详细内容（前10条）

1. ⭐ GSE320142 NKG2A抑制促进NK细胞-CD8+ T细胞相互作用，从而增强卵巢癌的抗癌免疫力

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、immunity、T cell、NK cell
• 📝 描述：Contributors : Teraza Lanickova ; Artemis Angelidou ; Michal Hensler ; Veronika Niederlova ; Jitka FucikovaSeries Type : OtherOrganism : Homo sapiensNatural killer (NK) cells contribute to tumor immunosurveillance, yet their phenotypic and functional heterogeneity and impact on anti-tumor immunity remain incompletely understood. Here, using an integrated set of transcriptomic, spatial, and functional assays, we demonstrate that advanced non-small cell lung carcinoma (NSCLC), which is generally considered an immunologically “hot” tumor – contains elevated levels of intratumoral cytotoxic NK1 (CD56dim) and NK3 subsets, which exhibit robust clinically relevant effector functions, localze preferentially within tumor cores, and spatially interact with CD8+ T cells in mature tertiary lymphoid structures (mTLSs). In contrast, the NK cell compartment of immunological “cold” tumors such as high-grade serous ovarian carcinoma (HGSOC) – which generally contains immature TLSs and ICI-resistant TCF1-TIM3+CD8+ CTLs – is enriched in functionally exhausted NK2 (CD56bright) NK cells expressing high levels of TIM3 and NKG2A. Functional studies in HGSOC patient samples and syngeneic mouse models reveal that bidirectional crosstalk between NK cells and CD8⁺ T cells is essential for anti-tumor immunity, and that disrupting this interaction—via CD8⁺ T cell or NK cell depletion—promotes NK cell exhaustion and CD8⁺ T cell dysfunction. Importantly, blockade of NKG2A restores NK cytotoxicity and promotes CD8⁺ T cell effector responses, and when combined with PD1 inhibition, significantly enhances survival in murine HGSOC models. Our findings highlight the NKG2A–HLA-E axis as a clinically actionable checkpoint in tumors with impaired NK cell–mediated immunity, and delineate the spatial and functional interplay between NK cells and CD8⁺ T cells as a determinant of anti-tumor immune efficacy.
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2. ⭐ GSE253585 调节性 T 细胞异质性的解卷积揭示了循环前体细胞在乳腺癌进展过程中作为免疫逃逸的传导者 [Visium]

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、immune、T cell、Visium
• 📝 描述：Contributors : Triet Bui ; Ernesto Rojas ; Julieann Puleo ; Aashna Jhaveri ; Simona Cristea ; Franziska Michor ; Kornelia PolyakSeries Type : OtherOrganism : Rattus norvegicusTumor-immune microenvironment is instrumental in shaping breast cancer tumor evolution. We previously identified an evolutionary bottleneck demarcating ductal carcinoma in situ (DCIS) from invasive ductal carcinoma (IDC). How the microenvironment evolves during such transition remains elusive. We dissected, in parallel, single-cell composition of DCIS and IDC patients and rat tumors that faithfully recapitulate human breast cancer. We discovered T cell diversity distinguishing DCIS and IDC and a novel cycling Treg state occupying the pseudotime bifurcation between DCIS and IDC, preceding more activated Treg subtypes. Multiscale analysis of patient cohorts as part of HTAN Consortium established that cycling Treg predicts recurrence in low-grade DCIS. We proved cycling Treg as Treg progenitors critical for immune escape and demonstrated that OX40 agonism restored immunotherapeutic sensitivity, where responders displayed increased inflammatory CAF subtype heterogeneity. Our study thus established cycling Treg’s importance in preserving immune escape and underscored its prognostic value to stratify future recurrence.
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3. ⭐ GSE310797 不同分期口腔鳞状细胞癌的单细胞和空间RNA测序

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、RNA-seq、spatial
• 📝 描述：Contributors : Fengtian Li ; Hu ChenSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Homo sapiensTo investigate the dynamic changes in the tumor microenvironment during the progression of oral squamous cell carcinoma (OSCC), we collected 16 treatment-naïve OSCC samples for single-cell RNA sequencing (scRNA-seq). Among these, 6 cases were additionally subjected to spatial transcriptomic profiling to capture the tissue architecture and spatial organization of the tumor microenvironment.
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4. ⭐ GSE312050 对调节性 T 细胞异质性的解卷积分析表明，增殖前体细胞是乳腺癌进展过程中免疫逃逸的调控者

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、immune、T cell
• 📝 描述：Contributors : Triet Bui ; Ernesto Rojas ; Julieann Puleo ; Simona Cristea ; Franziska Michor ; Kornelia PolyakSeries Type : Expression profiling by high throughput sequencingOrganism : Rattus norvegicusTumor-immune microenvironment is instrumental in shaping breast cancer tumor evolution. We previously identified an evolutionary bottleneck demarcating ductal carcinoma in situ (DCIS) from invasive ductal carcinoma (IDC). How the microenvironment evolves during such transition remains elusive. We dissected, in parallel, single-cell composition of DCIS and IDC patients and rat tumors that faithfully recapitulate human breast cancer. We discovered T cell diversity distinguishing DCIS and IDC and a novel cycling Treg state occupying the pseudotime bifurcation between DCIS and IDC, preceding more activated Treg subtypes. Multiscale analysis of patient cohorts as part of HTAN Consortium established that cycling Treg predicts recurrence in low-grade DCIS. We proved cycling Treg as Treg progenitors critical for immune escape and demonstrated that OX40 agonism restored immunotherapeutic sensitivity, where responders displayed increased inflammatory CAF subtype heterogeneity. Our study thus established cycling Treg’s importance in preserving immune escape and underscored its prognostic value to stratify future recurrence.
• 🔗 查看原文

5. ⭐ GSE253587 对调节性 T 细胞异质性的解卷积揭示了循环前体细胞在乳腺癌进展过程中免疫逃逸的调控作用

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、immune、T cell
• 📝 描述：Series Type : Expression profiling by high throughput sequencing ; OtherOrganism : Homo sapiens ; Rattus norvegicusThis SuperSeries is composed of the SubSeries listed below.
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6. ⭐ GSE253572 对调节性 T 细胞异质性的解卷积揭示了循环前体细胞在乳腺癌进展过程中免疫逃逸的调控作用

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、immune、T cell
• 📝 描述：Contributors : Triet Bui ; Ernesto Rojas ; Julieann Puleo ; Simona Cristea ; Franziska Michor ; Kornelia PolyakSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiens ; Rattus norvegicusTumor-immune microenvironment is instrumental in shaping breast cancer tumor evolution. We previously identified an evolutionary bottleneck demarcating ductal carcinoma in situ (DCIS) from invasive ductal carcinoma (IDC). How the microenvironment evolves during such transition remains elusive. We dissected, in parallel, single-cell composition of DCIS and IDC patients and rat tumors that faithfully recapitulate human breast cancer. We discovered T cell diversity distinguishing DCIS and IDC and a novel cycling Treg state occupying the pseudotime bifurcation between DCIS and IDC, preceding more activated Treg subtypes. Multiscale analysis of patient cohorts as part of HTAN Consortium established that cycling Treg predicts recurrence in low-grade DCIS. We proved cycling Treg as Treg progenitors critical for immune escape and demonstrated that OX40 agonism restored immunotherapeutic sensitivity, where responders displayed increased inflammatory CAF subtype heterogeneity. Our study thus established cycling Treg’s importance in preserving immune escape and underscored its prognostic value to stratify future recurrence.
• 🔗 查看原文

7. GSE317253 增强的线粒体自噬通过恢复上皮代谢适应性促进肺修复和再生 [AT2s RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolic、RNA-seq
• 📝 描述：Contributors : Ying Xi ; Pei Wu ; Jiawei ChenSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAlveolar Type II cells (AT2s) are the stem cells in the alveoli, responsible for both alveolar homeostasis and regeneration. Mitochondrial dysfunction has been reported in the AT2 cells from both chronic and acute injury induced alveolar diseases, including idiopathic pulmonary fibrosis (IPF) and viral pneumonia. Here, we demonstrate that genetic depletion of Ubiquitin Specific Peptidase 30 (USP30), a negative regulator of mitophagy, boosts mitophagy and restores mitochondrial function, leading to protection from injury induced AT2 apoptosis and increased AT2 stem cell activity. Both global Usp30 knockout (KO) and AT2-specific Usp30 KO protects the mice from bleomycin induced lung fibrosis and influenza puneumonia. Moreover, pharmaceutical inhibition of USP30 using a small molecule inhibitor effectively alleviates lung fibrosis and influenza pneumonia. Our study underscores a therapeutic potiential of USP30 inhibition for the treatment of injury induced alveolar diseases, offering a promising strategy for treating injury induced diseases
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8. GSE317252 增强的线粒体自噬通过恢复上皮代谢适应性促进肺修复和再生 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolic、RNA-seq
• 📝 描述：Contributors : Ying Xi ; Pei Wu ; Jiawei ChenSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAlveolar Type II cells (AT2s) are the stem cells in the alveoli, responsible for both alveolar homeostasis and regeneration. Mitochondrial dysfunction has been reported in the AT2 cells from both chronic and acute injury induced alveolar diseases, including idiopathic pulmonary fibrosis (IPF) and viral pneumonia. Here, we demonstrate that genetic depletion of Ubiquitin Specific Peptidase 30 (USP30), a negative regulator of mitophagy, boosts mitophagy and restores mitochondrial function, leading to protection from injury induced AT2 apoptosis and increased AT2 stem cell activity. Both global Usp30 knockout (KO) and AT2-specific Usp30 KO protects the mice from bleomycin induced lung fibrosis and influenza puneumonia. Moreover, pharmaceutical inhibition of USP30 using a small molecule inhibitor effectively alleviates lung fibrosis and influenza pneumonia. Our study underscores a therapeutic potiential of USP30 inhibition for the treatment of injury induced alveolar diseases, offering a promising strategy for treating injury induced diseases
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9. GSE320329 对土壤微生物群落的多组学表征揭示了琥珀酸和谷氨酸代谢在碳酸钙沉淀过程中的关键作用

• ✍️ 作者：未知作者
• 🏷️ 关键词：regex:micro(b|be|bial|organism)、metabolism
• 📝 描述：Contributors : Lin Tesia T. ; Anthony Winston ; McClure Ryan ; Mitchell HughSeries Type : Expression profiling by high throughput sequencingOrganism : Bacillus toyonensis ; Curtobacterium flaccumfaciens ; Microbacterium foliorum ; Rhodococcus qingshengiiMicrobially induced calcium carbonate precipitation (MICP) holds potential for soil stabilization and carbon sequestration efforts. While the biogeochemical pathways and enzymes driving MICP are known, the microbial metabolic networks and community dynamics underlying such processes remain poorly characterized. To address this gap, we interrogated a MICP-capable four-member consortium of soil bacteria termed carbon storing consortium - A (CSC-A). Prior work shows that CSC-A yields carbonate at a higher quantity compared to the sum of carbonate individually produced by each member, suggesting MICP is driven by consortium dynamics.Thus, we applied a multi-omic integration approach of genomics, transcriptomics, and metabolomics to investigate potential inter-species interactions that may influence the MICP phenotype. Genomic life history characterizations identified evidence of specialization by two members, while metatranscriptomic perturbation suggested that R. qingshengii is a keystone species when grown in urea, a key molecule to the MICP process. By comparing individual species’ metabolomes to the metabolic profile of a shared well, we identified over 200 metabolites predicted to be produced or consumed by CSC-A. Integrating both data types and mapping them to the KEGG reactome highlighted over 20 different enriched pathways with reactions related to glutamate metabolism, succinate metabolism, and branched chain amino acid biosynthesis. As succinate metabolism was a major node in this network we applied laboratory assays to confirm that succinate led to increased carbonate precipitation by CSC-A, a critical validation of our modeling approach. By isolating and identifying the interconnected metabolic components underlying MICP in CSC-A, we identified keystone taxa, metabolites, and pathways important for future optimization of the application of this consortium to carbonate precipitation.
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10. GSE315997 通过 USP7 抑制导致非经典 PRC1.1 复合物不稳定，从而诱导神经母细胞瘤中的神经元分化 [CHIP-Seq、CUT&RUN、PCGF1KO]

• ✍️ 作者：未知作者
• 🏷️ 关键词：Neuronal、ChIP-seq
• 📝 描述：Contributor : Nathaniel W MabeSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensPediatric cancers are frequently driven by genomic alterations that result in impaired differentiation during tissue development. To identify protein complex-level dependencies required for differentiation in neuroblastoma, a pediatric cancer of the developing peripheral nervous system, we curated a list of protein complexes using the CORUM database and mined the Dependency Map (DepMap) using single sample gene set enrichment analysis. This analysis identified the non-canonical PRC1.1 complex, which represses transcriptional activity through ubiquitination of histone 2A, lysine 119 (H2AK119Ub), as a selectively enriched dependency in neuroblastoma. Knockout of several PRC1.1 subunits reduced neuroblastoma growth, arrested the cell cycle, and induced a neuronal differentiation program. While no known direct inhibitors of PRC1.1 exist, co-dependency analysis of PRC1.1 subunits against all other genes in DepMap identified that the deubiquitinase USP7 strongly correlated with PRC1.1 dependency. Treatment with XL177A, a small molecule inhibitor of USP7, significantly reduced neuroblastoma growth in both cellular and animal models. Integrated RNA- and ChIP-sequencing showed that both PRC1.1 knockout and USP7 inhibition resulted in highly correlated transcriptional alterations and reduced H2AK119Ub deposition on chromatin, suggesting that USP7 inhibition reduced neuroblastoma growth through a PRC1.1-dependent mechanism. Mechanistically, global proteomics and ubiquitinomics revealed that USP7 inhibition disrupted non-canonical PRC1 complex assembly, resulting in destabilization of PRC1.1 and subsequent proteolysis. Our findings expand our understanding of the chromatin complexes required to maintain a de-differentiated state in neuroblastoma and suggest the therapeutic potential for USP7 inhibitors in the treatment of this disease.
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1. 细胞液滴内部的隐藏结构为癌症和肌萎缩侧索硬化症的治疗开辟了新的靶点。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Biomolecular condensates were long believed to be simple liquid blobs inside cells. Researchers have now uncovered that some are actually supported by fine protein filaments forming an internal scaffold. When this structure is disrupted, cells fail to grow and divide properly. The discovery suggests scientists may one day design drugs that target condensate architecture to fight cancer and neurodegenerative disease.
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2. 你越害怕衰老，你的身体衰老的速度可能就越快。

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging
• 📝 描述：Worrying about getting older—especially fearing future health problems—may actually speed up aging at the cellular level, according to new research from NYU. In a study of more than 700 women, those who felt more anxious about aging showed signs of faster biological aging in their blood, measured using cutting-edge “epigenetic clocks.” Fears about declining health had the strongest link, while concerns about beauty or fertility didn’t appear to have the same biological impact.
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3. 大多数美国人体内发现的 PFAS 与生物体快速衰老有关。

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging
• 📝 描述：“Forever chemicals” known as PFAS have quietly infiltrated everything from nonstick pans to food packaging—and now new research suggests some of them may be speeding up the aging process itself. In a nationally representative U.S. study, two lesser-known PFAS compounds, PFNA and PFOSA, were found in 95% of participants and strongly linked to faster biological aging in men aged 50 to 64.
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• GSE315996 通过 USP7 抑制导致非经典 PRC1.1 复合物不稳定，从而诱导神经母细胞瘤神经元分化 [ChIP-Seq NGP]
• GSE307922 通过 USP7 抑制导致非经典 PRC1.1 复合物不稳定，从而诱导神经母细胞瘤中的神经元分化 [RNA-Seq]
• GSE307920 通过 USP7 抑制导致非经典 PRC1.1 复合物不稳定，从而诱导神经母细胞瘤中的神经元分化 [ChIP-Seq]
• GSE303748 CHD1 是 MYC 驱动的乳腺癌中的合成致死脆弱性 [ATAC-seq]
• GSE303747 CHD1 是 MYC 驱动的乳腺癌中的合成致死脆弱性 [RNA-Seq]
• GSE291677 乳酸和组蛋白H3K18乳化与视网膜基因表达的代谢调控相关
• GSE290710 乳腺癌中 LINC00636 和 CD47 调控的双功能超级增强子内的 InDel 基因组变异 [RNA-seq]
• GSE290709 乳腺癌中 LINC00636 和 CD47 调控的双功能超级增强子内的 InDel 基因组变异 [ATAC-seq]
• GSE320584 利用 STEMdiff™ 肝类器官生长培养基和 STEMdiff™ 肝类器官分化培养基，对 hPSC 来源的肝细胞样细胞生成的增殖性和分化性肝类器官进行单细胞 RNA 测序分析
• GSE320206 通过调节巨噬细胞功能，利用 CEL 增强 M1 巨噬细胞来源外泌体对三阴性乳腺癌的免疫治疗
• GSE320108 将拷贝数、甲基化和融合检测整合到一次检测中：一种用于儿童和成人罕见肿瘤诊断的纳米孔测序方法
• GSE312326 DKC1 通过失调鞘脂生物合成促进结直肠癌进展和治疗耐药性
• GSE320378 roX RNA 缺失导致的剂量补偿缺陷可通过重新校准 X/常染色体化学计量得到挽救 [RNA-seq]
• GSE320376 roX RNA 缺失导致的剂量补偿缺陷可通过重新校准 X/常染色体化学计量比来挽救 [ChIP-seq]
• GSE307263 人类髓系发育驱动大脑环境中的分化潜能 [ChIP-seq]
• GSE307262 人类髓系发育驱动大脑环境中的分化潜能 [ATAC-seq]
• GSE301256 增强的线粒体自噬通过恢复上皮细胞代谢功能促进肺部修复和再生
• GSE299717 人类髓系发育驱动大脑环境中的分化潜能 [RNA-seq]
• GSE295598 流感感染后肺泡 II 型细胞的时间序列 RNA 测序
• GSE289669 MEK/ERK信号通路阻断H3K9me3异染色质的形成，从而促进人类中胚层和内胚层的分化。[RNA-Seq]
• GSE289666 MEK/ERK信号通路阻断H3K9me3异染色质的形成，从而增强人类中胚层和内胚层的分化。[ChIP-Seq]
• GSE223315：携带Cysltr1缺陷小鼠的EMT6肿瘤祖细胞和髓系细胞的单细胞RNA表达数据
• GSE320427 绵羊单细胞转录组对称性破缺图谱
• GSE316009 通过抑制USP7导致非经典PRC1.1复合物不稳定，从而诱导神经母细胞瘤神经元分化
• GSE312830 CRYPTID-exon：从 RNA-seq 数据中简化隐蔽外显子的检测
• GSE311135 巨噬细胞对球孢子菌的吞噬作用促进其分化为寄生型
• GSE310927 PRMT5抑制引发功能性ATM缺陷并使胰腺癌对CHK1阻断敏感
• GSE301413 发现一种对血液恶性肿瘤具有强效抗癌活性的旁系同源选择性p300蛋白降解剂
• GSE299479 肺类器官模型展示了组成驱动的上皮可塑性和免疫极化
• GSE295985 LGR5+隐窝基底柱状细胞中诱导的异常NOTUM+程序维持了结直肠癌中的免疫抑制微环境
• GSE288838 高分辨率染色质图谱显示，CTCF 将减数分裂环锚定到染色体轴上。[Hi-C]
• GSE228867 对照 siRNA 和 PHGDH-siRNA 处理的人类永生化表皮细胞 (HaCaT 细胞) 的表观基因组分析
• GSE309203 ZNF200 与 DDX17 相互作用，调控 RBP-J 的转录活性。[ChIP-Seq]
• GSE308112 ZNF200 与 RBP-J 启动子区域的 DDX17 相互作用，从而调节 RBP-J 的转录活性。[ATAC-Seq]
• GSE307595 H1299 细胞系中 ZNF200 RNA-seq
• GSE320415 芍药籽油通过抑制PI3K/Akt/mTOR和NF-κB信号通路缓解UVB诱导的角质形成细胞炎症、氧化应激和光老化
• GSE320026 蛋白质稳态检查点控制 EGFR 稳定性和细胞适应性，由 lncRNA 定义 [RNA-seq]
• GSE316115 RNA-seq 分析 E18.5 小鼠胚胎肺揭示 Svep1 敲除胚胎中肺泡成熟和气道分化受损
• GSE308447 肾盂肾炎可降低血清胆固醇并减轻动脉粥样硬化的严重程度，即使存在全身性炎症
• GSE290690 E3泛素连接酶HUWE1的缺失会损害Kras诱导的肺腺癌肿瘤发生并诱导衰老表型
• GSE290688 七叶苷靶向斑马鱼幼体中的 Keap1/Nrf2/ARE 信号通路
• GSE290687 E13.5 对照组和 Isl1 cKO 视网膜的 RNA-Seq
• GSE284673 L-亮氨酸摄取抑制剂对结核分枝杆菌mc2 6206全基因组转录组谱的影响