Omics A Journal of Integrative Biology最新文献

{"title":"Triadic Carrier-Free Nanomedicines: Natural Product-Based Nanoarchitectures for Cancer Therapy.","authors":"Diyar Salahuddin Ali, Hazha Omar Othman, Rebwar Omar Hassan, Suren Azad Ramadhan, Soran Mahmoud Hameed, Kovan Dilawer Issa, Esra Tariq Anwer","doi":"10.1177/15578100261495868","DOIUrl":"https://doi.org/10.1177/15578100261495868","url":null,"abstract":"<p><p>Triadic carrier-free nanomedicines are an emerging class of anticancer nanoassemblies in which therapeutic efficacy derives solely from the self-assembly and/or prodrug behavior of natural-product building blocks, without exogenous carriers. This review systematically evaluates the design principles, assembly mechanisms, biological activities, pharmacokinetics, safety, and translational status of natural-product-based triadic systems composed of two phytochemicals and a third functional modulator (peptide, nucleic acid fragment, or secondary drug). We summarize current <i>in vitro</i> and <i>in vivo</i> evidence showing that preclinical studies on these triadic carrier-free nanomedicines have reported markedly enhanced cytotoxicity, improved tumor accumulation, and reduced off-target toxicity in selected models compared with free-drug mixtures or conventional nanocarriers. However, these benefits have so far been demonstrated in a limited range of tumor types and experimental conditions and require confirmation in broader, clinically oriented investigations. The novelty of this review lies in providing a focused framework that integrates molecular self-assembly forces, multistimuli responsiveness, and mechanistic crosstalk among three natural-product-derived components, while critically outlining key barriers to manufacturability, long-term biodistribution and toxicity, and regulatory pathways that must be addressed to advance triadic carrier-free nanomedicines toward human cancer therapy.</p>","PeriodicalId":19530,"journal":{"name":"Omics A Journal of Integrative Biology","volume":" ","pages":"15578100261495868"},"PeriodicalIF":2.0,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An Immune Exclusion Index Identifies T/NK Cell Effector Deficiency and a Barrier-Like Microenvironmental State in MMRp/MSS Endometrial Cancer.","authors":"Jie Wang, Yu Wang, Liyan Duan, Kunming Li, Yingya Li, Yanping Jia, Yu Wang","doi":"10.1177/15578100261495854","DOIUrl":"https://doi.org/10.1177/15578100261495854","url":null,"abstract":"<p><p>Mismatch repair-proficient or microsatellite stable (MMRp/MSS) endometrial cancer derives limited benefit from immune checkpoint inhibitor monotherapy, and immune exclusion may reflect both barrier-like tumor-stromal programs and insufficient T cell/natural killer cell (T/NK-cell) effector activity. We integrated The Cancer Genome Atlas uterine corpus endometrial carcinoma (TCGA-UCEC), Clinical Proteomic Tumor Analysis Consortium (CPTAC)-UCEC, GSE17025, GSE21882, and GSE251923 to derive and evaluate an immune exclusion index (IEI) in candidate MMRp/MSS tumors. IEI was derived from a 112-gene biologically constrained candidate pool using Cox elastic-net modeling in the TCGA candidate MMRp/MSS cohort (243 tumors, 39 death events). The weighted 9-gene IEI showed apparent association with poor overall survival in the same TCGA cohort (unadjusted hazard ratio [HR] = 5.06, 95% confidence interval [CI] 2.80-9.14, <i>p</i> = 7.77e-08; adjusted HR = 2.00, 95% CI 1.37-2.93, <i>p</i> = 3.62e-04). Median stratification gave HR = 8.15. Gene Expression Omnibus cohorts supported the adverse phenotype direction but not independent MMRp/MSS survival validation; CPTAC and GSE251923 supported RNA-protein and spot-level marker consistency. IEI provides an interpretable framework for candidate T/NK-low, barrier-like microenvironmental states.</p>","PeriodicalId":19530,"journal":{"name":"Omics A Journal of Integrative Biology","volume":" ","pages":"15578100261495854"},"PeriodicalIF":2.0,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genomic Amplification of <i>CCNE1</i> Is Associated with an Immunosuppressive Tumor Microenvironment and Adverse Clinical Outcome in High-Grade Serous Ovarian Cancer.","authors":"Annapurna Vadaparty, Durgadevi Veeraiyan, Guruguhan Sivakumar, Soumyabrata Roy, Akhileshwar Namani, Tapas Patra","doi":"10.1177/15578100261495840","DOIUrl":"https://doi.org/10.1177/15578100261495840","url":null,"abstract":"<p><p>High-grade serous ovarian cancer (HGSOC) is the most lethal gynecological malignancy, with a poor 5-year survival rate. Many patients also experience relapse of the disease due to chemotherapy resistance, highlighting an urgent need for new therapeutic modalities. Among the genomic alterations implicated in HGSOC progression, amplification of cyclin E1 (<i>CCNE1</i>) has emerged as a frequent and clinically significant event, occurring in ∼19% of cases. In this hypothesis-generating study, we explore the prognostic relevance of <i>CCNE1</i> amplification, focusing on its role in shaping the tumor microenvironment (TME). We conducted an <i>in silico</i> analysis utilizing exome sequencing, clinical, and transcriptome data from HGSOC patients available in The Cancer Genome Atlas. <i>CCNE1</i> amplification correlates with significantly reduced overall and disease-free survival in HGSOC patients. Differential gene expression and pathway analyses predicted that <i>CCNE1</i>-amplified tumors associate with replication stress, elevated mitotic activity, and increased chromosomal instability. Importantly, these tumors showed a predicted reprogrammed immune landscape, characterized by elevated stromal content, increased infiltration of M2 macrophages, myeloid-derived suppressor cells, and cancer-associated fibroblasts, alongside reduced expression of antigen-presenting machinery, particularly Human Leukocyte Antigen (HLA) class II genes. Further analysis highlighted a strong association between replication stress and upregulation of Transforming Growth Factor-beta (TGF-β) signaling pathways, which likely contribute to the observed immunosuppressive microenvironment. Together, our data suggested that <i>CCNE1</i> amplification is associated with tumor progression not only through enhanced proliferation but also by adopting an immune-suppressive TME. These observations suggest the potential of targeting the TME or replication stress response pathways in <i>CCNE1</i>-amplified HGSOC as a therapeutic strategy to improve patient outcomes.</p>","PeriodicalId":19530,"journal":{"name":"Omics A Journal of Integrative Biology","volume":" ","pages":"15578100261495840"},"PeriodicalIF":2.0,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149128220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Candidate Inflammation-Microenvironment Progression Signature for Colorectal Cancer Liver Metastasis: Bulk Transcriptomic Discovery, TCGA-COAD Prognosis, and Spatial Localization.","authors":"Peiying Han, Ye Tan, Aidong Chen, Lei Hu","doi":"10.1177/15578100261495849","DOIUrl":"https://doi.org/10.1177/15578100261495849","url":null,"abstract":"<p><p>Colorectal cancer liver metastasis (CRLM) is biologically heterogeneous, and transcriptomic signals from metastatic tissue can be confounded by host liver background. We integrated GSE50760 bulk transcriptomes, The Cancer Genome Atlas colon adenocarcinoma (TCGA-COAD) survival data, GSE17536 external survival data, and GSE225857 spatial transcriptomes to derive and assess a candidate inflammation-microenvironment progression signature. Differential expression between liver metastases and primary colorectal tumors was analyzed with limma using Benjamini-Hochberg false discovery rate correction. Genes with CRLM differential expression, concordant primary-tumor progression direction, and no typical hepatic-background annotation were retained. The resulting 39-gene score was calculated as the mean up-module expression minus the mean down-module expression. Liver metastases showed 418 upregulated and 88 downregulated genes. In TCGA-COAD, the score was associated with worse overall survival and remained associated after adjustment for age, sex, and American Joint Committee on Cancer stage (hazard ratio [HR] per 1 standard deviation [SD] 1.25; <i>p</i> = 0.038). In GSE17536, the score was associated with disease-free/recurrence-free survival (HR per 1 SD 1.72; <i>p</i> = 0.0021). Spatial analysis showed higher lesion-level scores in liver metastases than primary lesions, with L1/L2 heterogeneity. This candidate signature requires independent and prospective validation before clinical use.</p>","PeriodicalId":19530,"journal":{"name":"Omics A Journal of Integrative Biology","volume":" ","pages":"15578100261495849"},"PeriodicalIF":2.0,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149128140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Composition-Aware Analysis of Public Testis Transcriptomes Identifies Reproducible Tissue-State Signatures in Nonobstructive Azoospermia.","authors":"Zhibang Zhang","doi":"10.1177/15578100261495843","DOIUrl":"https://doi.org/10.1177/15578100261495843","url":null,"abstract":"<p><p>Whole-testis transcriptomes can conflate loss of germ cells with transcriptional changes in retained somatic compartments. We used public human testis datasets to determine whether a composition-aware transcriptional pattern is reproducible in nonobstructive azoospermia (NOA). Donor-level single-cell analysis showed marked depletion of recovered spermatocyte and spermatid states in NOA. We held a germline signature and a GSE149512-derived stromal/macrophage-associated signature fixed during evaluation in two independent obstructive azoospermia (OA) comparator cohorts. In GSE145467 (10 OA and 10 NOA), NOA showed lower germline scores and higher tissue-state scores (Hedges' <i>g</i> = 1.70 for the tissue-state score, 95% confidence interval [CI] 0.92-3.77; exact permutation <i>p</i> = 0.00108). The same direction was observed in GSE9210 (11 OA and 47 NOA; <i>g</i> = 3.69, 95% CI: 2.28-7.26; 100,000-draw permutation <i>p</i> = 0.000010). The original mixed-control bulk cohort was retained only as a within-cohort sensitivity analysis because its within-cohort remodeling axis was strongly correlated with the NOA label (<i>r</i> = 0.899; variance inflation factor = 5.19). Small spermatocyte-focused data provided exploratory, rather than confirmatory, cell-state observations. These results support a reproducible bulk tissue-state pattern in NOA, but do not establish absolute cell-number changes, cell-intrinsic mechanisms, microdissection testicular sperm extraction prediction, or clinical utility.</p>","PeriodicalId":19530,"journal":{"name":"Omics A Journal of Integrative Biology","volume":" ","pages":"15578100261495843"},"PeriodicalIF":2.0,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149128145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Global Phosphoproteome Analysis Identifies CLK4 Co-Regulatory Pathways Driving Tumor-Specific Dysregulation.","authors":"Apoorva Pai, Leona Dcunha, Athira Perunelly Gopalakrishnan, Samseera Ummar, Athira C Rajeev, Rajesh Raju","doi":"10.1177/15578100261470540","DOIUrl":"10.1177/15578100261470540","url":null,"abstract":"<p><p>Dual-specificity protein kinase CLK4 plays a pivotal role in regulating alternative mRNA splicing, DNA repair, and various cellular processes through precise phosphorylation. In this study, we analyzed 3825 global human cellular phosphoproteome studies, identifying 430 qualitative profiles and 55 quantitative differential datasets featuring high-confidence Class-1 phosphosites (localization probability ≥ 75%; A-score ≥ 13). Notably, S136 and S138 emerged as predominant phosphorylation sites outside the kinase domain. These sites showed frequent detection and differential expression in liver, lung, and head and neck cancers, as documented in PhosphositePlus. We identified a high-confidence set of co-regulated phosphoproteins, including SQSTM1, SRRT, RPS6, TP53BP1, TNKS1BP1, THUMPD1, OTUD4, and TCEA1. These proteins link CLK4 to critical pathways, including RNA splicing, autophagy, DNA damage response, and cancer progression. Binary interactors, including SRRM2, Interacts with SPT6 1 (IWS1), RBBP6, ZC3H18, BUD13, and DYRK1A, further connect CLK4 to RNA processing and splicing. Predicted downstream substrates, such as CCNL2, CDK11B, PRDX6, YTHDC1, RBM15, SRRM1, SFSWAP, HNRNPU, and DOCK7, highlight CLK4's broad regulatory scope. Upstream kinases were also predicted for S136 and S138. Site-resolved analyses revealed tumor-specific dysregulation of CLK4 phosphorylation at key residues. Co-occurring phosphosite alterations and nearby somatic mutations suggest disrupted CLK4 regulation in cancer. Overall, this study provides a comprehensive phosphoproteomic resource that maps CLK4's co-regulatory networks, paving the way for mechanistic investigations and targeted cancer therapies.</p>","PeriodicalId":19530,"journal":{"name":"Omics A Journal of Integrative Biology","volume":" ","pages":"594-608"},"PeriodicalIF":2.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148550011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative Analysis of Hub Genes and miRNAs Reveals Inflammatory and Structural Signatures in Fibromyalgia and Their Modulation Following Manual Therapy.","authors":"Michele de Moura Gonçalves, Ariana Mendes Freire, Adriana Mary Mestriner Felipe de Melo, Gisele da Silva Peixoto Zandona, Elisabete Castelon Konkiewitz, Eduardo Henrique Loreti","doi":"10.1177/15578100261468867","DOIUrl":"10.1177/15578100261468867","url":null,"abstract":"<p><p>Fibromyalgia is a chronic pain syndrome characterized by widespread musculoskeletal pain, fatigue, sleep disturbances, and cognitive dysfunction, with substantial impact on quality of life and functional capacity. Despite its high prevalence, its underlying molecular mechanisms remain incompletely understood, and reliable biomarkers are lacking. This study performed an integrative analysis of publicly available transcriptomic datasets combined with protein-protein interaction network analysis, hub gene identification, and investigation of microRNA (miRNA)-mediated posttranscriptional regulation, in addition to evaluating molecular modulation following therapeutic intervention. Differentially expressed genes consistently identified across independent cohorts revealed two major molecular axes: An inflammatory-immune axis involving cytokine and interferon-related pathways, including <i>IL6</i>, <i>TNF</i>, <i>CXCL8</i>, and <i>STAT1</i>, and a structural axis associated with extracellular matrix organization, including <i>COL1A1</i>, <i>COL3A1</i>, <i>FN1</i>, and <i>ITGB1.</i> Integration with miRNA data demonstrated reduced expression of regulatory miRNAs linked to inflammatory and structural pathways, suggesting impaired posttranscriptional control. Therapeutic modulation analysis further demonstrated reduced expression of inflammatory genes and increased expression of structural genes following manual therapy, indicating partial reversibility of these molecular alterations. Collectively, these findings support the presence of multilevel molecular dysregulation in fibromyalgia and highlight potential biomarkers and therapeutic targets associated with inflammatory and peripheral structural mechanisms.</p>","PeriodicalId":19530,"journal":{"name":"Omics A Journal of Integrative Biology","volume":" ","pages":"585-593"},"PeriodicalIF":2.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148472078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>LIMK1</i> and <i>PKM</i> as Integratively Identified Transcriptomic Signatures in Inflammatory Bowel Disease.","authors":"Houshu Tu, Menglin Chen, Panpan Zhu, Ling He, Jing Hong","doi":"10.1177/15578100261472246","DOIUrl":"10.1177/15578100261472246","url":null,"abstract":"<p><p>Inflammatory bowel disease (IBD) involves complex immunometabolic dysregulation. Mitochondria-associated endoplasmic reticulum membranes (MAMs) link metabolic adaptation and inflammatory signaling, but gene expression features associated with MAM-related transcriptomic states in IBD remain unclear. Public transcriptomic datasets were integrated with a curated MAM-related gene set and herbal target information. Differential expression analysis, weighted gene coexpression network analysis, and machine learning-assisted feature selection were used to identify candidate genes. A two-gene nomogram was constructed and evaluated in discovery and independent validation datasets. Functional enrichment, immune deconvolution, regulatory network prediction, molecular docking, 200-ns molecular dynamics simulations, and preliminary quantitative polymerase chain reaction validation were performed. <i>LIMK1</i> and <i>PKM</i> were identified as candidate transcriptomic signature genes associated with IBD status and MAM-related transcriptional states, showing discriminatory performance in independent datasets. Both genes were associated with cytokine-cytokine receptor interaction and drug metabolism-cytochrome P450 pathways and were linked to macrophage-related immune states. Structural analyses suggested stable predicted binding between <i>PKM</i> and 1-(4-hydroxybenzyl)-4-methoxy-9,10-dihydrophenanthrene-2,7-diol and structurally plausible interactions between <i>LIMK1</i> and palmatine. Preliminary tissue-level validation supported the disease-associated expression pattern of <i>PKM</i>, whereas <i>LIMK1</i> showed a consistent but nonsignificant upward trend. <i>LIMK1</i> and <i>PKM</i> may represent candidate transcriptomic signatures associated with MAM-related regulatory states in IBD. These findings should be interpreted as hypothesis-generating associations rather than evidence of MAM localization, functional causality, or therapeutic efficacy. Further protein-level and functional validation is required.</p>","PeriodicalId":19530,"journal":{"name":"Omics A Journal of Integrative Biology","volume":" ","pages":"609-630"},"PeriodicalIF":2.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148713120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human Extracellular Vesicles, Metabolites, and Metabolomics: A Comprehensive Review.","authors":"Mohammed A Al-Zubaidi","doi":"10.1177/15578100261467517","DOIUrl":"10.1177/15578100261467517","url":null,"abstract":"<p><p>Metabolomics is a powerful systems-level approach and has the potential to serve as an important part for understanding the biochemical pathways and metabolic phenotypes in physiological and pathological states. Extracellular vesicles (EVs), which include apoptotic bodies, microvesicles, and exosomes, have emerged alongside metabolomics as active mediators of intercellular communication, transporting diverse cargo that mirrors the cellular origin and metabolic status of their parent cell. EVs are enriched with lipids, proteins, nucleic acids, and biologically active metabolites involve in signal transduction, metabolic regulation, and pathogenic mechanisms of a disease. Nevertheless issues related to heterogeneity of vesicles, purity of isolation, and detection sensitivity of metabolites, the study of EV metabolomics still methodologically and analytically challenging. This review offers a critical synthesis of current knowledge in EV metabolomics including analytical technology, statistical and computational approaches, and emerging clinical applications. In addition, a specific focus on methodological variability, contamination chances, and limitations in existing research study design that affect reproducibility and translation. Furthermore, multi-omics integration and machine learning are reviewed as promising approaches to enhance the discovery of biomarkers and interpretation of the biological system. Finally, highlighting the key research gap and future research directions to steer the advancement of clinically related applications in translational medicine.</p>","PeriodicalId":19530,"journal":{"name":"Omics A Journal of Integrative Biology","volume":" ","pages":"561-570"},"PeriodicalIF":2.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148437557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Joint Analysis of QTL Data Provided Insights into the Connection of Transcriptome and Proteome and the Impact of Omics Platforms.","authors":"Majid Nikpay","doi":"10.1177/15578100261467514","DOIUrl":"10.1177/15578100261467514","url":null,"abstract":"<p><p>This study investigated the connection between the transcriptome and proteome by integrating eQTL (Expression Quantitative Trait Locus) and pQTL (Protein Quantitative Trait Locus) datasets generated using different technologies. eQTL data were obtained from the eQTLGen (microarray-based) and INTERVAL (RNA-Seq-based) studies, while pQTL data were derived from the UK Biobank (Olink platform) and deCODE (SomaScan platform) studies. A total of 1162 genes common to all four datasets were analyzed. Mendelian randomization (MR) identified 211 genes whose transcript levels significantly (<i>p</i> < 5e-8) predicted protein levels, whereas genetic correlation analysis detected 67 genes with shared genetic regulation. Negative transcript-protein associations were observed for 12% of genes identified by MR and 7% of those identified through genetic correlation. Cross-platform comparisons showed the strongest concordance between eQTL and pQTL effect sizes in the INTERVAL-UK Biobank panel and the weakest in the eQTLGen-deCODE panel. Colocalization analysis further confirmed these findings and indicated genes with strong eQTL-pQTL overlap predominantly encode intracellular proteins, whereas genes with weak overlap tend to encode glycosylated secreted proteins. Integrating both the transcriptome and proteome for biomarker discovery and locus annotation is important, as the overall genetic architectures of the blood transcriptome and proteome are not the same. RNA-Seq and Olink platforms provide more accurate measurements of RNA and protein levels.</p>","PeriodicalId":19530,"journal":{"name":"Omics A Journal of Integrative Biology","volume":" ","pages":"571-577"},"PeriodicalIF":2.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148592836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}