Cavill R, Pishva E
Epigenetics (Dec 2026)

DNA methylation (DNAm) signatures are highly cell type-specific, yet most epigenome-wide association studies (EWAS) are performed on bulk tissue, potentially obscuring critical cell type-specific patterns. Existing computational tools for detecting cell type-specific DNAm changes are often limited by the accuracy of cell type deconvolution algorithms. Here, we introduce CEAM (Cell-type Enrichment Analysis for Methylation), a robust and interpretable framework for cell type enrichment analysis in DNA methylation data. CEAM applies over-representation analysis with cell type-specific CpG panels from Illumina EPIC arrays derived from nuclei-sorted cortical post-mortem brains from neurologically healthy aged individuals. The constructed CpG panels were systematically evaluated using both simulated datasets and published EWAS results from Alzheimer's disease, Lewy body disease, and multiple sclerosis. CEAM demonstrated resilience to shifts in cell type composition, a common confounder in EWAS, and remained robust across a wide range of differentially methylated positions, when upstream modeling of cell type composition was modeled with sufficient accuracy. Application to existing EWAS findings generated in neurodegenerative diseases revealed enrichment patterns concordant with established disease biology, confirming CEAM's biological relevance. The workflow is publicly available as an interactive Shiny app (https://um-dementia-systems-biology.shinyapps.io/CEAM/) enabling rapid, interpretable analysis of cell type-specific DNAm changes from bulk EWAS.]]> Wed, 31 Dec 1969 19:00:00 EST Machine learning and multi-omics-based identification of hub paternal imprinted genes PEG11/RTL1, PEG9/DLK1, PEG6/NDN, and PEG5/NNAT in sperm of couples experiencing idiopathic recurrent pregnancy loss. Hashemi Karoii D, Najafi SMA, Favaedi R, Esmaeili Borzabadi V, Sabbaghian M, Amirchaghmaghi E, Shahhoseini M
Comput Biol Med (Jan 2026)

Idiopathic recurrent pregnancy loss (IRPL), defined as two or more consecutive pregnancy losses without an identifiable cause, affects 1-2 % of couples in their reproductive years. While maternal factors have been extensively studied, paternal contributions remain underexplored. Paternally imprinted genes are essential for spermatogenesis, embryonic development, and placental function, and their epigenetic dysregulation may contribute to IRPL.]]> Wed, 31 Dec 1969 19:00:00 EST DNA methylation of genes involved in lipid metabolism drives adiponectin levels and metabolic disease. Sinke L, Delerue T, Wilson R, Lu X, Xia Y, Costeira R, Nasr MK, Beekman M, Franke L, Zhernakova A, Fu J, Gieger C, Herder C, Koenig W, Peters A, Ordovas JM, Dörr M, Grabe HJ, Nauck M, Bell JT, Teumer A, Snieder H, Waldenberger M, Slagboom PE, Heijmans BT
Diabetologia (Jan 2026)

Despite playing critical roles in the pathophysiology of type 2 diabetes and other metabolic disorders, the molecular mechanisms underlying circulating adipokine levels remain poorly understood. By identifying genomic regions involved in the regulation of adipokine levels and adipokine-mediated disease risk, we can improve our understanding of type 2 diabetes pathogenesis and inter-individual differences in metabolic risk.]]> Wed, 31 Dec 1969 19:00:00 EST From genes to lifestyle: A multi-dimensional framework for Alzheimer's disease prevention and therapy. Su L, Wang Y
Ageing Res Rev (Jan 2026)

Alzheimer's disease (AD) is a complex neurodegenerative disorder driven by multilayered molecular and cellular mechanisms that cannot be fully elucidated through single-omics approaches. Consequently, large-scale multi-omics integration-encompassing transcriptomics, epigenomics (e.g., methylation), and genetic association studies (GWAS/eQTL/mQTL)-has uncovered critical genetic and epigenetic networks underlying disease risk and progression.Based on these integrative insights, this review emphasized several genes-including KLHL21, SCN2B, ZNF415, and PITRM1-as potential contributors to AD pathogenesis. Notably, single-cell and spatial transcriptomics analyses revealed specific enrichment of these genes in astrocytes, underscoring the pivotal role of this cell type in Aβ clearance, tau propagation, and neuroinflammation. Exercise interventions were shown to selectively modulate the expression of these genes, providing molecular support for the preventive and therapeutic potential of non-pharmacological lifestyle strategies. Drug repurposing analyses using DrugBank have identified promising therapeutic candidates, including FDA-approved agents (e.g., valproic acid, raloxifene, and clomipramine) and naturally derived compounds (e.g., quercetin and fisetin), which may modulate key AD-related pathways. Furthermore, emerging evidence of miRNA-gene regulatory networks suggested an additional layer of post-transcriptional control that may regulate responses to pathological stimuli. Collectively, these integrative insights advocated for a multidimensional precision medicine framework that spans genetic, cellular,network, and lifestyle levels of regulation. This shift from single-target therapeutics to an integrated "gene-cell-network-lifestyle" paradigm open new theoretical and translational avenues for delaying or mitigating AD progression.]]> Wed, 31 Dec 1969 19:00:00 EST Using Epigenetic Data to Deconvolute Immune Cells in Cancer from Blood Samples. Boughanem H, Ouzounis S, Callari M, Sanz-Pamplona R, Macias-Gonzalez M, Katsila T
Methods Mol Biol (2026)

DNA methylation plays a crucial role in regulating gene expression and is a hallmark of epigenetic dysregulation in human tumors. High-throughput DNA methylation profiling can unravel intricate patterns in cancer. Moreover, understanding immune cell dynamics is essential for comprehending cancer progression and treatment response. Using DNA methylation data in immune cells, we can apply deconvolution algorithms estimate proportions of major immune cell types, providing insights into immune status and its implications in cancer. Functional analysis can identify specific overrepresented or underrepresented immune cell subsets, potentially uncovering novel biomarkers or therapeutic targets. This pipeline presents a detailed workflow in RStudio for DNA methylation studies and immune cell deconvolution, enhancing reproducibility and efficiency. The workflow integrates preprocessing, analysis, and visualization steps, facilitating robust inference of cell-type proportions from DNA methylation data.]]> Wed, 31 Dec 1969 19:00:00 EST [Expression of Concern] Gene therapy for human colorectal cancer cell lines with recombinant adenovirus 5 based on loss of the insulin‑like growth factor 2 imprinting. Sun H, Pan Y, He B, Deng Q, Li R, Xu Y, Chen J, Gao T, Ying H, Wang F, Liu X, Wang S
Int J Oncol (Jan 2026)

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, for the immunohistochemical data shown in Fig. 2B and C, the PBS/TUNEL panel in Fig. 2B appeared to be strikingly similar to the PBS/E1A panel shown in Fig. 2C. Furthermore, for the E1A experiments portrayed in Fig. 2C, portions of the data panels shown for the H101 and E1A groups also appeared to be strikingly similar, albeit with rotation of one of the panels. The authors were contacted by the Editorial Office to offer an explanation for this possible anomaly in the presentation of the data in this paper, although up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [International Journal of Oncology 46: 1759‑1767, 2015; DOI: 10.3892/ijo.2015.2852].]]> Wed, 31 Dec 1969 19:00:00 EST Regions of Homozygosity Identified with a Chromosomal Microarray in a Korean Population: Distribution, Frequency, and Clinical Interpretation. Kim J, Min S, Seol CA, Seo EJ
Ann Lab Med (Jan 2026)

Single nucleotide polymorphism-based chromosomal microarray analysis (CMA) can detect regions of homozygosity (ROHs), which may be associated with medical conditions; however, limited ROH data, especially in East Asians, complicates clinical interpretations. We characterized ROH distributions and frequencies in a Korean population using CMA, highlighting clinically relevant findings, including suspected uniparental disomy (UPD), using standardized criteria.]]> Wed, 31 Dec 1969 19:00:00 EST Multiomics Insights into Epigenetic Mechanisms and Their Role as Biomarkers for Acute Coronary Syndrome. D'Agostino A, Rosalinda M, Salvatore M, Monica F
Heart Fail Clin (Jan 2026)

Acute coronary syndrome (ACS) is a complex cardiovascular condition driven by chronic inflammation, immune system imbalances, and epigenetic alterations. Recent research highlights the crucial role of epigenetic modifications in disease progression. Furthermore, differentially methylated regions influence expression in genes associated with immune signaling and cellular functions in ACS patients. ACS is a multifactorial disease driven by complex interactions between genetic, epigenetic, and environmental factors. By leveraging multiomics approaches, clinicians and researchers can uncover novel pathophysiological mechanisms and refine therapeutic strategies for improved cardiovascular outcomes in ACS patients. Integrating multiomics technologies with machine learning-driven analysis is revolutionizing our understanding of ACS.]]> Wed, 31 Dec 1969 19:00:00 EST Ferroptosis in renal cell carcinoma: integrative multi-omics insights and therapeutic perspectives. Wang X, Li J, Zhang Y, Huang R, Zhang P, Hu H
Int J Surg (Dec 2025)

Renal cell carcinoma(RCC)exhibits marked heterogeneity in its molecular landscape and clinical behavior.Ferroptosis,an iron-dependent and lipid peroxidation-driven form of cell death,has emerged as a biologically relevant process in RCC pathogenesis.This review summarizes recent advances in the multi-omics dissection of ferroptosis in RCC,including findings from genomics,epigenomics,transcriptomics,proteomics,metabolomics,and microbiomics.Key molecular regulators such as VHL,SLC7A11,GPX4,and ACSL4 are highlighted for their roles in ferroptosis sensitivity or resistance.In parallel,insights from single-cell and spatial omics offer new perspectives on cell-type specificity and microenvironmental context.We also discuss the implications of ferroptosis in therapeutic modulation,including potential integration with immune checkpoint inhibitors and metabolic interventions.This review aims to provide a coherent overview of ferroptosis in RCC and inform future mechanistic studies and translational strategies.]]> Wed, 31 Dec 1969 19:00:00 EST From renal development to pathology: An analysis of the multilevel role of insulin‑like growth factor 2 (Review). Sun Y, Hao W, Liu W, Hu W
Mol Med Rep (Jan 2026)

Insulin‑like growth factor 2 (IGF2) is a multifunctional polypeptide hormone that serves important roles in embryonic development, metabolic regulation and disease pathogenesis. IGF2 expression is tightly regulated by genomic imprinting, which restricts transcription to the paternal allele. IGF2 modulates cellular processes, including proliferation, differentiation and metabolic homeostasis, by activating downstream signaling cascades via binding to IGF1 receptor, insulin receptor isoform A and IGF2 receptor. IGF2 is important for kidney development, promoting both nephron formation, and the functional maintenance of renal tubules and glomeruli. Aberrant IGF2 expression is associated with the pathogenesis of diverse renal diseases, including acute kidney injury, chronic kidney disease, diabetic nephropathy, renal cell carcinoma and Wilms' tumor. Under pathological conditions, IGF2 promotes renal fibrosis and promotes tumor expansion and progression by activating key signaling pathways such as the PI3K/Akt and TGF‑β pathways. Due to these roles, IGF2 has attracted growing clinical interest as a potential therapeutic target. The present review presents a comprehensive analysis of the structure and function of IGF2, its roles in renal pathophysiology, and its therapeutic potential, while outlining future research directions.]]> Wed, 31 Dec 1969 19:00:00 EST Multi-omics study of molecular and genetic bases of orthostatic hypotension. Zelenova E, Daniel V, Bruttan M, Artemieva L, Spektor E, Mamchur A, Kashtanova D, Ivanov M, Abushinova G, Matkava L, Rumyantseva A, Ivashechkin A, Grebnev P, Golubnikova L, Mitrofanov S, Akopyan A, Beloshevskaya O, Saliyeva T, Tarasova I, Strazhesko I, Yudin V, Makarov V, Keskinov A, Tkacheva O, Yudin S, Skvortsova V
Clin Epigenetics (Dec 2025)

Orthostatic hypotension is a sharp decrease in blood pressure when an individual transitions from a supine to an upright position. OH affects at least 30% of older adults. It is attributed to the dysfunction of the autonomic innervation and decreased vascular bed capacity. Genomic (n = 2526), methylomic (n = 910), and transcriptomic (n = 391) data from centenarians aged 90 years and older were used to examine molecular and genetic factors for OH. No statistically significant genetic predictors of OH were identified. However, the study revealed numerous epigenetic markers of OH indicative of general aging, such as DNA hypomethylation. The predictive DNA methylation-based model for orthostatic hypotension demonstrated an average accuracy of 79%. The transcriptome analyses highlighted associations between OH and inflammation pathways, as well as other age-related biological processes. Integrated omics and clinical data have identified six key mechanisms associated with orthostatic hypotension: metabolic dysregulation, impaired muscle tone, altered cell proliferation, inflammation, humoral regulation, and neural regulation.]]> Wed, 31 Dec 1969 19:00:00 EST