详细内容（前10条）

1. ⭐ GSE302321 共靶向 EZH2 和 TEAD 通过 Hippo 通路突变癌症中的肿瘤固有免疫信号通路诱导细胞凋亡 - 来自 EZH2 基因破坏的 ChIP-seq 数据

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune、ChIP-seq、pathway
• 📝 描述：Contributors : Antja-Voy Hartley ; Shweta Kukreja ; Sonsoles L Veiga ; Rong Li ; Xintao Qiu ; Henry W Long ; Pasi A JänneSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensTEA/TEF-domain [TEAD] inhibitors are being evaluated in clinical trials for cancers with alterations in the Hippo pathway including mesothelioma. We recently developed and showcased the potency of TEAD palmitoylation inhibitors MYF-03-69 and MYF-03-176 in mesothelioma cell lines. However, TEAD inhibition results in cell cycle arrest in cell line models with Hippo pathway alterations without inducing cell death, potentially limiting their long-term clinical efficacy. Using a genome-wide CRISPR/Cas9 screen, we identified EZH2 as a critical modulator of the cellular response to TEAD inhibition. Compared to single agent treatments, EZH2i/TEADi robustly triggered apoptosis and suppressed the growth of Hippo-mutated cells in vitro and in vivo. Mechanistically, EZH2i/TEADi-treated cells exhibited heightened activation of tumor-intrinsic innate immune signaling which resulted in DNA damage and subsequent apoptosis. Taken together, we propose this novel combinatorial strategy as a potential approach to enhancing the anti-tumor efficacy of single agent TEAD targeting therapies in Hippo pathway altered tumors. This GEO accession includes the data series associated with ChIP-seq derived from genetic disruption of EZH2.
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2. ⭐ GSE307120 融合驱动的致癌程序塑造易位性肾细胞癌的免疫微环境

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、immune、regex:onco(logy|logist|gene|genic)
• 📝 描述：Contributors : Prathyusha Konda ; Srinivas R ViswanathanSeries Type : Expression profiling by high throughput sequencing ; Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensRenal cell carcinomas comprise multiple molecularly distinct cancers but most are treated empirically with therapies designed for clear cell RCC (ccRCC), the most common subtype, due to incomplete understanding of subtype-specific biology. We analyzed single-cell transcriptomes and chromatin accessibility profiles from translocation renal cell carcinoma (tRCC), an aggressive RCC defined by oncogenic TFE3 gene fusions.
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3. ⭐ GSE287826 健康人和 MASH 患者的肝细胞空间转录组学分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : FENG WANG ; Ekihiro Seki ; Yoon Seok RohSeries Type : OtherOrganism : Homo sapiensSpatial transcriptomics of hepatocytes was employed to identify differentially expressed genes between healthy tissues and those from MASH patients.
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4. ⭐ GSE287820 对喂食 NCD 和 FFD 饮食的 24 周龄小鼠肝组织中的肝细胞进行空间转录组学分析。

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : FENG WANG ; Ekihiro Seki ; Yoon Seok RohSeries Type : OtherOrganism : Mus musculusSpatial transcriptomics analysis of hepatocytes was performed to identify differentially expressed genes in liver tissues of 24-week-old mice maintained on NCD and FFD diets.
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5. ⭐ GSE327192 树突状细胞介导的抗原呈递调控癌症中三级淋巴结构发育 [MERFISH]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、dendritic cell、antigen
• 📝 描述：Contributors : Laszlo Halasz ; Raphael Mattiuz ; Brian Soong ; Miriam MeradSeries Type : OtherOrganism : Homo sapiens ; synthetic constructTertiary lymphoid structures (TLS) correlate with favorable responses to immunotherapy, yet the mechanisms governing their formation and maintenance in tumors remain poorly defined. Through high-resolution spatial mapping across human tumors, we identified a consistent accumulation of CCR7⁺ mature dendritic cells (DC) within TLS. To dissect their function, we developed a non-small cell lung cancer (NSCLC) model that recapitulates mature TLS formation. Using this model, we demonstrate that TLS induction requires IFNγ-driven maturation of type 1 conventional dendritic cells (cDC1), their migration to tumor-draining lymph nodes (tdLN), and the subsequent recruitment of tdLN-primed T cells into the tumor microenvironment. As tumors progress, TLS persist even in the absence of tdLN T cell egress, coinciding with impaired cDC1 migration to tdLN and their retention within intratumoral stromal hubs enriched in CCR7 ligands. Timed depletion of cDC1 or blockade of their localization to these hubs disrupts TLS maintenance. Strikingly, concomitant genetic ablation of both MHC class I and II on cDC1 abolishes the maintenance of TLS, T follicular helper (TFH) cells, germinal center formation, tumor-specific IgG production, and the differentiation of progenitor exhausted CD8⁺ T cells. These findings establish that local cDC1-mediated antigen presentation to CD8⁺ and CD4⁺ T cells is a central orchestrator of anti-tumor TLS programs and compelling targets for therapeutic intervention.
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6. ⭐ GSE322553 树突状细胞介导的抗原呈递调节癌症中三级淋巴结构发育。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、dendritic cell、antigen
• 📝 描述：Contributors : Laszlo Halasz ; Raphael Mattiuz ; Miriam MeradSeries Type : OtherOrganism : Homo sapiensTertiary lymphoid structures (TLS) correlate with favorable responses to immunotherapy, yet the mechanisms governing their formation and maintenance in tumors remain poorly defined. Through high-resolution spatial mapping across human tumors, we identified a consistent accumulation of CCR7⁺ mature dendritic cells (DC) within TLS. To dissect their function, we developed a non-small cell lung cancer (NSCLC) model that recapitulates mature TLS formation. Using this model, we demonstrate that TLS induction requires IFNγ-driven maturation of type 1 conventional dendritic cells (cDC1), their migration to tumor-draining lymph nodes (tdLN), and the subsequent recruitment of tdLN-primed T cells into the tumor microenvironment. As tumors progress, TLS persist even in the absence of tdLN T cell egress, coinciding with impaired cDC1 migration to tdLN and their retention within intratumoral stromal hubs enriched in CCR7 ligands. Timed depletion of cDC1 or blockade of their localization to these hubs disrupts TLS maintenance. Strikingly, concomitant genetic ablation of both MHC class I and II on cDC1 abolishes the maintenance of TLS, T follicular helper (TFH) cells, germinal center formation, tumor-specific IgG production, and the differentiation of progenitor exhausted CD8⁺ T cells. These findings establish that local cDC1-mediated antigen presentation to CD8⁺ and CD4⁺ T cells is a central orchestrator of anti-tumor TLS programs and compelling targets for therapeutic intervention.
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7. ⭐ GSE312124 MAPK驱动的胶质瘤进展和肿瘤相关免疫反应的重编程

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune、glioma
• 📝 描述：Contributors : Joanna Phillips ; Elaheh HashemiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensGlioma evolution is associated with disease progression and therapeutic resistance. We recently identified a group of MAPK-driven glioma with CDKN2A homozygous deletion that are low-grade and immune enriched. However, Over time, these tumors can progress to aggressive, higher-grade tumors. While low-grade tumors may be amenable to immunotherapeutic strategies, it is unknown how the tumor and its microenvironment evolve.
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8. ⭐ 利用 GS​​E272421 空间转录组立体测序揭示了单中心 Castleman 病的功能区室化。

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Series Type : OtherOrganism : Homo sapiensThe cell-of-origin of UCD and the cell-cell communication in lymphnode tissue in UCD context is still not well-studied. We performed stereo-seq to profile heteigeneous cell population within UCD lymphnode tissue as well as to determine their importance for UCD development. Distinct subpopulations of Follicular dendritic cells were identified in the microenvironment that contribute the growth of the disease.
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9. ⭐ GSE338894 一种口服有效的、肠道富集的AhR激动剂通过调节炎症、屏障稳态和纤维化，在结肠炎中显示出治疗效果

• ✍️ 作者：未知作者
• 🏷️ 关键词：inflammation、gut、regex:gut(-?microbiome)?
• 📝 描述：Contributors : Pan Ren-You ; Zhang Yongli ; Zhang YongliSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusInflammatory bowel disease (IBD) is characterised by chronic intestinal inflammation, epithelial barrier dysfunction, and maladaptive stromal remodelling that can progress to fibrosis. Current therapies primarily target inflammatory pathways and rarely achieve durable remission or structural disease modification, highlighting a major unmet clinical need. Here, we evaluated the therapeutic potential of YUQ-A1007, an orally active, gut-enriched small-molecule aryl hydrocarbon receptor (AhR) agonist, across multiple translational models of colitis. The anti-inflammatory, barrier-restorative, and anti-fibrotic effects of YUQ-A1007 were assessed using in vitro cell systems, patient-derived colonic biopsies and organoids, permeability assays, and three murine colitis models. YUQ-A1007 partially activated AhR signalling, suppressed pro-inflammatory cytokine production, enhanced regulatory T cell differentiation, increased tight junction protein expression, and inhibited fibrotic gene programs. In vivo, oral YUQ-A1007 administration reduced disease severity, restored epithelial barrier integrity, and broadly downregulated inflammatory cytokines, chemokines, fibrosis-associated genes, pro-inflammatory mesenchymal stromal cell biomarkers, and matrix metalloproteinases. In ulcerative colitis patient-derived colonic explants, YUQ-A1007 dose-dependently reduced inflammatory mediator secretion while preserving barrier function. Collectively, these findings support further development of YUQ-A1007 as a gut-targeted AhR therapeutic for ulcerative colitis and broader inflammatory bowel disease.
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10. GSE336471 KRAS突变驱动的RASA2通过TGFB2依赖的非经典Hedgehog/GLI1激活促进胰腺癌转移

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、KRAS
• 📝 描述：Contributors : Taochen He ; Qiangda Chen ; Yanfei An ; Zhihang Xu ; Zhenlai Jiang ; Jiande Han ; Yuqi XieSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensKRAS mutations are a major driver of pancreatic ductal adenocarcinoma (PDAC), promoting tumor initiation, progression, and metastasis. RASA2, a Ras GTPase-activating protein, modulates KRAS protein levels in wild-type contexts, yet its role in KRAS-mutant PDAC remains unclear. Here, we systematically investigated the biological function and molecular mechanisms of RASA2 in KRAS-mutant PDAC. Integrative analyses of multiple datasets and patient-derived samples demonstrated that RASA2 is consistently upregulated in KRAS-mutant PDAC and significantly associated with poor prognosis and metastatic progression. Gain- and loss-of-function studies revealed that RASA2 markedly enhances PDAC cell migration and invasion in both KRAS-mutant and KRAS-wild-type models, indicating that its pro-metastatic activity is largely independent of KRAS mutational status. Transcriptomic profiling and mechanistic interrogation uncovered that RASA2 activates GLI1 through a TGFB2-dependent, Sonic Hedgehog–independent non-canonical Hedgehog signaling pathway. Mechanistically, RASA2 directly interacts with the transcriptional regulator RTF1, facilitating H2BK120 ubiquitination at the TGFB2 promoter and thereby augmenting TGFB2 transcription. This epigenetic activation of TGFB2 subsequently drives non-canonical Hedgehog/GLI1 signaling to confer pro-metastatic traits. Pharmacologic inhibition of TGFB2 signaling or genetic silencing of GLI1 effectively abrogated RASA2-driven migratory, invasive, and metastatic phenotypes both in vitro and in vivo. Collectively, our findings identify RASA2 as a critical mediator of PDAC metastasis downstream of oncogenic KRAS and uncover a previously unrecognized RASA2–RTF1–H2BK120ub1–TGFB2–GLI1 signaling axis. KRAS mutation drives RASA2 upregulation, while the pro-metastatic activity of RASA2 is largely independent of KRAS mutational status. These findings reveal a previously unrecognized mechanism by which oncogenic KRAS promotes metastatic progression through RASA2-dependent epigenetic and transcriptional reprogramming and nominate the RASA2–TGFB2–GLI1 axis as a potential therapeutic target in PDAC
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1. 科学家测试了39种甜味剂，发现了意想不到的肠道影响。

• ✍️ 作者：未知作者
• 🏷️ 关键词：gut、regex:gut(-?microbiome)?
• 📝 描述：A large laboratory study found that many commonly used sweeteners can directly change the growth of gut bacteria. Researchers identified more than 100 cases in which sweeteners behaved differently when combined with medications, caffeine, or flavorings. The combination of isosteviol and the antidepressant duloxetine was especially disruptive, reducing beneficial bacteria and overall microbial diversity.
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2. 一种治疗阿尔茨海默病的新药可以修复DNA损伤并减轻脑部炎症。

• ✍️ 作者：未知作者
• 🏷️ 关键词：inflammation、Alzheimer
• 📝 描述：A drug originally developed for spinal cord injury may offer a fresh approach to treating Alzheimer’s disease. In mouse studies, KCL-286 repaired dangerous DNA damage, reduced inflammation, and targeted multiple disease-related pathways instead of focusing on just amyloid or tau. Since it has already cleared an initial human safety trial, researchers believe it could move more quickly into Alzheimer’s clinical testing.
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3. DeepDETAILS——基于批量测序样本对细胞类型特异性转录调控过程进行高分辨率重建

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：DeepDETAILS combines artificial intelligence with RNA sequencing and chromatin data to reconstruct cell-specific gene regulation from bulk tissue sequencing experiments…
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4. 这种糖衣疗法使小鼠对抗致命脑癌的存活率提高了50%。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：A new experimental treatment may have found a way to outsmart glioblastoma’s toughest defense: the blood-brain barrier. Researchers used sugar-coated nanoparticles to ferry genetic instructions that restore a key tumor-suppressing protein directly into brain cancer cells. In mouse studies, the therapy increased median survival by 50% while shrinking tumors without noticeable damage to other organs.
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5. 人工智能标记出超过25万篇可疑的癌症研究论文

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：A powerful new AI tool has uncovered what could be one of the biggest integrity problems in modern science. After analyzing 2.6 million cancer research papers published between 1999 and 2024, researchers identified more than 250,000 studies with writing patterns resembling papers suspected of being produced by fraudulent “paper mills.”
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• 利用GSE327205对MIA诱导的骨关节炎小鼠背根神经节（DRG）进行RNA测序分析，比较针灸治疗组和非治疗组：重点关注神经免疫串扰基因
• GSE317860 CD1d-KO 和 WT 小鼠 E0771 乳腺肿瘤中髓系细胞的单细胞 RNA 测序
• GSE332732 肾脏特异性 Glut2 敲除 (rGlut2 KO) 小鼠肾脏的全基因组亚硫酸氢盐测序
• GSE338103 连接组蛋白 H1.0 和 JUNB 相互作用维持谱系特异性和年龄依赖性染色质结构以保护细胞身份 [ATAC-seq]
• GSE338101 连接组蛋白 H1.0 和 JUNB 相互作用维持谱系特异性和年龄依赖性染色质结构以保护细胞身份 [RNA-Seq]
• GSE337790 血管功能是 FLASH 辐射后肠道再生增强的基础 [bulk RNAseq]
• GSE318154 多模态单细胞分析鉴定出 nclTECs，并将染色质重塑与 TEC 分化和自身抗原表达模式联系起来 [scATAC-seq]
• GSE337660 四种基因型的受冷胁迫秀丽隐杆线虫动物的 RNA-seq
• GSE328666 胸腺素β4通过抑制MAPK信号通路减轻脓毒症相关的急性肾损伤
• GSE338910 对用抗 CD3/CD28 刺激 4 小时的 T 细胞进行 RNA 测序
• GSE337851 转谷氨酰胺酶 2 缺失增强星形胶质细胞到神经元的代谢支持并减轻反复轻度创伤性脑损伤后的亚急性病理
• GSE331205 肾脏特异性 Glut2 敲除 (rGlut2 KO) 小鼠肾脏的单核多组 RNA 和 ATAC 测序
• GSE301610 空间分析揭示 TREM2+ 巨噬细胞在人类肺结核中结核分枝杆菌致病机制中的核心作用
• GSE298793 限时喂养通过减少肥胖小鼠肾脏中 CD8+ T 细胞的浸润来阻止肾脏纤维化和损伤
• GSE338456 乳腺癌相关成纤维细胞来源的外泌体 miR-1290 促进三阴性乳腺癌细胞增殖
• GSE338102 连接组蛋白 H1.0 和 JUNB 相互作用维持谱系特异性和年龄依赖性染色质结构以保护细胞身份 [CUT&Run]
• GSE331176 嘌呤和嘧啶类细菌环状二核苷酸介导的吞噬体激活 STING
• GSE302413 菖蒲内酯对高脂饮食组和常规饮食组胰腺肿瘤基因表达的影响
• GSE263214 跨组织研究揭示藏茶对小鼠代谢的重编程作用
• GSE338821 造血干细胞长期培养前后的 RNA 谱 [RNA-Seq]
• GSE338728 KAT7驱动的CCAR2乳酸化促进巨噬细胞胞外陷阱的形成并加速动脉粥样硬化的进展
• GSE338640 血管功能是 FLASH 辐射后肠道再生增强的基础
• GSE338639 血管功能是 FLASH 辐射后肠道再生增强的基础 [scRNAseq]
• GSE318155 多模态单细胞分析鉴定出 nclTECs，并将染色质重塑与 TEC 分化和自身抗原表达模式联系起来 [scMultiome-seq]