DNA and cell biology最新文献

{"title":"SLC25A30 Regulates Mitochondrial Autophagy Through the PINK1/PARKIN Signaling Pathway to Alleviate Sepsis-Associated Acute Kidney Injury.","authors":"Mingyu Xu, Yuchen Wang, Wuyang Lv, Yingyue Ding, Jing Liu, Ruxue Diao, Xiaotong Ma, Mengjiao Yin, Yingyu Jin","doi":"10.1177/10445498261442835","DOIUrl":"10.1177/10445498261442835","url":null,"abstract":"<p><p>This study aims to investigate the expression of the SLC25 subfamily in sepsis-associated acute kidney injury (SA-AKI) and the role of <i>SLC25A30</i> in regulating PINK1/PARKIN-mediated mitophagy. Transcriptome sequencing of renal tissues from lipopolysaccharide (LPS)-induced SA-AKI rats at multiple time points revealed time-dependent differential expression of SLC25 genes. At 12 h post-LPS injection (renal injury peak), 11 differentially expressed genes were identified. Intersection with Gene Expression Omnibus datasets and Gene Ontology enrichment highlighted 11 codifferentially expressed genes enriched in mitochondrial transmembrane transport. Notably, <i>SLC25A30</i> was significantly negatively correlated with KIM-1 (<i>r</i> = -0.96) and LCN2 (<i>r</i> = -0.98). <i>SLC25A30</i> was significantly downregulated in SA-AKI rat renal tissues and LPS-induced HK-2 cells, accompanied by upregulated PINK1/PARKIN, excessive mitophagy (elevated LC3B-II, decreased p62), and increased renal injury markers. <i>SLC25A30</i> overexpression inhibited PINK1/PARKIN, reversed excessive mitophagy, reduced KIM-1 and LCN2 levels, alleviated mitochondrial dysfunction, enhanced cell viability, and exerted cytoprotective effects. <i>PINK1</i> knockdown attenuated the regulatory effect of <i>SLC25A30</i> on excessive mitophagy, indicating a dependence on the PINK1/PARKIN pathway. In conclusion, downregulated <i>SLC25A30</i> is closely associated with excessive mitophagy in SA-AKI. <i>SLC25A30</i> overexpression inhibits excessive mitophagy via downregulating the PINK1/PARKIN pathway, improves mitochondrial function, and alleviates HK-2 cell injury, suggesting that <i>SLC25A30</i> may be a novel molecular target for SA-AKI-targeted therapy.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"327-342"},"PeriodicalIF":2.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147792939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Midbody Remnants as Signaling Centers in Cell Fate Determination and Tumorigenesis.","authors":"Hongbin Li, Xiaoli Ma, Jing Liang, Kai Xue, Wengui Shi, Wanying Lang","doi":"10.1177/10445498261448093","DOIUrl":"10.1177/10445498261448093","url":null,"abstract":"<p><p>During final cell division, the cleaved midbody is either released or asymmetrically retained as a midbody remnant (MBR). MBRs play critical roles in cell communication, signal transduction, and translation regulation, influencing cellular fate. Here, we synthesize their functions as RNA-processing granules, polarity regulators, and signaling platforms, emphasizing their role in primary cilia formation. In polarized epithelial cells, the MBR moves along the apical surface to the centrosome, delivering membrane components to permit ciliogenesis. In ductal carcinoma cells, MBR-localized Shc1-binding protein (SHCBP1) interacts with TBC1 domain family member 30 (TBC1D30 to antagonize Ras-related protein Rab-8 (Rab8) GTPase activity, blocking MBR-centrosome proximity and silencing ciliogenesis. Beyond ciliary regulation, MBRs integrate Wnt, PDGF, TGF-<i>β</i>, and genomic stability networks, acting as dynamic signaling hubs during cancer development. Regarding therapeutic strategies targeting MBRs, High SHCBP1 expression correlates with ciliary loss and poor prognosis in breast, pancreatic, and cholangiocarcinoma. Targeting the SHCBP1/Rab8 axis to restore ciliogenesis by reestablishing MBR-centrosome proximity offers a potential therapeutic strategy. In addition, secreted MBRs are enriched in signaling components and transcripts, serving as intercellular carriers of oncogenic cargoes and promising liquid biopsy biomarkers. In summary, by tracing MBRs from their postmitotic origin to their pathogenic roles, we highlight vulnerabilities within MBR regulatory networks and provide novel insights for cancer therapeutics.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"317-326"},"PeriodicalIF":2.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147824947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond the Tumor Mass: From Initiating Clones to Overt Isocitrate Dehydrogenase-Mutant Gliomas.","authors":"Jung Won Park, Jeong Ho Lee, Seok-Gu Kang","doi":"10.1177/10445498261435336","DOIUrl":"10.1177/10445498261435336","url":null,"abstract":"<p><p>Isocitrate dehydrogenase (<i>IDH</i>)-mutant gliomas are primary malignant brain tumors defined by recurrent mutations in <i>IDH1/2</i> genes and characterized by distinct molecular subtypes and relatively favorable clinical outcomes. Although these mutations represent early and defining events, recent data suggest that <i>IDH1</i> mutant glial progenitor cells can reside within the histologically normal-appearing peritumoral cortex, indicating that cells harboring the founding driver mutation can persist beyond the tumor mass while retaining nonmalignant features. These observations challenge a purely gene-centric view of gliomagenesis. In this essay, we review emerging data supporting a multistep and context-dependent model in which the mutant IDH enzyme establishes an epigenetically altered cellular state, with subsequent genetic alterations and lineage-specific constraints that shape malignant progression. We further discuss the conceptual distinction between the \"cell-of-mutation\" and the \"cell-of-origin\" and consider how temporal stratification of tumor evolution may inform stage-specific therapeutic strategies along the transition from initiating clones beyond the tumor mass to overt tumors.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"267-272"},"PeriodicalIF":2.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147492412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dent Disease 1 Associated with a Rare Novel Renal Chloride Channel 5 Variant in a Chinese Family.","authors":"Si-Yuan Zhang, Hao Huang, Zi-Jie Yu, Liang-Liang Fan, Jie-Yuan Jin, Qin Wang, Hui Xu, Lei Zhu, Yu-Xing Liu","doi":"10.1177/10445498261441112","DOIUrl":"10.1177/10445498261441112","url":null,"abstract":"<p><p>Dent disease 1, an X-linked recessive proximal tubulopathy most commonly caused by <i>CLCN5</i> variants, often presents with heterogeneous and nonspecific phenotypes that hinder clinical diagnosis in the absence of molecular data. We investigated a Chinese kindred with suspected hereditary renal disease using whole-exome sequencing and comprehensive <i>in silico</i> analyses and identified a novel frameshift variant in <i>CLCN5</i> (NM_001127899: c.2359dupG/p.R788Afs*24). Segregation analysis showed the proband to be hemizygous, with his mother and daughter as heterozygous carriers. Pathogenicity prediction, domain mapping against published <i>CLCN5</i> variants, and literature review indicate that this variant lies within a functionally critical, variant-hotspot region of the protein where truncating variants correlate with classic Dent disease 1 phenotypes. Molecular docking and structural modeling further predict destabilization of the H⁺/Cl^- exchange transporter 5 (CLC-5) dimer and reduced adenosine triphosphate (ATP)/adenosine diphosphate (ADP) binding affinity attributable to the frameshift, providing mechanistic plausibility for impaired channel function. Collectively, genetic, bioinformatic, and structural evidence support the p.R788Afs24 mutant as a likely pathogenic allele underlying the proband's renal phenotype, expanding the variant spectrum of <i>CLCN5</i> and underscoring the necessity of genetic testing for accurate diagnosis and management of Dent disease 1.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"273-280"},"PeriodicalIF":2.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147625291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bacteriophage-Encoded Small RNAs: Emerging Tools for Phage Therapy and Antibacterial Intervention.","authors":"Aviezer Silverman, Sahar Melamed","doi":"10.1177/10445498261431525","DOIUrl":"10.1177/10445498261431525","url":null,"abstract":"<p><p>Bacteriophages (phages) are viruses that specifically infect bacteria and play a central role in shaping microbial communities and bacterial evolution. Beyond their protein-coding genes, phage genomes were found recently to encode small RNAs (sRNAs) that act post-transcriptionally to regulate host and viral gene expression. These phage-encoded sRNAs can influence infection dynamics, modulate host physiology, and determine the balance between lytic and lysogenic cycles. A prominent example is the phage lambda sRNA PreS, which enhances phage DNA replication by increasing translation of the host <i>dnaN</i> mRNA, linking host replication capacity to phage propagation. This review examines emerging evidence that phage-encoded sRNAs constitute a versatile and underappreciated class of molecular tools. We discuss how such RNAs could be repurposed as precision antibacterial agents in an era of increasing antibiotic resistance and outline key challenges and opportunities for developing RNA-based alternatives to conventional phage therapy.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"259-262"},"PeriodicalIF":2.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147438552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An Assembly of the Global Phosphoproteomic Network of an Underexplored Kinase CDK17: Possible Implications in Cell Cycle Regulation.","authors":"Ashika Bangera, Fathimathul Lubaba, Athira Perunelly Gopalakrishnan, Prathik Basthikoppa Shivamurthy, Rajesh Raju, Poornima Ramesh","doi":"10.1177/10445498261433751","DOIUrl":"10.1177/10445498261433751","url":null,"abstract":"<p><p>Cyclin-dependent kinase 17 (CDK17) is an understudied member of the PCTAIRE family of CDKs, with phosphorylation-guided molecular mechanism being underexplored. In this study, an in-depth mass spectrometry-based phosphoproteomics data integration and harmonization, coupled with replicable statistical analysis, was performed to understand the phosphorylation landscape of CDK17. High-confidence phosphorylation sites of CDK17 were derived from 711 phosphoproteomics profiling studies, where 176 datasets showed differential phosphorylation of CDK17. Among 13 identified phosphorylation sites of CDK17, S180, S137, and S146 were prominently detected in 75% of all the datasets. Notably, sequence conservation of CDK17 (S146, S137, and S180) with CDK16 (S119, S110, and S153) and CDK18 (S98, S89, and S132), respectively, was observed, where CDK16 (S119) is a part of the binding motif for multiple upstream kinases, 14-3-3 protein, and CCNYL1. Furthermore, conserved co-regulatory patterns of other proteins were identified as compared with CDK17 phosphorylation, which revealed 19 upstream kinases, 164 downstream substrates, and several interactors of CDK17, which conserved co-regulatory patterns across diverse biological contexts. Statistical analysis revealed phosphoregulation of CDK17 through other kinases, regulation of CDK17 substrates, protein-protein interactions, and conserved co-differential regulation in multiple datasets. Specifically, this analysis derived through global data integration with a replicable analytical framework lays a groundwork for experimental validation of CDK17 phosphorylation in its functional regulation.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"281-293"},"PeriodicalIF":2.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147482870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"First-in-Class Small Molecule Inhibitor of Oncogene <i>AVIL</i> in Glioblastoma.","authors":"Zhongqiu Xie, Sophia Xie, Hui Li","doi":"10.1177/10445498261431994","DOIUrl":"10.1177/10445498261431994","url":null,"abstract":"<p><p>Glioblastoma multiforme (GBM) is the most prevalent and aggressive malignant primary brain tumor, marked by rapid growth, extensive invasiveness, and a median survival of only ∼15 months despite current multimodal therapy. To identify new therapeutic vulnerabilities, we investigated the actin-regulatory protein <i>AVIL</i>, previously implicated through a <i>MARS-AVIL</i> gene fusion in rhabdomyosarcoma. Comprehensive genomic and transcriptomic analyses across REMBRANDT, TCGA, and CGGA datasets revealed recurrent <i>AVIL</i> amplification and consistently elevated AVIL expression in GBM compared with normal brain tissue. <i>AVIL</i> was overexpressed across all GBM molecular subtypes and glioma stem cell (GSC) states but was nearly undetectable in normal astrocytes, neural stem cells, and brain tissues. Functional studies demonstrated that <i>AVIL</i> is both necessary and sufficient for glioma genesis: <i>AVIL</i> silencing eradicated GBM cells <i>in vitro</i> and suppressed xenograft growth <i>in vivo</i>, while <i>AVIL</i> overexpression enhanced proliferation, migration, and transformation. Mechanistically, <i>AVIL</i> drives tumor progression through actin cytoskeleton remodeling and activation of the FOXM1-LIN28B oncogenic pathway. Using a small molecule microarray screen, we identified a selective <i>AVIL</i>-binding compound (compound A) that potently inhibited GBM cell growth with minimal toxicity to normal astrocytes. Gene expression changes induced by compound A mirrored those following <i>AVIL</i> knockdown, indicating on-target activity. Compound A demonstrated robust antitumor efficacy in multiple preclinical GBM models, including orthotopic xenografts, GSC-derived tumors, patient-derived xenografts, and temozolomide-resistant GBM with favorable pharmacokinetics and blood-brain barrier penetration. The minimal <i>AVIL</i> expression in normal tissues and lack of phenotype in <i>AVIL</i>-deficient mice underscore its potential as a low-toxicity therapeutic target. Together, these findings establish <i>AVIL</i> as a critical oncogenic driver in GBM and introduce a first-in-class <i>AVIL</i> inhibitor with strong translational promise for precision neuro-oncology.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"263-266"},"PeriodicalIF":2.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13535569/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147392041","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Estrogen, Dopamine, and Learning.","authors":"Carla E M Golden, Christine M Constantinople","doi":"10.1177/10445498261427138","DOIUrl":"10.1177/10445498261427138","url":null,"abstract":"<p><p>Estrogenic hormones act throughout the brain, yet the basic mechanisms by which hormones influence neural circuit dynamics and computations, especially during complex behaviors, are unclear. Exogenous estrogenic hormones modulate dopamine signaling in the nucleus accumbens, which is thought to promote synaptic plasticity for reward-based learning. We recently found that elevated estrogenic activity predicts enhanced phasic dopamine and behavioral sensitivity to past rewards that could be explained by reduced expression of dopamine reuptake proteins in the nucleus accumbens core. Our computational and decision theoretical approach allowed us to characterize estrogenic modulation of dopamine at broad levels of description and opens up new avenues of research on hormone-neuromodulatory interactions during cognitive behaviors.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"187-190"},"PeriodicalIF":2.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147391963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SLFN11 Enhances PARPi Sensitivity in Ovarian Cancer via Ubiquitin-Mediated Stabilization.","authors":"Minjie Liu, Hongfeng Li, Fang Zhang, Jia Bian, Laifu Fang","doi":"10.1177/10445498261422919","DOIUrl":"10.1177/10445498261422919","url":null,"abstract":"<p><p>Schlafen family member 11 (<i>SLFN11</i>), implicated in cancer drug resistance, may improve poly(ADP-ribose) polymerase inhibitor (PARPi) efficacy. This study investigates <i>SLFN11</i>'s role in epithelial ovarian cancer (EOC) progression and its influence on PARPi sensitivity, particularly in <i>BRCA</i>-wild-type contexts, with a focus on its emerging function in proteostasis regulation. <i>SLFN11</i> expression in EOC and adjacent tissues was evaluated via immunohistochemistry, quantitative polymerase chain reaction (PCR), and Western blot. Functional assays-including cell viability, transwell migration, wound healing, and colony formation-assessed <i>SLFN11</i>'s effects on SKOV3 cells (<i>BRCA</i>-wild-type) proliferation and invasiveness. PARPi sensitivity in SKOV3 cells with <i>SLFN11</i> knockdown or overexpression (OE) was tested using Cell Counting Kit (CCK)-8 and Terminal deoxynucleotidyl transferase (TdT) dUTP Nick-End Labeling (TUNEL) assays. Protein stability and ubiquitination levels of <i>PARP1/2</i> were analyzed as the central mechanism. <i>SLFN11</i> mRNA and protein levels were markedly lower in EOC tissues compared with normal tissues. Silencing <i>SLFN11</i> enhanced EOC cell proliferation, migration, and invasion, whereas OE inhibited these malignant behaviors. <i>SLFN11</i> knockdown reduced PARPi-induced apoptosis and drug sensitivity, while its OE amplified these responses. Mechanistically, we demonstrate that <i>SLFN11</i> suppresses global proteotoxic ubiquitination, thereby specifically stabilizing PARP1/2 proteins and potentiating PARPi-mediated DNA damage through enhanced chromatin trapping. <i>SLFN11</i> enhances PARPi sensitivity in EOC by stabilizing PARP1/2 via inhibition of proteotoxic ubiquitination, supporting its role as a biomarker in a <i>BRCA</i>-wild-type EOC cell model where PARPi efficacy is limited by intrinsic resistance. While the application of PARPi in other subtypes of EOC still requires further validation, <i>SLFN11</i> may improve PARPi response and could be explored as a strategy to address PARPi resistance.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"226-240"},"PeriodicalIF":2.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147461286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Silent Signals: The Expanding Role of Cell-Free DNA in Women's Health, Pregnancy, and Reproductive Medicine.","authors":"Matin Dolatabadi, Mahdieh Mondanizadeh","doi":"10.1177/10445498261426174","DOIUrl":"10.1177/10445498261426174","url":null,"abstract":"<p><p>Cell-free DNA (cfDNA) is an emerging biomarker detectable in various bodily fluids, with promising implications across a wide range of clinical domains. Its minimally invasive nature, short half-life, and ability to reflect tissue-specific genetic and epigenetic alterations position cfDNA as a key tool in women's health diagnostics. This narrative review aims to explore the biological characteristics, release mechanisms, and clinical utility of cfDNA in gynecological cancers, pregnancy-related disorders, and assisted reproductive technologies (ART), highlighting current applications, benefits, limitations, and future perspectives. A comprehensive literature review was conducted using databases including PubMed, Scopus, Web of Science, and Google Scholar. Relevant peer-reviewed articles from January 2005 to March 2025 were analyzed to summarize advances in cfDNA detection techniques, clinical applications, and emerging technologies in women's health. In gynecology, cfDNA-especially circulating tumor DNA-has shown promise in early cancer detection, mutation analysis, and disease monitoring. In prenatal medicine, fetal cfDNA (cffDNA) in maternal plasma enables highly accurate, noninvasive screening for chromosomal abnormalities and pregnancy complications such as preeclampsia and intrauterine growth restriction. In reproductive medicine, cfDNA derived from follicular fluid and embryo culture media may serve as a novel biomarker for assessing oocyte and embryo quality. cffDNA offers a noninvasive method for fetal genetic evaluation in pregnancy loss cases, enabling the detection of chromosomal abnormalities to inform clinical management. Technological innovations such as fragmentomics, methylation analysis, and artificial intelligence are enhancing the analytical power and clinical relevance of cfDNA. cfDNA offers a transformative, noninvasive approach for improving diagnosis, prognosis, and personalized care in women's health. While clinical implementation still faces technical and standardization challenges, emerging tools and multi-omics integration are expected to strengthen the role of cfDNA in precision medicine. Future large-scale studies and validation across diverse populations are essential to support its routine clinical adoption.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"201-213"},"PeriodicalIF":2.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147438546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}