详细内容（前10条）

1. ⭐ GSE318408 血管 STING 激活促进小细胞肺癌中 NK 细胞的抗肿瘤免疫 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immunity、NK cell、scRNA
• 📝 描述：Contributors : Marco Campisi ; Tatsuya Osaki ; David A Barbie ; Navin R MahadevanSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensSmall cell lung cancer (SCLC) typically displays a “cold” tumor microenvironment with a paucity of immune infiltrate. Neuroendocrine SCLC cells also profoundly repress MHC-I expression, rendering them vulnerable to NK cell-mediated cytotoxicity. Here, we confirm that neuroendocrine SCLC cells are sensitive to NK cell mediated attack, yet quantitative spatial profiling of the SCLC immune microenvironment in patient samples reveals that effector immune cells, including NK cells, are excluded from MHC-Ilow/neg SCLC regions. To study this biology, we develop dynamic single cell RNA sequencing of microphysiological immune tumor environments (DynaMITE-seq) and integrate findings with spatial transcriptomics in patient tissue, unveiling the microvasculature as a major checkpoint restricting NK cell extravasation/recruitment. We demonstrate that activation of vascular Stimulator of Interferon Genes (STING) signaling restores NK cell infiltration and killing of neuroendocrine SCLC, suggesting a strategy to overcome this key SCLC immunologic barrier and prime therapeutic response to DLL3-targeted CAR-NK cell therapy.
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2. ⭐ GSE318867 血管 STING 激活促进小细胞肺癌中 NK 细胞的抗肿瘤免疫 [空间转录组]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immunity、NK cell
• 📝 描述：Contributors : Marco Campisi ; Ian Dryg ; Jason Weirather ; David A Barbie ; Navin R MahadevanSeries Type : OtherOrganism : Homo sapiensSmall cell lung cancer (SCLC) typically displays a “cold” tumor microenvironment with a paucity of immune infiltrate. Neuroendocrine SCLC cells also profoundly repress MHC-I expression, rendering them vulnerable to NK cell-mediated cytotoxicity. Here, we confirm that neuroendocrine SCLC cells are sensitive to NK cell mediated attack, yet quantitative spatial profiling of the SCLC immune microenvironment in patient samples reveals that effector immune cells, including NK cells, are excluded from MHC-Ilow/neg SCLC regions. To study this biology, we develop dynamic single cell RNA sequencing of microphysiological immune tumor environments (DynaMITE-seq) and integrate findings with spatial transcriptomics in patient tissue, unveiling the microvasculature as a major checkpoint restricting NK cell extravasation/recruitment. We demonstrate that activation of vascular Stimulator of Interferon Genes (STING) signaling restores NK cell infiltration and killing of neuroendocrine SCLC, suggesting a strategy to overcome this key SCLC immunologic barrier and prime therapeutic response to DLL3-targeted CAR-NK cell therapy.
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3. ⭐ GSE318663 血管STING激活促进NK细胞在小细胞肺癌中的抗肿瘤免疫

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immunity、NK cell
• 📝 描述：Series Type : Genome binding/occupancy profiling by high throughput sequencing ; Expression profiling by high throughput sequencing ; OtherOrganism : Homo sapiensThis SuperSeries is composed of the SubSeries listed below.
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4. ⭐ GSE319188 通过 LHRH-NanoTi 靶向递送 TGF-β 抑制剂可逆转卵巢癌中 NAT10/ac4C 介导的顺铂诱导的免疫抑制性肿瘤微环境

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、tumor microenvironment
• 📝 描述：Contributor : Fei LvSeries Type : OtherOrganism : Mus musculusBackground: Platinum-based chemotherapy for ovarian cancer is frequently compromised by the development of resistance, a process often accompanied by an immunosuppressive tumor microenvironment. The molecular mechanisms linking cisplatin resistance to immune evasion remain poorly understood, hindering the development of effective combination therapies.Results: This study reveals that cisplatin-induced immunosuppression and resistance are driven by a reduction in N-acetyltransferase 10 (NAT10)-mediated N4-acetylcytidine (ac4C) modification, which produces two parts of unfavorable effects: 1) activating the DNA damage repair pathway, thereby confers resistance to cisplatin; 2) enhancing the expression of TGF-β via NAT10’s interaction with ribosomal proteins RPS3 and RPS6. The elevated TGF-β increases the infiltration of myeloid-derived suppressor cells (MDSCs), M2 macrophages, exhausted CD8+ T cells, and regulatory T cells (Tregs) within the tumor microenvironment. To target this pathway, we developed a LHRH receptor-targeted nanodelivery system for a TGF-β inhibitor, which synergized with cisplatin to achieve superior antitumor efficacy by effectively reversing the immunosuppressive microenvironment.Conclusions: Our study defines the NAT10/ac4C–TGF-β axis as a pivotal mechanism coordinating cisplatin resistance and immunosuppression in ovarian cancer. These findings propose targeted inhibition of TGF-β signaling as a promising therapeutic strategy to overcome platinum resistance by revitalizing the antitumor immune response.
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5. ⭐ GSE318885 SMARCA4 通过 H3K27 乙酰化调节 PROX1 促进前列腺癌的谱系可塑性和恩扎卢胺耐药性 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、resistance、ATAC-seq
• 📝 描述：Contributors : Chenwei Wu ; Mayao Luo ; Shidong Lv ; Qiang WeiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensEnzalutamide resistance is a dynamic process often culminating in the aggressive progression to neuroendocrine prostate cancer (NEPC). This lineage plasticity is hypothesized to be driven by underlying epigenetic alterations, yet the core molecular drivers remain unclear. Elucidating these factors is of significant clinical importance for overcoming resistance. To model this transition, we established a dynamic gradient-resistant cell model simulating the clinical response to enzalutamide, and found robust upregulation of the chromatin remodeling factor SMARCA4 in resistant cells. Both in vitro and in vivo experimental results demonstrated that inhibiting SMARCA4 effectively suppresses tumor progression and reverses neuroendocrine transformation. Mechanistically, integrated multi-omics analysis, correlation studies, and protein interaction experiments revealed the transcription factor PROX1 as a crucial downstream target of SMARCA4, where its inhibition alone was sufficient to reverse the aggressive malignancy and neuroendocrine characteristics of resistant cells. We further demonstrated that SMARCA4 enhances H3K27ac levels and chromatin accessibility at the PROX1 locus to regulate its expression. Importantly, the tumor-suppressive effect of SMARCA4 knockdown could be rescued by histone deacetylase inhibitors (HDACi), achieving a level of recovery comparable to PROX1 overexpression. In summary, this study defines a core epigenetic pathway, showing that increased SMARCA4 activity promotes luminal-to-neuroendocrine transformation by enhancing histone acetylation and chromatin accessibility at the PROX1 locus. Targeting the SMARCA4-PROX1 axis provides a valuable therapeutic strategy for combating enzalutamide resistance and NEPC progression.
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6. ⭐ GSE318884 SMARCA4 通过 H3K27 乙酰化调控 PROX1 促进前列腺癌的谱系可塑性和恩扎卢胺耐药性 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、resistance、RNA-seq
• 📝 描述：Contributors : Chenwei Wu ; Mayao Luo ; Shidong Lv ; Qiang WeiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensEnzalutamide resistance is a dynamic process often culminating in the aggressive progression to neuroendocrine prostate cancer (NEPC). This lineage plasticity is hypothesized to be driven by underlying epigenetic alterations, yet the core molecular drivers remain unclear. Elucidating these factors is of significant clinical importance for overcoming resistance. To model this transition, we established a dynamic gradient-resistant cell model simulating the clinical response to enzalutamide, and found robust upregulation of the chromatin remodeling factor SMARCA4 in resistant cells. Both in vitro and in vivo experimental results demonstrated that inhibiting SMARCA4 effectively suppresses tumor progression and reverses neuroendocrine transformation. Mechanistically, integrated multi-omics analysis, correlation studies, and protein interaction experiments revealed the transcription factor PROX1 as a crucial downstream target of SMARCA4, where its inhibition alone was sufficient to reverse the aggressive malignancy and neuroendocrine characteristics of resistant cells. We further demonstrated that SMARCA4 enhances H3K27ac levels and chromatin accessibility at the PROX1 locus to regulate its expression. Importantly, the tumor-suppressive effect of SMARCA4 knockdown could be rescued by histone deacetylase inhibitors (HDACi), achieving a level of recovery comparable to PROX1 overexpression. In summary, this study defines a core epigenetic pathway, showing that increased SMARCA4 activity promotes luminal-to-neuroendocrine transformation by enhancing histone acetylation and chromatin accessibility at the PROX1 locus. Targeting the SMARCA4-PROX1 axis provides a valuable therapeutic strategy for combating enzalutamide resistance and NEPC progression.
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7. GSE319552 酮体和糖酵解代谢是新生儿败血症炎症的关键调节因子

• ✍️ 作者：未知作者
• 🏷️ 关键词：inflammation、metabolism
• 📝 描述：Contributors : Björn Klabunde ; Ole Bæk ; Duc Ninh NguyenSeries Type : Expression profiling by high throughput sequencingOrganism : Sus scrofaNeonatal sepsis is a life-threatening condition in preterm infants, primarily due to a dysregulated immunometabolic response to infection. Sepsis and infection mortality are associated with excessive glycolysis-induced inflammation, impaired mitochondrial oxidative phosphorylation (OXPHOS) and loss of disease tolerance. Reduced glucose intake can reverse these dysregulations, but it is unclear how the mechanistic control of glycolysis-OXPHOS balance drives defense strategies and infection outcomes. Here, in a preterm piglet model of neonatal sepsis, glycolysis inhibition with 2-deoxyglucose (2-DG) completely prevents acute infection mortality, reduces systemic inflammation and markers of liver injury, accompanied by enhanced mitochondrial metabolism and disease tolerance. Strikingly, this protection by 2-DG is conferred despite elevated blood glucose levels and higher bacterial burdens than the infected controls. Alternatively, partial replacement of glucose intake with the ketone beta-hydroxybutyrate (BHB) abolishes sepsis-related mortality via improving disease tolerance and clinical parameters.
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8. GSE319314 小胶质细胞线粒体通过代谢和转录重编程支持人类3D体外脑模型中的神经元成熟

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolic、Neuronal
• 📝 描述：Contributors : Sydney P Sterben ; Charitha C Anamala ; Sahan B Kansakar ; Vaishnavi Koduri ; Volha LiaudanskayaSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensAutism Spectrum Disorder (ASD) is a neurodevelopmental condition characterized by disrupted neuronal circuit maturation. Emerging evidence implicates microglial function and mitochondrial regulation as contributors to ASD-associated biology, yet the mechanisms linking these processes to neuronal development remain poorly defined. Neuronal maturation requires tightly coordinated metabolic and transcriptional remodeling, in which mitochondria play a central role in regulating the developmental tempo and metabolic identity, while microglia modulate neuronal synaptic network maturation; however, whether microglia influence neuronal development through direct mitochondrial contributions remains unknown. Here, using a 3D human in vitro brain model, we show that microglial mitochondria can act as transferable cues that promote metabolic, mitochondria-dynamic, and transcriptional aspects of neuronal maturation. Neurons treated with microglial mitochondria exhibited enhanced oxidative metabolism, improved mitochondrial dynamics, and activation of gene programs associated with nervous system development and neurogenesis. These effects were accompanied by increased expression of dendritic maturation markers, supporting the view that transferred mitochondria can contribute to the regulation of neuronal state. However, full structural and synaptic maturation required the combined action of microglia-derived mitochondria and secreted signaling factors. Together, this study identified microglial mitochondrial transfer as a contributor to neuronal maturation with potential relevance to developmental trajectories disrupted in ASD.
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9. GSE319246 ApoE4 通过 AsxL1/LXRα–H3K4me3 轴的表观遗传重编程驱动阿尔茨海默病中的小胶质细胞脂质失调

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer、epigenetic
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusBackground The ε 4 allele of apolipoprotein E gene (ApoE) stands as the greatest genetic risk factor for late-onset Alzheimer’s disease (AD). Although microglia accumulating lipid droplets (LDAM) have been implicated in AD pathogenesis, the mechanistic link between ApoE4 and microglial lipid dysregulation remains elusive. Methods We employed a multi-omics approach, combining snRNA-seq and locus-specific epigenetic analysis, alongside microglia-specific gene manipulation in ApoE-targeted replacement (TR) mice. Primary microglia were challenged with cholesterol to simulate lipid overload conditions. Results In mid-life ApoE4-TR mice, microglia within the dentate gyrus developed pronounced lipid droplet accumulation, concurrent with impaired Aβ clearance and a pro-inflammatory shift. snRNA-seq unveiled a unique microglial cluster in ApoE4 mice, enriched for lipid-metabolism genes and marked by the pronounced downregulation of the hub gene AsxL1. Mechanistically, ApoE4 attenuated the AsxL1–LXRα interaction, leading to reduced H3K4me3 occupancy at promoters of lipid-efflux genes such as Abca1. Crucially, CRISPR-mediated, microglia-specific overexpression of AsxL1 restored H3K4me3 levels, normalized cholesterol efflux, and rescued Aβ phagocytic deficits in vivo. Conclusions Our findings define an epigenetic pathway whereby ApoE4 drives microglial dysfunction via the AsxL1–LXRα–H3K4me3 axis, fostering the LDAM phenotype. Enhancing AsxL1 function presents a promising therapeutic avenue for countering ApoE4-mediated pathogenesis in AD.
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10. GSE319228 体内抑制子宫肌瘤中的TDO2导致肿瘤转录组广泛改变

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、transcriptome
• 📝 描述：Contributors : Tsai-Der Chuang ; Abigail Wiseman ; Gabriela Alfaro ; Sayna Pejouhesh Jahromi ; Sepideh Pejouhesh Jahromi ; Daniel Baghdasarian ; Omid KhorramSeries Type : Non-coding RNA profiling by high throughput sequencing ; Expression profiling by high throughput sequencingOrganism : Homo sapiensThis study aimed to characterize large and small RNA transcriptomic changes in fibroid xenografts from mice treated with the TDO2 inhibitor 680C91 for two months.
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1. 大型研究发现，孕期接种mRNA新冠疫苗与自闭症之间没有关联

• ✍️ 作者：未知作者
• 🏷️ 关键词：vaccine
• 📝 描述：Researchers tracked more than 400 toddlers to see whether mRNA COVID-19 vaccination during or just before pregnancy was linked to autism or developmental delays. After detailed assessments of speech, motor skills, behavior, and social development, they found no meaningful differences between vaccinated and unvaccinated groups. Experts say the results provide strong reassurance about vaccine safety in pregnancy.
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2. 人工智能揭示了驱动阿尔茨海默病的隐藏基因控制中心

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：Scientists have created the most detailed maps yet of how genes control one another inside the brains of people with Alzheimer’s disease. Using a powerful new AI-based system called SIGNET, the team uncovered cause-and-effect relationships between genes across six major brain cell types, revealing which genes are truly driving harmful changes. The most dramatic disruptions were found in excitatory neurons, where thousands of genetic interactions appear to be extensively rewired as the disease progresses.
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3. 科学家发现神经会积极促进胰腺癌的发生发展。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Scientists have uncovered a hidden partnership between pancreatic cancer and the nervous system. Support cells in the pancreas lure nerve fibers, which then release signals that accelerate early cancer growth. This creates a self-sustaining loop that helps tumors take hold. Blocking the nerve activity significantly reduced tumor growth in experiments, suggesting a new treatment strategy.
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4. 科学家发现了一种能让癌细胞快速重编其DNA的酶

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Researchers have uncovered the enzyme behind chromothripsis, a chaotic chromosome-shattering event seen in about one in four cancers. The enzyme, N4BP2, breaks apart DNA trapped in tiny cellular structures, unleashing a burst of genetic changes that can help tumors rapidly adapt and resist therapy. Blocking the enzyme dramatically reduced this genomic destruction in cancer cells.
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• GSE309579 整合单细胞 RNA 和 ATAC 测序揭示胶质母细胞瘤中剂量敏感、簇特异性的调控动态
• GSE294799 对发育中的斑马鱼和人类内胚层进行功能基因组学分析，揭示了控制脊椎动物器官发生的高度保守的顺式调控模块[RNA-seq]
• GSE294761 对发育中的斑马鱼和人类内胚层进行功能基因组学分析，揭示了控制脊椎动物器官发生的高度保守的顺式调控模块 [ATAC-seq]
• GSE254727 拓扑信息调控元件集合协调细胞身份基因表达程序[scRNA-Seq]
• GSE254726 拓扑信息调控元件集合协调细胞身份基因表达程序[scATAC-Seq]
• GSE301801 对经对照组、胆固醇辅助正常批次、毒性批次和皮脂酸处理的野生型 C57BL/6 小鼠进行批量 RNA-seq 分析
• GSE298692 ChIP-seq 分析 MM.1S 细胞中的 H3K4me3、H3K27ac、H3K27me3、p-STAT3、POU2AF1 和 ELL2
• GSE296093 mRNA疫苗通过非常规途径启动CD8 T细胞
• GSE162175 不同形式衰老的转录组学
• GSE319394 低氧条件下 Siniperca chuatsi MFF-1 细胞的 RNA-seq 分析
• GSE319347 人类 iMGL 和 iMGL-运动神经元共培养物与 cGAS 抑制剂的批量 RNA 测序
• GSE319344 脑膜淋巴管内皮细胞的丢失导致具有清除功能的新型血管网络的形成。
• GSE319333 非小细胞肺癌 (NSCLC) 中 mtdsRNA 水平的特征分析
• GSE319316 局部负反馈塑造了减数分裂DNA断裂的全基因组模式
• GSE319292 暴露于持续亚最大允许浓度 (MCL) 和超最大允许浓度 (MCL) 亚砷酸钠和贫铀的斑马鱼幼体转录组数据
• GSE319045 Irx3 通过调节炎症和纤维化通路改善心肌梗死后心脏功能障碍
• GSE319035 P21+TREM2+-衰老巨噬细胞促进炎症衰老和代谢功能障碍相关的脂肪肝疾病[NAFLD_time_course]
• GSE319006 靶向 HDAC 和蛋白质稳态以根除静止癌细胞
• GSE318940 Smarca4 协调染色质可及性和代谢程序以维持造血干细胞功能
• GSE318900 利用大型语言模型和扩散框架解码和重构启动子架构：高通量启动子强度测序源数据
• GSE318654 人类脊髓背角和腹角的分子图谱定义了神经元类型的排列和神经胶质细胞的性别差异
• GSE318004 NIK 驱动的髓系细胞 IL-23 产生是自身免疫性炎症发展的关键因素 [16S rRNA-seq]
• GSE291249 匹配的左心房和右心房颤动人类队列中DNA甲基化水平的表观基因组学研究
• GSE290099 人类副流感病毒3型感染后人肺组织的免疫反应——经典通路和治疗