IF 5.2 2区生物学

Cells Pub Date : 2025-09-20 DOI: 10.3390/cells14181472

Nasser Adjei, Bruce Ladenheim, Michael T McCoy, Vikrant Palande, Jean Lud Cadet, Atul P Daiwile

{"title":"RNA Sequencing Identified Differentially Expressed Genes in the Mesocorticolimbic and Nigrostriatal Systems of Compulsive METH-Taking Rats.","authors":"Nasser Adjei, Bruce Ladenheim, Michael T McCoy, Vikrant Palande, Jean Lud Cadet, Atul P Daiwile","doi":"10.3390/cells14181472","DOIUrl":"10.3390/cells14181472","url":null,"abstract":"Methamphetamine (METH) is an extremely addictive drug which continues to cause significant harm to individuals and communities. In the present study we trained male rats to self-administer METH for 20 days, followed by 9 days of foot shock exposure. All rats escalated their METH intake during the first 20 days. The rats that continued to self-administer METH in the presence of aversive stimuli were termed shock-resistant (SR), while those that reduced their intake were shock-sensitive (SS). RNA sequencing showed numerous differentially expressed genes (DEGs) in the prefrontal cortex, nucleus accumbens, dorsal striatum, and midbrain. Ingenuity pathway analysis linked DEGs to addiction-related mechanisms. We identified shared genes with similar expression patterns across four brain regions (SR: Fos and Ahsp; SS: Tet1, Cym, and Tmem30c). The identified genes play key roles in addiction-related brain functions, such as neuronal activity, stress response, and epigenetic regulation, and their importance in METH addiction is highlighted. These genes represent promising targets for developing new treatments aimed at reversing neuroadaptations caused by METH use.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468296/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148157","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}

引用次数: 0

Temporal Dynamics of Extracellular Matrix Remodeling in Anthracycline-Induced Cardiotoxicity. 蒽环类药物引起心脏毒性的细胞外基质重构的时间动力学。

IF 5.2 2区生物学

Cells Pub Date : 2025-09-20 DOI: 10.3390/cells14181471

Fibi Meshrkey, Somaya Y Ibrahim, Rushita A Bagchi, William J Richardson

{"title":"Temporal Dynamics of Extracellular Matrix Remodeling in Anthracycline-Induced Cardiotoxicity.","authors":"Fibi Meshrkey, Somaya Y Ibrahim, Rushita A Bagchi, William J Richardson","doi":"10.3390/cells14181471","DOIUrl":"10.3390/cells14181471","url":null,"abstract":"Anthracyclines are widely used chemotherapeutic agents with proven efficacy against a broad range of malignancies, but their clinical utility is limited by a well-documented, dose-dependent cardiotoxicity. While this toxicity has traditionally been attributed to direct cardiomyocyte injury, emerging evidence highlights the pivotal role of cardiac fibroblasts (CFs) in the development and progression of anthracycline-induced cardiotoxicity. This review examines the diverse effects of anthracycline focusing on doxorubicin (DOX) and CFs across the temporal phases of cardiac injury. DOX activates fibroblast-driven extracellular matrix remodeling and promotes fibrosis through enhanced collagen production and the induction of cellular senescence, thereby exacerbating early myocardial inflammation and dysfunction. Clinically, anthracycline cardiotoxicity may present as acute (within days), subacute (within weeks), or chronic progressive forms manifesting either early (within one year) or late (up to decades post-treatment). While early manifestations may be reversible with timely detection and management, late-phase cardiotoxicity is often irreversible, characterized by declining left ventricular ejection fraction and heart failure. A deeper understanding of the molecular and cellular contributions of CFs may uncover novel therapeutic targets to prevent or attenuate anthracycline-related cardiac damage.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468079/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148166","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}

引用次数: 0

Dicer1 Depletion Leads to DNA Damage Accumulation and Cell Death in a RET/PTC3 Papillary Thyroid Cancer Mouse Model, Thereby Inhibiting Tumor Progression. 在RET/PTC3乳头状甲状腺癌小鼠模型中，Dicer1缺失导致DNA损伤积累和细胞死亡，从而抑制肿瘤进展。

IF 5.2 2区生物学

Cells Pub Date : 2025-09-19 DOI: 10.3390/cells14181465

Maria Rojo-Pardillo, Alice Augenlicht, Geneviève Dom, Jukka Kero, Bernard Robaye, Carine Maenhaut

{"title":"Dicer1 Depletion Leads to DNA Damage Accumulation and Cell Death in a RET/PTC3 Papillary Thyroid Cancer Mouse Model, Thereby Inhibiting Tumor Progression.","authors":"Maria Rojo-Pardillo, Alice Augenlicht, Geneviève Dom, Jukka Kero, Bernard Robaye, Carine Maenhaut","doi":"10.3390/cells14181465","DOIUrl":"10.3390/cells14181465","url":null,"abstract":"Beyond well-known genetic drivers, microRNA dysregulation has emerged as a key contributor to thyroid tumorigenesis. Central to this process is Dicer1, a ribonuclease essential for microRNA maturation, whose expression is often reduced in papillary thyroid carcinoma (PTC). Evidence from previous studies suggest Dicer1 functions as a context-dependent haplo-insufficient tumor suppressor gene: partial loss may promote tumor development, whereas complete loss may disrupt essential cellular functions, causing cell death and tumor suppression. However, the effects of partial or complete Dicer1 loss in thyroid cancer remain unclear. To explore this, we genetically inactivated one (heterozygous) or both (homozygous) Dicer1 alleles specifically in thyroid follicular cells of a RET/PTC3 transgenic mouse model using an inducible Cre-Lox system. Our findings deepen the current understanding of the RET/PTC3-driven PTC model by revealing an increased number of vimentin-positive cells and disruption in redox homeostasis. Additionally, whereas heterozygous Dicer1 loss did not alter tumor progression in RET/PTC3 mice, total loss reduced tumor growth and led to accumulated DNA damage and cell death. These findings highlight the crucial role of Dicer1 dosage in thyroid cancer progression and underscore its potential as a therapeutic target for aggressive PTC and other malignancies characterized by aberrant Dicer1 expression.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468101/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147956","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}

引用次数: 0

Wings of Discovery: Using Drosophila to Decode Hereditary Spastic Paraplegia and Ataxias. 发现之翼：利用果蝇解码遗传性痉挛性截瘫和共济失调。

IF 5.2 2区生物学

Cells Pub Date : 2025-09-19 DOI: 10.3390/cells14181466

Rachele Vivarelli, Chiara Vantaggiato, Maria Teresa Bassi, Filippo Maria Santorelli, Maria Marchese

{"title":"Wings of Discovery: Using Drosophila to Decode Hereditary Spastic Paraplegia and Ataxias.","authors":"Rachele Vivarelli, Chiara Vantaggiato, Maria Teresa Bassi, Filippo Maria Santorelli, Maria Marchese","doi":"10.3390/cells14181466","DOIUrl":"10.3390/cells14181466","url":null,"abstract":"Hereditary spastic paraplegia (HSP) and hereditary ataxias (HA) are clinically and genetically heterogeneous neurodegenerative disorders that primarily affect motor coordination and neural integrity. Despite distinct pathological features, such as pyramidal tract degeneration in HSP and spinocerebellar pathway involvement in HA, these conditions share overlapping genetic pathways and mechanisms. The fruit fly Drosophila melanogaster has emerged as a powerful model organism for investigating the molecular basis of rare diseases, including HSP and HA. Its genetic tractability, rapid life cycle, and high degree of gene conservation with humans make it a cost-effective and ethically viable platform for disease modelling. In this review, we provide a comprehensive overview of Drosophila-based models for HSP and HA. We highlight the use of advanced genetic tools, including RNA interference, CRISPR/Cas9, and the GAL4/UAS system, as well as behavioral and neuroanatomical assays to model disease features. Furthermore, we discuss the application of genetic \"avatars\" and high-throughput drug screening platforms to test therapeutic candidates. Collectively, these models have deepened our understanding of the pathophysiology of HSP and HA, offering valuable insights for the development of targeted therapies and approaches to personalized medicine.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12469124/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147940","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}

引用次数: 0

Beyond Spherical: Unveiling the Significance of Oval Blastocyst Morphology on Euploidy and Implantation Success. 超越球形：揭示卵形囊胚形态对整倍体和着床成功的意义。

IF 5.2 2区生物学

Cells Pub Date : 2025-09-19 DOI: 10.3390/cells14181468

Jakub Wyroba, Agnieszka Kuczyńska, Klaudia Kasperkowicz, Katarzyna Kostarczyk, Pawel Kordowitzki, Joanna Kochan

{"title":"Beyond Spherical: Unveiling the Significance of Oval Blastocyst Morphology on Euploidy and Implantation Success.","authors":"Jakub Wyroba, Agnieszka Kuczyńska, Klaudia Kasperkowicz, Katarzyna Kostarczyk, Pawel Kordowitzki, Joanna Kochan","doi":"10.3390/cells14181468","DOIUrl":"10.3390/cells14181468","url":null,"abstract":"The selection of the most suitable embryo, based on the morphology and shape, for embryo transfer is a critical aspect of the in vitro fertilization (IVF) process, as its precision can significantly enhance the overall effectiveness of IVF and contribute to a healthy birth. This study aimed to compare the chromosomal status and implantation potential of oval-shaped blastocysts versus normal-shaped blastocysts on day 5 post-ICSI (intracytoplasmic sperm injection). Initially, the frequency of oval blastocysts was assessed by analyzing 1328 embryos from 610 ICSI cycles. Subsequently, 80 patients undergoing ICSI and PGT-A (preimplantation genetic testing for aneuploidy), who had both normal and oval blastocysts in the same cycle, were selected to evaluate the euploid rate relative to blastocyst morphology. Finally, the implantation outcomes of fresh embryo transfers involving oval and normal-shaped blastocysts, neither of which had undergone PGT-A, were analyzed. Half of the blastocysts from each group were transferred after assisted hatching (AH), and the other half were transferred without AH. Blastocyst shape does not appear to correlate with an increased risk of aneuploidy but does influence hatching ability. Following AH, the implantation potential of elongated blastocysts is equivalent to that of normally shaped blastocysts, suggesting AH is beneficial for oval embryos. Consequently, the transfer of oval blastocysts is considered as safe and effective as the transfer of normally shaped embryos.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468772/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147942","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}

引用次数: 0

Role of Nucleotide P2 Receptors in the Immune System: Focus on Effector T Cells. 核苷酸P2受体在免疫系统中的作用：聚焦于效应T细胞。

IF 5.2 2区生物学

Cells Pub Date : 2025-09-19 DOI: 10.3390/cells14181467

Romuald Brice Babou Kammoe, Chakib Hamoudi, Fawzi Aoudjit

引用次数: 0

Frog Skin Antimicrobial Peptide 3-13 and Its Analogs Alleviate Atherosclerosis Cholesterol Accumulation in Foam Cells via PPARγ Signaling Pathway. 青蛙皮肤抗菌肽3-13及其类似物通过PPARγ信号通路缓解动脉粥样硬化泡沫细胞中的胆固醇积累。

IF 5.2 2区生物学

Cells Pub Date : 2025-09-19 DOI: 10.3390/cells14181470

Xue-Feng Yang, Zi-Meng Hao, Xin-Yu Cui, Wan-Qi Liu, Meng-Miao Li, De-Jing Shang

{"title":"Frog Skin Antimicrobial Peptide 3-13 and Its Analogs Alleviate Atherosclerosis Cholesterol Accumulation in Foam Cells via PPARγ Signaling Pathway.","authors":"Xue-Feng Yang, Zi-Meng Hao, Xin-Yu Cui, Wan-Qi Liu, Meng-Miao Li, De-Jing Shang","doi":"10.3390/cells14181470","DOIUrl":"10.3390/cells14181470","url":null,"abstract":"Atherosclerosis (AS), a major contributor to cardiovascular disease, hypertension, and stroke, is associated with significant morbidity and mortality. Antimicrobial peptides (AMPs) 3-13, W3R6, and chensinin-1b were engineered based on the sequence of chensinin-1, originally isolated from the skin secretion of Rana chensinensis. This study investigated their therapeutic potential in ApoE-/- AS mice and THP-1-derived foam cells, focusing on the regulation of cholesterol metabolism. AMP 3-13 markedly reduced body weight gain, aortic root plaque formation, and plasma cholesterol levels in ApoE-/- mice. Transcriptomic analysis revealed that AMP 3-13 significantly altered gene expression related to cholesterol metabolism and the PPAR signaling pathway. Specifically, AMP 3-13 upregulated PPARγ, ABCA1, and ABCG1, while downregulating CD36 in aortic root plaques. In THP-1-derived foam cells, AMP 3-13 and its analogs activated the PPARγ-ABCA1/ABCG1 axis, enhancing cholesterol efflux. Concurrently, they inhibited CD36 expression by competing with PPARγ for promoter binding, thereby reducing ox-LDL uptake. These findings suggested that AMP 3-13 and its analogs represented promising therapeutic agents for AS through their ability to reduce cholesterol accumulation in foam cell.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468074/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147968","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}

引用次数: 0

Orlistat Confers Neuroprotection in Traumatic Brain Injury by Modulating Microglial Lipid Metabolism. 奥利司他通过调节小胶质脂质代谢对创伤性脑损伤的神经保护作用。

IF 5.2 2区生物学

Cells Pub Date : 2025-09-19 DOI: 10.3390/cells14181469

Chenxuan Yu, Yu Ni, Yuxuan Xiong, Huayu Kang, Zhengqiao Jiang, Yuan Liu, Xincheng Zhang, Yanchao Liu, Kai Zhao, Sheng Wang, Chao Gan, Huaqiu Zhang

{"title":"Orlistat Confers Neuroprotection in Traumatic Brain Injury by Modulating Microglial Lipid Metabolism.","authors":"Chenxuan Yu, Yu Ni, Yuxuan Xiong, Huayu Kang, Zhengqiao Jiang, Yuan Liu, Xincheng Zhang, Yanchao Liu, Kai Zhao, Sheng Wang, Chao Gan, Huaqiu Zhang","doi":"10.3390/cells14181469","DOIUrl":"10.3390/cells14181469","url":null,"abstract":"Traumatic brain injury (TBI) represents a major cause of mortality and disability worldwide, particularly affecting young adults and elderly populations. This study investigates the neuroprotective potential of orlistat (ORL), a gastrointestinal lipase inhibitor, in a murine TBI model. Behavioral, histological, and molecular analyses demonstrated that ORL significantly attenuated TBI-induced neurological damage. Microglial depletion experiments revealed that ORL's neuroprotective effects were largely mediated through microglial modulation. In vitro and in vivo studies showed that ORL suppressed microglial activation, phagocytosis, and migration. Single-cell RNA sequencing identified upregulation of lipoprotein lipase (LPL) in a TBI-induced microglial subpopulation. Molecular docking predicted ORL-LPL binding, suggesting direct enzymatic inhibition. Transcriptomic and metabolomic analyses further revealed ORL's modulation of microglial metabolic pathways and inflammatory responses. Our findings position ORL as a promising repurposed therapeutic for TBI through its novel mechanism of targeting microglial LPL-mediated neuroinflammation.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468502/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148212","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}

引用次数: 0

Tumor-Associated Macrophages in Glioblastoma: Mechanisms of Tumor Progression and Therapeutic Strategies. 胶质母细胞瘤中的肿瘤相关巨噬细胞：肿瘤进展机制和治疗策略。

IF 5.2 2区生物学

Cells Pub Date : 2025-09-18 DOI: 10.3390/cells14181458

Jianan Chen, Qiong Wu, Anders E Berglund, Robert J Macaulay, James J Mulé, Arnold B Etame

{"title":"Tumor-Associated Macrophages in Glioblastoma: Mechanisms of Tumor Progression and Therapeutic Strategies.","authors":"Jianan Chen, Qiong Wu, Anders E Berglund, Robert J Macaulay, James J Mulé, Arnold B Etame","doi":"10.3390/cells14181458","DOIUrl":"10.3390/cells14181458","url":null,"abstract":"Glioblastoma (GBM) is an aggressive brain tumor with a highly immunosuppressive microenvironment that promotes tumor progression and therapy resistance. Tumor-associated macrophages (TAMs), comprising up to 50% of the tumor mass, are recruited via chemokine axes such as CCL2/CCR2, CX3CL1/CX3CR1, and CXCL12/CXCR4 and adopt an M2-like immunosuppressive phenotype, facilitating immune escape and angiogenesis. Key signaling pathways, including CSF1R, STAT3, NF-κB, PI3K/Akt, and HIF-1α, regulate TAM function, making them promising therapeutic targets. Strategies such as TAM depletion, reprogramming, and immune checkpoint blockade (PD-1/PD-L1, and CD47-SIRPα) have shown potential in preclinical models. Emerging approaches, including CAR-macrophage (CAR-M) therapy, nanotechnology-based drug delivery, and exosome-mediated modulation, offer new avenues for intervention. However, clinical translation remains challenging due to GBM's heterogeneity and adaptive resistance mechanisms. Future research should integrate multi-omics profiling and AI-driven drug discovery to refine TAM-targeted therapies and improve patient outcomes. This review provides a comprehensive analysis of TAM-mediated immune regulation in GBM and explores evolving therapeutic strategies aimed at overcoming its treatment barriers.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468907/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148004","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}

引用次数: 0

Patient-Derived Tumor Organoids to Model Cancer Cell Plasticity and Overcome Therapeutic Resistance. 病人来源的肿瘤类器官模拟癌细胞可塑性和克服治疗耐药性。

IF 5.2 2区生物学

Cells Pub Date : 2025-09-18 DOI: 10.3390/cells14181464

Roberto Coppo, Masahiro Inoue

{"title":"Patient-Derived Tumor Organoids to Model Cancer Cell Plasticity and Overcome Therapeutic Resistance.","authors":"Roberto Coppo, Masahiro Inoue","doi":"10.3390/cells14181464","DOIUrl":"10.3390/cells14181464","url":null,"abstract":"Cancer cell plasticity, defined as the ability of tumor cells to reversibly adopt distinct functional states, plays a central role in tumor heterogeneity, therapy resistance, and disease relapse. This process enables cells to enter stem-like, dormant, or drug-tolerant persister states in response to treatment or environmental stress without undergoing genetic changes. Such reversible transitions complicate and limit current treatments. Conventional cancer models often fail to capture the complexities of these adaptive states. In contrast, patient-derived tumor organoids (PDOs), which retain the cellular diversity and structure of primary tumors, provide a unique system for investigating plasticity. This review describes how PDOs can model cellular plasticity, such as the emergence of drug-tolerant persister cells and the interconversion between cancer stem cell states across multiple tumor types. We particularly focused on colorectal cancer organoids, for which research on the mechanism of plasticity is the most advanced. Combined with single-cell analysis, lineage tracing, and functional assays, PDOs can help identify the molecular pathways that control plasticity. Understanding these mechanisms is important for developing therapies to prevent treatment failure and control disease progression.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12469014/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148225","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}

引用次数: 0

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