Frontiers in Cell and Developmental Biology最新文献

{"title":"Cell division during Xenopus gastrulation influences neuroectoderm patterning.","authors":"Ian Velloso, Rodrigo Araujo, Marko Horb, Jose G Abreu","doi":"10.3389/fcell.2026.1798565","DOIUrl":"https://doi.org/10.3389/fcell.2026.1798565","url":null,"abstract":"<p><p>Oriented cell division is emerging as a fundamental morphogenetic mechanism driving tissue elongation and axis formation. Although <i>Xenopus laevis</i> embryos can undergo gastrulation and neurulation in the absence of cell division, the specific contribution of mitosis during gastrulation remains poorly defined. Here, we systematically examine the role of cell division during gastrulation in neural plate formation and anterior-posterior (A-P) patterning. Using Hydroxyurea and Aphidicolin (HUA) to block cell division, combined with in situ hybridization and time-lapse imaging, we analyzed division dynamics and developmental outcomes in the dorsal mesoderm and neuroectoderm. Consistent with previous work, we find that cell division is dispensable for dorsal mesoderm patterning and neural tube closure. Strikingly, however, inhibition of cell division during gastrulation profoundly disrupts neural plate patterning, leading to severe head and trunk defects that manifest at tailbud stages. This phenotype is accompanied by markedly reduced expression of key anterior neural markers (<i>bf1 and krox20</i>), indicating a failure to properly specify the forebrain, midbrain, and hindbrain domains. These defects reveal an essential role for cell division in early neural regionalization rather than in tissue formation per se. Moreover, quantitative analysis shows that cell divisions are abundant throughout the gastrulating ectoderm and exhibit strong A-P orientation, particularly in the dorsal posterior region. Together, our results identify A-P oriented cell division as a conserved and previously underappreciated mechanism required for neural plate elongation and anterior neural patterning during vertebrate development.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1798565"},"PeriodicalIF":4.6,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13144160/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development and clinical validation of a nursing risk prediction model for chemotherapy-induced febrile neutropenia in patients with cancer.","authors":"Fang Xie, Dongmei Zheng, Na Chen, Jie Zhang, Nan Wang, Qin Yi, Lihuai Wang","doi":"10.3389/fcell.2026.1779406","DOIUrl":"https://doi.org/10.3389/fcell.2026.1779406","url":null,"abstract":"<p><strong>Background: </strong>Febrile neutropenia (FN) is one of the most serious yet potentially preventable complications of systemic chemotherapy. However, practical tools that support nursing-led early risk stratification and workflow-ready preventive actions remain limited.</p><p><strong>Methods: </strong>We performed a real-world cohort study including 2,125 patients with cancer receiving systemic chemotherapy at a single institution. Patients were randomly split (7:3) into a derivation cohort (70%) and an internal validation cohort (30%). Candidate predictors were prespecified to ensure bedside nursing assessability and routine clinical availability, incorporating both conventional clinical/laboratory factors and nursing-relevant indicators (e.g., nutritional risk, mucositis, and self-monitoring adherence). Predictors were selected using penalized regression, followed by multivariable logistic modeling to estimate FN risk in the first evaluable chemotherapy cycle. Model performance was assessed by discrimination and calibration, and clinical utility was examined using decision curve analysis. A nomogram and risk-stratified nursing pathways were developed to translate predicted risk into actionable surveillance and preventive care.</p><p><strong>Results: </strong>The final nursing-oriented model showed good discrimination and satisfactory calibration in both the derivation and validation cohorts. Decision curve analysis indicated net benefit across a clinically relevant range of threshold probabilities. Risk stratification based on predicted probabilities was associated with graded increases in FN incidence and adverse clinical outcomes.</p><p><strong>Conclusion: </strong>This nursing-oriented FN prediction model provides individualized early-cycle FN risk estimation and operational risk stratification to support targeted surveillance and preventive nursing interventions. External validation across diverse institutions and nursing documentation systems is warranted.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1779406"},"PeriodicalIF":4.6,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13144087/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stem cell activation in organ culture reveals novel transcriptional programs underlying metabolic, fibrotic, vascular, and immune dysregulation in uterine leiomyomas.","authors":"Paula Vázquez, Ana Salas, Silvia Beltrán-Flores, Francisco Montes de Oca, Araceli Delgado, Teresa A Almeida","doi":"10.3389/fcell.2026.1804196","DOIUrl":"https://doi.org/10.3389/fcell.2026.1804196","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background and objective: &lt;/strong&gt;Uterine leiomyomas may arise from somatic stem or progenitor cells, leading to abnormal activation, proliferation, and clonal expansion. In organ cultures of myometrium and leiomyoma, differentiated cells decline after 7 days, whereas resident stem cells may persist within their niches and subsequently become activated, proliferate, and repopulate tissue slices. This study investigated gene expression programs that regulate the proliferation and differentiation of myometrial and &lt;i&gt;MED12&lt;/i&gt;-mutant leiomyoma stem cells during long-term organ culture.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Comparison of normal and tumor tissues at baseline and after culture revealed several fibroid transcriptional signatures that were preserved during prolonged &lt;i&gt;ex vivo&lt;/i&gt; culture. The &lt;i&gt;MED12&lt;/i&gt; mutation persisted in the repopulated fibroid slices, supporting the hypothesis that fibroids originate from stem or progenitor cells harboring &lt;i&gt;MED12&lt;/i&gt; mutation. Both tissues activated hypoxia and stemness-associated programs, including robust induction of &lt;i&gt;HMGA1&lt;/i&gt;, &lt;i&gt;HMGA2&lt;/i&gt;, and &lt;i&gt;PLAG1&lt;/i&gt;. Myometrium induced KITLG/KIT expression, a limited number of CD49b (ITGA2)-stem-positive and Ki67-positive proliferating cells, indicating restrained proliferation, likely mediated by upregulation of &lt;i&gt;ITGA2-AS1&lt;/i&gt;. Additionally, myometrial slice cultures were enriched for immune and endothelial/vascular programs, including several SOX family members. In contrast, leiomyoma cultures exhibited widespread CD24/CD73 expression, focal CD49b clusters, high Ki67 positivity, metabolic reprogramming toward complex carbohydrate degradation, SLC-mediated transport, and a low-PLIN2/high-ACLY signature. Uterine leiomyoma cultures repressed genes involved in vascular homeostasis (e.g., &lt;i&gt;PLPP3&lt;/i&gt;) and preferentially activated pathways related to smooth muscle excitability and vesicle secretion. Extracellular matrix (ECM) remodeling was strongly pro-fibrotic in leiomyomas, with significant upregulation of several TGFB-regulated and related genes, a disrupted balance of KLF regulators, including loss of the anti-fibrotic repressor &lt;i&gt;KLF10&lt;/i&gt; and induction of the pro-fibrotic &lt;i&gt;KLF5&lt;/i&gt; factor, and broad upregulation of integrins. Differential expression of multiple HOX genes further distinguished ECM regulation between tissues. From niche survival to pro-fibrotic expansion, the study delineates checkpoints primed for intervention, highlighting potential therapeutic opportunities targeting profibrotic signaling, metabolic dependencies, and integrin-mediated ECM interactions.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;Long-term organ culture recapitulates key molecular features of fibroids and reveals tissue-specific mechanisms governing stem cell activation and differentiation. These findings identify potential therapeutic opportunities and establish long-term organ culture as a robust, physiologically relevant platform for investigating norma","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1804196"},"PeriodicalIF":4.6,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13143910/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NELL-1: role and mechanisms in disease pathogenesis and development.","authors":"Fang Mi, Qingrong Yue, Xi Deng, Lijun Jian, Yongkang Wu","doi":"10.3389/fcell.2026.1783756","DOIUrl":"https://doi.org/10.3389/fcell.2026.1783756","url":null,"abstract":"<p><p>NELL-1 (NEL-like protein 1) is a multifunctional secreted glycoprotein that has been implicated in a variety of biological processes, including skeletal development, immune regulation, and tumorigenesis. Despite its significance, the regulatory mechanisms of NELL-1 across different tissues, the diversity of its signaling pathways, and its context-dependent roles in disease are not fully elucidated. This gap in understanding hinders the systematic development and clinical translation of potential applications. Current research suggests that NELL-1 influences skeletal development and regeneration through pathways such as Wnt/β-catenin, MAPK, and Runx3-Indian hedgehog (Ihh). Additionally, it plays crucial roles in conditions such as membranous nephropathy, various tumors, and neurodevelopmental disorders. The distinct isoforms of NELL-1, such as NELL-1₅₇₀ and NELL-1-ΔE, exhibit specific functional properties and hold significant therapeutic promise, particularly in bone regeneration and tumor suppression. This review aims to provide a comprehensive analysis of the molecular mechanisms of NELL-1 in osteogenesis, chondrogenesis, immune regulation, and tumor suppression. It also explores various strategies to enhance its stability and targeting, including PEG modification and nanoparticle delivery systems. In conclusion, NELL-1 represents a key molecule with multi-tissue, multi-disease regulatory potential, and its value in both basic research and clinical translation is increasingly prominent. Future research should focus on its tissue-specific mechanisms, isoform functional optimization, and the development of safe and effective delivery systems to advance its applications in precision medicine.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1783756"},"PeriodicalIF":4.6,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13144030/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advancements in artificial intelligence for cancer diagnosis and prognosis prediction: current applications and emerging opportunities.","authors":"Qingmiao Shi, Na Lou, Chen Xue","doi":"10.3389/fcell.2026.1769097","DOIUrl":"https://doi.org/10.3389/fcell.2026.1769097","url":null,"abstract":"<p><p>Cancer continues to be a leading cause of mortality worldwide, presenting substantial challenges to public health systems. The traditional approaches to cancer diagnosis and prognosis prediction exhibit certain limitations with respect to accuracy, comprehensiveness, dynamic monitoring, and personalization. With the advancement of artificial intelligence (AI) technologies, novel diagnostic and predictive methods are increasingly addressing these shortcomings. This review provides a comprehensive overview of the primary AI algorithms applied in oncology, including machine learning, deep learning, and large language models. It further examines the distinctive characteristics and appropriate use cases of AI algorithms, highlighting their specific roles in cancer screening, diagnostic accuracy, and outcome forecasting. Additionally, the review discusses emerging trends and persistent challenges, aiming to provide actionable insights that support clinical decision-making and advance scientific innovation in this rapidly evolving field. In conclusion, this review systematically outlines recent advances in AI applications for cancer diagnosis and prognostic prediction, with the objective of facilitating a transformative shift in oncology from experience-based practices toward data-driven precision medicine.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1769097"},"PeriodicalIF":4.6,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13144042/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New Frontiers in modeling the lipedema microenvironment <i>in vitro</i>.","authors":"Khushi Soni, Rosalyn D Abbott","doi":"10.3389/fcell.2026.1816014","DOIUrl":"https://doi.org/10.3389/fcell.2026.1816014","url":null,"abstract":"<p><p>Lipedema is a chronic and often debilitating adipose tissue disorder that primarily affects women. The disease is characterized by disproportionate and symmetrical accumulation of subcutaneous fat in the extremities. Despite the high prevalence of lipedema, which affects ∼10% of women, and its significant impact on patient quality of life, lipedema is understudied and often misdiagnosed as other disorders (obesity or lymphedema). In this review, we explore the current understanding of lipedema through clinical, tissue, and cellular lenses, and examine suspected pathological mechanisms, including hormonal influences (such as estrogen), adipocyte hypertrophy and hyperplasia, increased extracellular matrix (ECM) fibrosis, and specialized immune cell involvement, including M2 macrophage infiltration. Recent advancements in adipose tissue engineering, including organoids, fat-on-a-chip platforms, and the use of induced pluripotent stem cells (iPSCs) are explored as platforms to study lipedema pathogenesis.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1816014"},"PeriodicalIF":4.6,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13139339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeted autophagy: research progress on the regulatory potential of periodontitis prevention and treatment.","authors":"Yujia Wang, Zhaojiang Fu, Yingtao Wu","doi":"10.3389/fcell.2026.1708337","DOIUrl":"https://doi.org/10.3389/fcell.2026.1708337","url":null,"abstract":"<p><p>Chronic periodontitis is a multifactorial inflammatory disease primarily caused by bacterial pathogens, leading to progressive destruction of both soft and hard periodontal tissues. While dental plaque biofilm has been universally recognized as the primary etiological factor in periodontitis development, disease progression is also influenced by local irritants and systemic modulators, making its pathogenesis complex and widely studied. Autophagy, an essential cellular self-protection mechanism, plays a pivotal role in maintaining intracellular homeostasis, responding to stress stimuli, and defending against microbial invasion. Recently, this process has emerged as a key research focus in periodontal pathology. This study investigates the dynamic changes and functional variations of autophagy during different stages of periodontitis, aiming to elucidate its precise role in disease initiation and progression.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1708337"},"PeriodicalIF":4.6,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13139059/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insights gained from single-cell sequencing analysis of ischemic stroke.","authors":"Yanqin Mei, Teng Guan, Longsheng Fu, Jiming Kong, Yanni Lv","doi":"10.3389/fcell.2026.1784660","DOIUrl":"https://doi.org/10.3389/fcell.2026.1784660","url":null,"abstract":"<p><p>Ischemic stroke represents a significant global health hazard, causing substantial morbidity, mortality, and long-term disability worldwide. The brain's complexity necessitates targeting ischemic stroke dysfunction syndrome. Single-cell RNA sequencing (scRNA-seq) offers unbiased, high-resolution analysis of cell heterogeneity, revealing cellular markers and types. Limited therapeutic options and drug discovery hinder stroke treatment, but scRNA-seq provides insights into new targets and biomarkers. Since 2019, over 50 studies on scRNA-seq in ischemic stroke have been published. This review summarizes ischemic stroke research based on scRNA-seq technology, detailing stroke features from various perspectives. We tabulated 22 brain and 7 blood cell types post-stroke. 13 cell types that frequently reported in ischemic stroke and undergone extensive heterogeneity studies were summarized. A summary was given of investigations into subcluster categorization, function-related subclusters, and newly discovered subclusters from scRNA-seq. Immune cell or non-immune cellular interactions and their regulatory influences were also explored. Additionally, the review covered age-related issues, advantages and disadvantages, technological innovations, and scope in ischemic stroke. Despite the moniker \"single-cell,\" the analysis transcends individual entities, acknowledging the systemic variability of cellular types. Single-cell sequencing technologies, by their nature, interrogate entire tissues, distilling information from thousands of cells into a comprehensive average. Looking ahead, there is anticipation for broader scRNA-seq application in ischemic stroke research, promising deeper understanding of cellular complexities.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1784660"},"PeriodicalIF":4.6,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13139180/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autophagy-lysosome networks in oligodendrocytes: a dynamic framework for myelin integrity.","authors":"Isabel Jiménez-Ridruejo, Ainhoa Plaza-Zabala","doi":"10.3389/fcell.2026.1818512","DOIUrl":"https://doi.org/10.3389/fcell.2026.1818512","url":null,"abstract":"<p><p>Oligodendrocytes generate and maintain myelin, a highly specialized membrane system essential for efficient signal propagation and long-term white matter integrity. The extreme biosynthetic demands and unique architecture of myelinating oligodendrocytes place exceptional pressure on intracellular quality control pathways. In this context, autophagy-lysosome networks have emerged as central regulators of oligodendrocyte biology, operating beyond bulk degradation to coordinate membrane remodeling, organelle homeostasis, and selective protein turnover. Here, we synthesize current evidence demonstrating that autophagy is dynamically regulated across the oligodendrocyte lineage and fulfills stage-specific roles, from precursor maintenance and differentiation-associated remodeling to long-term maintenance of compact myelin. We highlight advances revealing selective autophagic degradation of myelin proteins, the spatial distribution of autophagy within myelinating cells, and functional interactions between autophagy, endo-lysosomal trafficking, and myelin integrity. We also discuss emerging concepts of functional heterogeneity within autophagy-related compartments and context-dependent routing of myelin-associated cargo. Finally, we outline key open questions that define current gaps in our understanding of oligodendroglial autophagy. By framing autophagy as an integrated regulatory network rather than a single pathway, this review provides a conceptual foundation for understanding myelin biology under physiological conditions and establishes a basis for future studies on white matter vulnerability.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1818512"},"PeriodicalIF":4.6,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13139324/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835894","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting R-loops: diverse RNA helicases in R-loop resolution and their potential as targets for cancer therapy.","authors":"Katherine Herrera, Kaoru Takasaki, Takahiko Murayama","doi":"10.3389/fcell.2026.1822277","DOIUrl":"https://doi.org/10.3389/fcell.2026.1822277","url":null,"abstract":"<p><p>RNA helicases are enzymes that remodel RNA secondary structures and RNA-protein complexes using ATP-driven motor forces. They are known to participate in many essential cellular processes, including transcription, splicing, translation, RNA decay, and ribosome assembly. However, the functional diversity of RNA helicases and the multitude of associated cofactors make it difficult to grasp the full picture of their roles in these processes. Here, we focus exclusively on the R-loop-unwinding activities of RNA helicases and the cofactors involved in this process. R-loops are three-stranded nucleic acid structures that are mainly formed during transcription between newly synthesized mRNA and its template DNA. Timely resolution of R-loops by RNA helicases is required to prevent the DNA damage and replication stress that can result from collisions between transcription and DNA replication machinery acting aberrantly on the same DNA strand. Although R-loop resolution is critical for genome stability and cell proliferation, our understanding of the responsible helicases and their mechanisms remains incomplete. In this review, we summarize recent findings on R-loop-resolving helicases, discuss key questions and approaches for future investigation, and consider the potential of targeting these helicases for cancer therapy.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1822277"},"PeriodicalIF":4.6,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13139199/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835679","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}