geneimprint : Hot off the Press

'; ?> 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, 05 Feb 2026 03:33:23 EST Thu, 05 Feb 2026 03:33:23 EST jirtle@radonc.duke.edu james001@jirtle.com Emerging Role of ctDNA Fragmentomics and Epigenetic Signatures in the Early Detection, Minimal Residual Disease Assessment, and Precision Monitoring of Renal Cell Carcinoma. Kamli H, Khan NU
J Cell Mol Med (Feb 2026)

Renal cell carcinoma (RCC) presents a significant global health challenge, with a substantial proportion of patients diagnosed with advanced or metastatic disease due to the limitations of current diagnostic imaging and the lack of validated non-invasive biomarkers. These conventional methods, including computed tomography and magnetic resonance imaging, often lack the sensitivity and specificity to differentiate benign from malignant small renal masses reliably or to detect minimal residual disease (MRD) post-treatment. This review explores the transformative potential of liquid biopsy, explicitly focusing on circulating tumour DNA (ctDNA) fragmentomics and epigenetic signatures, to overcome these clinical hurdles. This review also explores how the analysis of ctDNA fragmentation patterns-such as size distribution, end motifs, and nucleosome footprints-provides a mutation-independent method to enhance RCC detection, even in low-shedding tumours. Concurrently, RCC-specific epigenetic alterations, particularly DNA methylation profiles, offer particular biomarkers for early detection, tumour classification, and prognostication. This Review examines evidence that integrating these multi-analyte approaches-combining fragmentomic and epigenetic data-synergistically improves diagnostic accuracy, enables sensitive MRD assessment, and allows precision monitoring of treatment response and tumour evolution. Despite existing technical and biological challenges, the convergence of ctDNA fragmentomics and epigenetic profiling heralds a new era for the non-invasive, dynamic, and personalised management of RCC, promising to improve patient outcomes through earlier intervention and tailored therapeutic strategies.]]> Wed, 31 Dec 1969 19:00:00 EST Limitations and opportunities in multi-omics integration for neurodevelopmental, neurodegenerative and psychiatric disorders: A systematic review. Behrens LMP, Fernandes GDS, GonÃ§alves GF, Nunes FVM, Weimer RD, Moreira JCF, Dorn M
Neuroscience (Feb 2026)

Recent advances in high-throughput technologies have led to an increased generation of biological data across genomics, transcriptomics, proteomics, epigenomics, and metabolomics. However, a major challenge remains: effectively integrating these multi-omics datasets to allow a more holistic understanding of the complex, interconnected mechanisms underlying human diseases. Neurodevelopmental, neurodegenerative, and psychiatric disorders are particularly multifactorial and heterogeneous, making them candidates for multi-omics approaches. In this context, this systematic review assesses the current state of multi-omics integration in neurological research. Records retrieved from five major databases were processed, and 156 studies were included for further analysis. The most frequently studied conditions were Alzheimer's Disease, Depressive Disorder and Parkinson's Disease, with epigenomics-transcriptomics and metagenomics-metabolomics emerging as the most common omics pairings. The field remains dominated by studies integrating pairs of omics layers. Only a limited number of computational tools are currently being applied to the integration of more than two omics layers, highlighting a gap in comprehensive multi-omics modeling. Despite progress, key challenges persist, including data accessibility and the need for standardized frameworks to allow cross-study comparisons. Moreover, most computational findings lack experimental validation in wet-laboratory settings. Future research should address these challenges, develop scalable algorithms for integrating multi-omics data, and leverage large, open-access datasets. Integrating computational predictions with experimental validation could help researchers prioritize high-confidence biomarkers relevant to clinical applications. Collaborative efforts among bioinformaticians, clinicians, and experimentalists will be essential to translating these advances into clinically actionable solutions.]]> Wed, 31 Dec 1969 19:00:00 EST A cell type enrichment analysis tool for brain DNA methylation data (CEAM). MÃ¼ller 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 Multi-omic screening for pleural mesothelioma in Asbestos-Exposed Populations: A literature review and Recommendations. Zwijsen K, Heirwegh E, Schillebeeckx E, Marcq E, Covaci A, de Beeck KO, van Meerbeeck JP, Raskin J, Janssens A, Snoeckx A, Lamote K
Lung Cancer (Feb 2026)

Pleural mesothelioma (PM) is an aggressive thoracic cancer related to historical exposure to asbestos fibres. Symptoms often appear at an advanced stage, leading to delayed diagnosis and dismal prognosis. Early diagnosis is thus crucial in improving patient outcome. Current biomarker research for early detection focuses on different -omics research fields (genomics, proteomics, transcriptomics, metabolomics and volatomics), however with no clinically useful result. Moreover, currently no screening program is advocated for asymptomatic individuals with an established asbestos exposure. The aim of this review is to summarise the advances in different -omics fields and to pinpoint state-of-the art biomarkers with the highest potential to serve as primary targets in clinical trials for early PM detection or screening.]]> Wed, 31 Dec 1969 19:00:00 EST : a computational suite for DNA methylation sequencing data analysis. Loyfer N, Rosenski J, Kaplan T
Life Sci Alliance (Apr 2026)

Next-generation methylation-aware sequencing of DNA sheds light on the fundamental role of methylation in cellular function in health and disease, increasing the number of covered CpG sites from hundreds of thousands in previous array-based approaches to tens of millions across the whole genome. While array-based approaches are limited to single-CpG resolution, next-generation sequencing allows for a more detailed, single-molecule fragment-level analysis; however, existing tools to fully use this capability are not yet well developed. Here, we present , an extensive computational suite tailored for methylation sequencing data. allows fast access and ultracompact anonymized representation of high-throughput methylome data, obtained through various library preparation and sequencing methods, with a custom epiread file format achieving a compression factor of over 100x from the input BAM file. In addition, contains state-of-the-art algorithms for genomic segmentation, biomarker identification, genetic and epigenetic data integration, and more. offers fragment-level analysis and informative visualizations, across multiple genomic regions and samples.]]> Wed, 31 Dec 1969 19:00:00 EST Cell-free DNA epigenomic profiling enables noninvasive detection and monitoring of translocation renal cell carcinoma. Garinet S, Semaan K, Li J, Zhang Z, Konda P, Sadagopan A, Canniff J, Phillips N, Klega K, Pandey M, Savignano H, Davidsohn MP, Lyons K, Medda A, Khanna P, Achom M, Fortunato BJ, Nawfal R, El Hajj Chehade R, O'Toole J, Horst J, Freeman D, Trowbridge R, Chau CH, Figg WD, Berchuck JE, Crompton BD, Seo JH, Choueiri TK, Freedman ML, Baca SC, Viswanathan SR
J Clin Invest (Feb 2026)

TFE3 translocation renal cell carcinoma (tRCC), an aggressive kidney cancer driven by TFE3 gene fusions, is frequently misdiagnosed owing to morphologic overlap with other kidney cancer subtypes. Conventional liquid biopsy assays that detect tumor DNA via somatic mutations or copy number alterations are unsuitable for tRCC since it often lacks recurrent genetic alterations and because fusion breakpoints are highly variable between patients. We reasoned that epigenomic profiling could more effectively detect tRCC because the driver fusion constitutes an oncogenic transcription factor that alters gene regulation. By defining a TFE3-driven epigenomic signature in tRCC cell lines and detecting it in patient plasma using ChIP-seq, we distinguished tRCC from clear-cell RCC (AUC = 0.86) and samples of individuals without evidence of cancer (AUC = 0.92) at low tumor fractions (<1%). This work establishes a framework for noninvasive epigenomic detection, diagnosis, and monitoring of tRCC, with implications for other mutationally quiet, fusion-driven cancers.]]> Wed, 31 Dec 1969 19:00:00 EST Synergistic integration of clinical and multi-omics data for early MCI diagnosis using an attention-based graph fusion network. Yu S, Zhao J, Ouyang J, Wang X, Kou P, Zhu K, Liu P
J Neurosci Methods (Apr 2026)

Mild cognitive impairment (MCI), a precursor to Alzheimer's disease (AD), requires precise early diagnosis. Single-omics approaches often miss disease complexity, motivating integrative and interpretable solutions.]]> Wed, 31 Dec 1969 19:00:00 EST Polyploid cisplatin-resistant cancer cells have altered nuclear organization and epigenomic status. Gonye AL, Orzolek L, Cherry C, Patatanian M, Loftus LV, Truskowski K, Butler G, Pienta KJ, Amend SR
Neoplasia (Feb 2026)

Chemotherapy resistance remains a critical barrier in cancer treatment, partly driven by polyploid cells that survive therapy and contribute to tumor recurrence. Here, we investigated epigenomic and transcriptional changes associated with cisplatin-surviving polyploid cells compared to parental cancer cells in prostate cancer (PC3) and triple-negative breast cancer (MDA-MB-231) cell lines. We observed persistent dysregulation of chromatin compaction and altered nuclear structure in polyploid cells following cisplatin treatment. Genome-wide chromatin accessibility profiling via ATAC-seq revealed significant remodeling, notably decreased promoter accessibility at proliferation-associated loci and increased accessibility of distal regulatory elements linked to inflammation and stress response. RNA-seq analyses demonstrated a coordinated transcriptional shift away from proliferative signatures toward inflammatory and survival pathways, including activation of NFÎºB, interferon response, and integrated stress response pathways. Importantly, we identified subsets of genes showing concordant changes in promoter accessibility and transcriptional activity, directly linking chromatin remodeling to transcriptional reprogramming. These integrated findings highlight the role of chromatin dynamics and epigenetic plasticity in chemotherapy resistance, demonstrating that widespread chromatin accessibility changes facilitate the transition to a stress-adapted, polyploid cell state. This study provides new insights into the molecular mechanisms supporting cancer cell persistence after chemotherapy.]]> Wed, 31 Dec 1969 19:00:00 EST âfolate axis as a modulator of the epigenetic landscape in autoimmune diseases (Review). Navarro-RodrÃguez PM, Bajeca-Serrano RF, Turrubiates-HernÃ¡ndez FJ, Ceja-GÃ¡lvez HR, HernÃ¡ndez-Bello J, HernÃ¡ndez-RamÃrez CO, RamÃrez-de Los Santos S, MuÃ±oz-Valle JF
Int J Mol Med (Mar 2026)

The oneâcarbon metabolism pathway, regulated by the methylenetetrahydrofolate reductase (MTHFR) enzyme, represents a key nexus where genetic predisposition and nutrient status converge to shape the epigenetic landscape of autoimmune diseases. The objective of the present review is to synthesize evidence of how the âfolate axis drives epigenomic patterns in these conditions. One of the main diseases involved is rheumatoid arthritis, where drugânaÃ¯ve patients show Tâcell and synovial hypomethylation with cytokineâdriven DNMT suppression, a process aggravated by reduced folate availability and polymorphisms that constrain Sâadenosylmethionine supply. Similarly, in systemic lupus erythematosus, CD4 T cells exhibit global hypomethylation with an interferonâskewed signature (such as ), associated with impaired activity and a folateâdependent SAM:SAH imbalance that further diminishes DNMT function. Finally, in celiac disease, intestinal differential methylation, including LINEâ1 hypomethylation, is observed, driven by glutenâinduced villous atrophy and folate malabsorption. Overall, impaired oneâcarbon metabolism and âdependent methylation capacity may be key determinants of epigenomic dysfunction underlying autoimmune disease and its clinical severity.17.]]> Wed, 31 Dec 1969 19:00:00 EST Melatonin-enabled omics: understanding plant responses to single and combined abiotic stresses for climate-smart agriculture. Raza A, Li Y, Charagh S, Guo C, Zhao M, Hu Z
GM Crops Food (Dec 2026)

Climate change-driven single and combined abiotic stresses pose escalating threats to sustainable, climate-smart agriculture and global food security. Melatonin (MLT, a powerful plant biostimulant) has established noteworthy potential in improving stress tolerance by regulating diverse physiological, biochemical, and molecular responses. Therefore, this review delivers a comprehensive synopsis of MLT-enabled omics responses across genomics, transcriptomics, proteomics, metabolomics, miRNAomics, epigenomics, phenomics, ionomics, and microbiomics levels that collectively regulate plant adaptation to multiple abiotic stresses. We also highlight the crosstalk between these omics layers and the power of integrated multi-omics (panomics) approaches to harness the complex regulatory networks underlying MLT-enabled stress tolerance. Lastly, we argue for translating these omics insights into actionable strategies through advanced genetic engineering and synthetic biology platforms to develop MLT-enabled, stress-smart crop plants.]]> Wed, 31 Dec 1969 19:00:00 EST Erythropoietin Expression and Regulation: Piecing Together Known Mechanisms and Emerging Insights. Idriss S, Hoogewijs D, Girodon F, Gardie B
Am J Hematol (Mar 2026)

Erythropoietin (EPO) is a circulating glycoprotein hormone essential for red blood cell production. The history of EPO stretches from early observations of hypoxia in the mid-19th century to its gene cloning and the clinical use of recombinant forms. Structurally, EPO's extensive glycosylation shapes stability, receptor binding, and therapeutic potential, inspiring engineered analogs with distinct pharmacokinetics. Developmentally, EPO expression shifts from embryonic neural crest and fetal hepatocytes to renal interstitial fibroblasts after birth. EPO gene regulation integrates hypoxia-inducible factors, transcriptional repressors, enhancers, with HIF-2Î± as the principal activator, and post-translational mechanisms. Recent findings reveal genetic variants within the EPO gene in patients with erythrocytosis. Isoelectric focusing profiles of EPO in these patients was similar to the hepatic-derived EPO profiles in premature newborns, highlighting a dynamic and context-dependent regulation. These findings suggest that reactivation of EPO expression in the liver could be therapeutically valuable, given that hepatic-derived EPO exhibits enhanced activity. Clinically, erythropoiesis-stimulating agents transformed anemia management but raised safety concerns, leading to refined guidelines. The recent introduction of hypoxia-inducible factor prolyl hydroxylase inhibitors represents a new strategy that restores endogenous EPO production and coordinates iron metabolism through transient HIF stabilization. Outstanding challenges include the absence of faithful human EPO-producing cell models and incomplete understanding of the full molecular mechanisms controlling EPO expression and production. Combining insights from developmental biology, genetics, and epigenomics may open new avenues for therapies targeting disorders of erythropoiesis and oxygen homeostasis.]]> Wed, 31 Dec 1969 19:00:00 EST ChIP happens: from biochemical origins to the modern omics toolbox for understanding steroid hormone receptors. Grimes TF, Pope J, Stenning J, Smith TE, Kent DG, Baker S, Brackenbury WJ, Willems LI, Holding AN
Biochem J (Feb 2026)

Nuclear steroid hormone receptors (SHRs) are ligand-activated transcription factors that mediate cellular responses to steroid hormones (SHs) through regulating gene expression. Understanding the SHR function is crucial for elucidating SH-driven physiology and pathology, including their roles in normal development, metabolism and reproduction, alongside their aberrant function in cancer, endocrine disorders and inflammatory diseases. Investigating the mechanisms that underscore SHR signalling and regulation is therefore essential for advancing our knowledge of both normal physiology and disease and is vital to the development of novel therapeutic strategies. In this review, we examine a range of methods for studying SHR interactions with chromatin and coregulator proteins, from classical biochemical assays to more advanced approaches such as PL-MS, RIME and ChIP. We also highlight potential future innovations in the field, including in situ Calling Cards and UV-induced photocross-linking RIME (UVXL-RIME), that may overcome current methodological limitations, in turn enabling the study of SHRs in increasingly physiologically relevant contexts.]]> 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 T-cell exhaustion from a multiomics perspective: Differentiation mechanisms and regulatory networks in the journey from progenitor-Exhausted TÂ cells to terminally exhausted T cells. Zhu T, Teng X, Jiao Q, Ren Y, Wang Y, Feng M
Clin Transl Med (Feb 2026)

A central hurdle limiting the success of T-cell-based immunotherapies is the progressive dysfunction of T cells, known as exhaustion. Overcoming this exhausted state is therefore a pivotal objective in translational oncology and immunology. The advent of single-cell multiomics has fundamentally revised the once-prevailing view of exhaustion as a uniform endpoint. Instead, it is now recognised as a dynamic differentiation process comprising a spectrum of distinct cellular states. This spectrum is organised along a hierarchical axis, originating from progenitor-exhausted (Tpex) cells that retain proliferative potential and advancing towards terminally exhausted (Tex) populations with severely impaired effector functions. We undertake a comprehensive synthesis of multiomics data-spanning transcriptomic, epigenomic, metabolomic, proteomic and posttranslational modification (PTM)-proteomic layers-to decipher the interconnected regulatory programmes that dictate commitment along this exhaustion axis. From this integrated analysis, we derive a unified mechanistic framework that delineates the molecular drivers of Tpex cell fate determination and terminal exhaustion. Beyond its explanatory power for basic biology, this framework serves as a direct roadmap for therapeutic innovation, highlighting novel nodes for intervention aimed at reinvigorating the exhausted T-cell compartment. The practical application of these insights holds significant promise for enhancing the efficacy of established current immunotherapeutic platforms. KEY POINTS: This review is the first to integrate multi-omics evidence for constructing a dynamic regulatory map of T-cell exhaustion. It highlights the critical cross-omics synergistic mechanisms, such as metabolic reprogramming influencing epigenetic remodeling to drive cell fate. The multi-omics perspective presented directly informs novel therapeutic strategies.]]> Wed, 31 Dec 1969 19:00:00 EST ChromAcS: an automated and flexible GUI for end-to-end reproducible ATAC-seq analysis across multiple species. Hossain M, Mojumder A, Rashid SMM, Islam ABMMK
BMC Bioinformatics (Feb 2026)

]]> Wed, 31 Dec 1969 19:00:00 EST Radiogenomics: Current Understandings and Future Perspectives. Zhang X, Lai Q, Cao J, Ching JCF, Teng X, Zhang J, Lee SWY, Ren G, Cai J
MedComm (2020) (Feb 2026)

Radiogenomics is a rapidly developing field that links radiological image features (radiomics) to genomic-level data (genomics, transcriptomics, and epigenomics), addressing the limitations of single-omic approaches. Radiomics provides a noninvasive and cost-effective method to capture tissue-level characteristics, while genomics elucidates the underlying molecular mechanisms. The central hypothesis is that the formation of imaging phenotypes is associated with the genetic and molecular processes, and thus can reflect underlying biological activities. This review presents the fundamental principles ofÂ radiogenomicÂ analysis, covering key concepts in image analysis and gene analysis, as well as advanced analytical techniques for linking imaging and genomic data. Moreover, we summarize recent research findings across various human diseases, including oncology and nononcology, to highlight the current understandings and achievements in this field. Radiogenomics shows potential in clinical applications for elucidating disease mechanisms, detecting genomic variations noninvasively, and improving prognosis predictions. However, its implementation in clinical practice is limited by data scarcity, analytical methods, and barriers in translational processes. Future research should focus on enhancing data quality and establishing guidelines, developing analytical platforms, and validating current findings through animal models and clinical trials.]]> Wed, 31 Dec 1969 19:00:00 EST Dissecting methylation errors at imprinted genes in human spermatozoa: from molecular observations to clinical applicationsâ . Marques CJ, Sousa M, Carvalho F, Barros A
Biol Reprod (Feb 2026)

Epigenetic modifications regulate chromatin conformation and transcription factor accessibility to regulatory regions of the genome, controlling gene expression without altering the DNA sequence itself, and being stably transmitted throughout cell divisions. One of the most well studied epigenetic marks is DNA methylation, which controls the monoallelic, parental-origin dependent expression of imprinted genes. Paternal imprinting marks are established in the male germ line, so that mature gametes - the spermatozoa - transmit correct imprints to the future embryo. Anomalies in the establishment and/or maintenance of imprinting marks can interfere with embryonic and placental development and/or result in the birth of children affected by imprinting syndromes, such as Silver-Russell (SRS) and Beckwith-Wiedemann (BWS). Here, we review the literature on the observations of imprinting errors in the male gamete, in the context of disturbances in spermatogenesis resulting in male infertility, focusing on the observations described by our group and others. We provide a clinical perspective on the implementation of sperm methylation analysis as a tool to improve diagnostic and therapeutic strategies in Assisted Reproduction Technologies (ART) and highlight the importance of understanding the molecular mechanisms underlying spermatogenic defects and male infertility.]]> Wed, 31 Dec 1969 19:00:00 EST Epigenetic Age Estimation for Hawaiian False Killer Whales (Pseudorca crassidens) in the Absence of 'Known-Age' Individuals. Martien KK, Baird RW, Robertson KM, Kratofil MA, Mahaffy SD, West KL, Chivers SJ, Archer FI
Mol Ecol Resour (Feb 2026)

Epigenetic aging models hold great promise for enhancing many aspects of wildlife research and management. However, their utility is limited by the need to train models using known-aged animals, which are rare among wildlife species. We present a novel approach to developing methylation-based age prediction models that enables us to train models using samples from individuals whose chronological age is estimated with uncertainty based on photo-identification catalogue data. Our approach incorporates this uncertainty into model training by representing the age of each individual with a probability distribution rather than a point estimate. We similarly represent the methylation profiles of individuals as binomial distributions and produce a distribution of predicted age for each sample that reflects the uncertainty in both its age and methylation profile. We compared age models trained using a wide range of parameterisations, training data sets and analytical methods to determine how well they predicted the catalogue-based age estimates. The resulting model has a median absolute error of 1.70âyears, outperforming many published clocks trained with known-age samples. This approach significantly expands the range of species for which accurate methylation-based age models can be developed, particularly those of conservation concern where known-age samples are limited. By producing distributions of predicted age, it also enables researchers to accurately communicate the uncertainty in their age estimates to subsequent data users.]]> Wed, 31 Dec 1969 19:00:00 EST Single-nucleus multiple-organ chromatin accessibility landscape in the adult rat. Li R, Duan S, Deng Q, Ma W, Liu C, Gao P, Lu L, Yuan Y
Gigascience (Feb 2026)

The chromatin accessibility landscape is the basis of cell-specific gene expression. We generated a multi organ, single-nucleus chromatin accessibility landscape from the model organism Rattus norvegicus. For this single-cell atlas, we constructed 25 libraries via snATAC-seq from nine organs in the rat, with a total of over 110,000 cells. Cell classification integrating gene activity scores with known marker genes identified 77 cell types, which were strongly correlated with those in published mouse single-cell transcriptome atlases. We further investigated the enrichment of cell type- and organ-specific transcription factors (TFs), Shared and organ-specific features of endothelial and stromal cells, as well as cross-organ macrophage regulatory states, and the conservation and specificity of gene regulatory programs across species. Together, these findings provide a valuable foundation for dissecting tissue-specific regulatory logic and for advancing cross-organ and cross-species cell type annotation and functional inference in the rat model.]]> Wed, 31 Dec 1969 19:00:00 EST Deciphering SjÃ¶gren's disease: New insights and perspectives extend from advanced omics approaches and immunology. Chen H, Kaneko N, Ohyama Y, Moriyama M
J Autoimmun (Feb 2026)

SjÃ¶gren's disease (SjD), formerly termed SjÃ¶gren's syndrome, is a chronic autoimmune exocrinopathy that has seen substantial advances in basic research over the past decade. Classical experimental approaches have revealed immune dysregulation encompassing aberrant activation of the adaptive immune system, activation of humoral autoimmunity against autoantigens, and upstream participation of innate immune mechanisms. In parallel, with the rapid development of sequencing and omics technologies, researchers are able to use these high-throughput methods to gain a more unbiased, sytem-wide view of disease processes and pathegenesis in SjD. Among them, numerous disease-associated traits have been revealed by genomics and epigenomics, while transcriptomics, proteomics, and immunogenomics have also depicted a more detailed landscape of phenotypes and cell states of immune cells, as well as the roles of key molecules such as Toll-like receptors (TLRs) in promoting autoimmune responses, yielding profound insights for the understanding of SjD. Meanwhile, these diverse data analysis methods offer the researchers impotant tools to further invertigate and understand SjD in the future. The convergence of these modalities supports data-driven disease prediction, refined patient stratification, and identification of therapeutic targets, thereby expanding translational opportunities. Collectively, integrating innovative omics with classical methodologies provides a coherent framework for capturing the pathogenesis of SjD, linking system-wide views to experimental validation, and accelerating the path from pathobiology to precision therapeutics. This review summarizes recent advances in the understanding of the pathogenesis of SjD, lymphomagenesis in SjD, patient stratification and promising targeted therapy, and also outlines future perspectives and challenges to be addressed.]]> Wed, 31 Dec 1969 19:00:00 EST