详细内容（前10条）

1. ⭐ GSE325457 孕酮重塑激素受体阳性乳腺癌的肿瘤免疫微环境，使其向巨噬细胞驱动的免疫抑制方向发展

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immune、macrophage
• 📝 描述：Contributors : Eilidh I Chowanec ; Halyna Fedosyuk ; Julio C Tinoco ; Amanda Heard ; Harmony I Saunders ; Prabhakar Chalise ; Zachary C Hartman ; Mary A Markiewicz ; Jeffery Vahrenkamp ; Jason Gertz ; Christy R HaganSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusHormone receptor–positive (HR⁺) breast cancers comprise ~80% of breast cancer cases, yet endocrine resistance remains a clinical barrier. While estrogen receptor alpha (ER) biology is well characterized, the role of progesterone receptor (PR) signaling in tumor progression and immune evasion is less defined. Using the ER⁺/PR⁺ SSM2 murine mammary tumor model, we investigated progesterone’s influence on tumor growth and the immune microenvironment. Progesterone significantly accelerated tumor growth in vivo and enhanced proliferation in vitro. Single-cell RNA sequencing (scRNA-seq) revealed that progesterone treatment reshaped the tumor microenvironment, expanding the tumor cell compartment while markedly reducing immune populations. Tumor-intrinsic analyses showed downregulation of interferon and antigen presentation pathways, alongside upregulation of cell cycle and proliferation signaling. Within the immune compartment, progesterone reduced overall T cell infiltration, shifted CD4⁺ T cells toward a regulatory phenotype, and increased macrophages. Notably, lipid-associated macrophages (LAMs) with a high Apoe/Trem2 signature were markedly expanded and engaged in immunosuppressive Spp1–CD44 signaling with immune cells. CellChat analysis of inferred ligand–receptor interactions revealed LAM-driven communication networks that may impair the anti-tumor immune response. Analysis of human breast cancer scRNA-seq datasets confirmed that PRhi tumors harbored more LAMs than PRlo tumors, supporting the translational relevance of our findings. Collectively, these data establish progesterone signaling as a driver of immune suppression in HR⁺ breast cancer through coordinated effects on tumor cells, T cells, and macrophages. Targeting PR signaling or LAM subsets may represent novel therapeutic strategies to overcome immune evasion and sensitize HR⁺ tumors to immunotherapy.
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2. GSE312335 基于DISE诱导的短RNA开发泛癌疗法[DISE-071.RNAseq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNAseq
• 📝 描述：Contributors : Marcus Peter ; Elizabeth BartomSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensDeveloping two different DISE inducing sRNAs. The first is based on the 6mer seed GGGGGC (G5C) and the second on CAG trinucleotide repeat sequences.This RNA seq analysis was designed to identify the most deregulated genes in either HeyA8 or PC3 cells transfected with either of the two Di-sRNAs, each compared to the nontargeting control sNT8.
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3. GSE312334 基于DISE诱导的短RNA开发泛癌疗法[DISE-069.RNAseq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNAseq
• 📝 描述：Contributors : Marcus Peter ; Elizabeth BartomSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensDeveloping two different DISE inducing sRNAs. The first is based on the 6mer seed GGGGGC (G5C) and the second on CAG trinucleotide repeat sequences.This RNA seq analysis was designed to identify the most deregulated genes in ID8p53-/-Brca2-/- (DKO) cells transfected with either of the two Di-sRNAs, each compared to the nontargeting control sNT8.
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4. GSE311839 HNF1A-MODY 对十二指肠胰高血糖素表达细胞的影响 [批量 RNA 测序]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、regex:intestin(e|al)
• 📝 描述：Contributors : Ulrik Larsen ; Lucas Unger ; Simona CheraSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThis project investigates the impact of the Hnf1a hotspot mutation similar to HNF1A-MODY (Maturity-Onset Diabetes of the Young) on glucagon expressing cells in the intestine. RNA sequencing (RNA-seq) data was preformed on intestinal crypts isolated from duodenum from mutant and control Hnf1a mice to study the mutation’s effect on gene expression. By comparing the transcriptomcis profiles of these crypts, the study aims to uncover molecular mehcnaisms underlying the phenotype caused by HNF1A-MODY during adulhood.
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5. GSE281506 联合使用 Menin 和 MEK 抑制剂治疗预后不良的 KMT2A 重排 RAS 通路突变型急性髓系白血病

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、pathway
• 📝 描述：Contributors : Kimberly Stegmaier ; Gabriela AlexeSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensKMT2A-rearranged acute leukemias are especially prevalent in the pediatric population. The KMT2A-fusion proteins drive leukemogenic gene expression through an interaction with a chromatin complex that includes the scaffold protein menin, giving rise to aggressive acute leukemias. RAS pathway mutations are common in pediatric leukemia. In a cohort of 1605 patients enrolled on Children’s Oncology Group (COG) trials AAML0531 and AAML1031, we identified RAS pathway mutations in 43% of AML cases. The presence of RAS pathway mutations in KMT2A-r AML was associated with lower complete remission (CR) rate, poor event-free survival (EFS) and early relapses. We next sought to identify efficacious targeted drug combinations for this subset of childhood leukemia. We evaluated the combination of RAS/MAPK targeting using the MEK1/2 inhibitor selumetinib with the menin inhibitor revumenib. Treatment of acute leukemia cell lines and cultured leukemia cells from patient-derived xenograft (PDX) models resulted in a synergistic decrease in viability, promoted cell cycle arrest, and promoted downregulation of targets of MYC signaling by each drug alone and even more effectively with the combination. In vivo, the combination treatment of AML and ALL pediatric PDX models harboring KMT2A-r and RAS mutations reduced leukemia burden effectively compared with the single drug-treated cohorts. Tissues from treated mice showed a decrease in protein levels of MYC, P-ERK and MEIS1, highlighting effective target engagement of the drugs. Our preclinical study suggests a promising, readily translatable targeted treatment for KMT2A-r RAS pathway mutant leukemias.
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6. GSE328472 癌症治疗药物 TKI 奥希替尼诱导的心脏毒性是由 HDAC 依赖性表观遗传抑制驱动，并可被伏立诺他逆转

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、epigenetic
• 📝 描述：Contributor : Hind LalSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusOsimertinib, a third-generation EGFR tyrosine kinase inhibitor (TKI), has significantly improved outcomes in non–small cell lung cancer (NSCLC) patients harboring the T790M mutation; however, emerging clinical evidence indicates a substantial risk of cardiotoxicity. Here, we establish the first in vivo preclinical model of osimertinib-induced cardiotoxicity using transverse aortic constriction (TAC) in mice. Osimertinib treatment resulted in profound cardiac dysfunction, impaired hypertrophic remodeling, and increased markers of heart failure and fibrosis. Unbiased transcriptomic profiling revealed a maladaptive myocardial stress response characterized by activation of p53-associated cell death pathways, mitochondrial dysfunction, and negative enrichment of histone acetyltransferase (HAT) complexes, indicating epigenetic repression. Mechanistically, osimertinib-treated hearts exhibited increased expression of multiple histone deacetylase (HDAC) isoforms, reduced acetylation of key histones, and enhanced cardiomyocyte apoptosis via Bax/caspase-mediated pathways. There was only a minimal, transient effect on inflammation, supporting a type I, cell-autonomous cardiotoxic mechanism. Consistent with this, in vitro and in vivo analyses demonstrated suppression of pro-survival ERK/AKT signaling, mitochondrial dysfunction, and activation of intrinsic apoptotic pathways. Given the central role of HDAC activation, we tested whether pharmacologic HDAC inhibition could mitigate osimertinib-induced cardiotoxicity. Treatment with the FDA-approved HDAC inhibitor vorinostat (SAHA) restored histone acetylation, attenuated p53 activation, reduced cardiomyocyte death, and rescued cardiac function in osimertinib-treated mice. Translational studies in human NSCLC-derived PC9 cells further demonstrated that SAHA enhances osimertinib anti-tumor efficacy while alleviating cardiotoxicity. Collectively, these findings define HDAC-dependent epigenetic repression as a key mechanism underlying osimertinib-induced cardiotoxicity and identify HDAC inhibition as a therapeutically actionable strategy to improve both cardiac safety and cancer treatment efficacy.
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7. GSE327288 在患者来源的肿瘤免疫模型中模拟生理相关环境以靶向免疫冷的高级别浆液性肿瘤

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune
• 📝 描述：Contributors : Simona Plesselova ; Hailey Axemaker ; Kristin Calar ; Oduduabasi Isaiah ; Jared Wollman ; Somshuvra Bhattacharya ; Etienne Z Gnimpieba ; Darci M Fink ; Congzhou Wang ; Hiruni Sumanasiri ; Kristina W Thiel ; Maria Bell ; Pilar De la PuenteSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensHigh-grade serous tumors are immunologically cold, characterized by limited immune cell infiltration and reduced clinical outcome, primarily due to hypoxia and extensive extracellular matrix remodeling that disrupt tumor-stromal-immune interactions. However, current experimental models fail to fully capture oxygen and matrix microenvironmental features, limiting progress in understanding tumor-immune dynamics and developing effective treatments. Here, we demonstrate that patient-derived tumor-immune models, mimicking physiologically relevant oxygen levels and extracellular matrix remodeling, recapitulate the hypoxia-induced stromal/matrix dysregulation, which associates with impaired immune infiltration, and enable dissecting targeted opportunities via TGF-β signaling. The models incorporate cancer cells co-cultured with cancer-associated fibroblasts within 3D matrices bioengineered using human plasma or grown on decellularized human ovarian extracellular matrices. Immune cells were either included within the 3D constructs as a multiculture to study tumor-immune interactions or challenged to infiltrate the matrices. By bioengineering physiologically relevant oxygen levels, we uncovered that intratumoral hypoxia acts as a friend and a foe, causing hypoxia-induced stromal-driven impaired immune infiltration but enhancing the activation and cytotoxicity of CD8+ T cells. We also showed that targeting TGF-β signaling reversed the hypoxia-induced stromal-driven impaired immune infiltration. These female patient-relevant models may aid the development of targeted therapies to turn immunologically cold tumors into hot ones.
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8. GSE299200 在患者来源的肿瘤免疫可调模型中重现生理相关的氧水平和细胞外基质重塑，揭示了免疫冷的高级别浆液性肿瘤的靶向机会

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune
• 📝 描述：Contributors : Simona Plesselova ; Hailey Axemaker ; Kristin Calar ; Oduduabasi Isaiah ; Jared Wollman ; Somshuvra Bhattacharya ; Etienne Z Gnimpieba ; Darci M Fink ; Congzhou Wang ; Maria Bell ; Pilar de laPuenteSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensHigh grade serous tumors are immunologically cold, characterized by limited immune cell infiltration and reduced clinical outcome, primarily due to hypoxia and extensive extracellular matrix remodeling that disrupts tumor-stromal-immune interactions. However, current experimental models fail to fully capture oxygen and matrix microenvironmental features, limiting progress in understanding tumor-immune dynamics and developing effective treatments. Here we show that patient-derived tumor-immune tunable models mimicking physiologically relevant oxygen levels and extracellular matrix remodeling recapitulate the hypoxia-induced stromal/matrix dysregulation, which causes impaired immune infiltration, and enable dissecting targeted opportunities via TGF-β signaling. The models integrate cancer cells co-cultured with cancer associated fibroblasts and exposed to immune cells as multi-culture or challenged them to infiltrate into a 3D model bioengineered with autologous plasma from the matching patient or onto decellularized human ovaries. By bioengineering physiologically relevant oxygen levels of hypoxic tumors and physoxic ovaries, we uncovered that intratumoral hypoxia acts as a friend and a foe, causing hypoxia-induced stromal-driven impaired immune infiltration but enhancing the activation and cytotoxicity of CD8+ T cells. We also showed that targeting TGF-β signaling reversed the hypoxia-induced stromal-driven impaired immune infiltration. These human-relevant tunable models may aid the development of targeted therapies to turn immunologically cold tumors into hot ones.
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9. GSE325008 靶向 UHRF1：伊沙佐米柠檬酸盐类似物作为 KRAS 突变型胰腺癌的潜在治疗药物

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、KRAS
• 📝 描述：Contributor : Sivasundaram KarnanSeries Type : Expression profiling by arrayOrganism : Homo sapiensTo investigate the effect of Ixazomib Citrate Analogue (ICA) inKRAS mutant on gene expression, we have emoloyed whole genomic microarray expression profiling using cancer cells
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10. GSE310378 工程化水疱性口炎病毒用于癌症特异性递送强效免疫治疗有效载荷

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、regex:immuno(logy|therapy|suppression)
• 📝 描述：Contributors : Eileen Theune ; William Theune ; Kepeng WangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe lack of tumor-specific targeting by oncolytic viruses (OVs) restricts their therapeutic potential. Here, we report a “cap-linker” strategy to modify the vesicular stomatitis virus (VSV) glycoprotein (G protein, VSV-GIN). The modified VSV (Pro-VSVIN) loses its ability to infect cells until present in the tumor microenvironment, where the linker is cleaved by tumor-enriched matrix metalloproteases (MMPs). When Pro-VSVIN is armed with a single-chain IL-12 (Pro-VSVIN-IL-12) and systemically injected into MC38 tumor-bearing mice, Pro-VSVIN-IL-12 shows a markedly improved safety profile and eradicates tumors. The efficacy of Pro-VSVIN-IL-12 was further improved when combined with PD-1 checkpoint blockade. Compared to WT VSVIN that carries IL-12, intravenously injected Pro-VSVIN-IL-12 leads to strong Th1 immunity, near abolishment of regulatory T cells, and CD8+ T cell activation in tumors. This preclinical work demonstrates a new tumor-specific targeting strategy of VSV for enhanced immunotherapy safety with superior efficacy.
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1. 蛋白质运输堵塞或许可以解释衰老、记忆力衰退和阿尔茨海默病。

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、Alzheimer
• 📝 描述：Scientists at Stanford may have uncovered a hidden reason our brains decline with age. Studying the ultra-short-lived turquoise killifish, researchers discovered that the cellular machinery responsible for building proteins begins to jam and malfunction over time. Tiny structures called ribosomes start colliding and stalling while reading genetic instructions, triggering a chain reaction that leads to faulty proteins and harmful clumps linked to diseases like Alzheimer’s.
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2. 通用RNA特征揭示衰老和死亡的共同机制

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging
• 📝 描述：RNA sequencing across multiple mammalian species identified conserved gene expression signatures linked to aging, mortality, chronic disease, and lifespan-modulating…
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3. 这种番茄豆浆汁在短短四周内就减轻了炎症。

• ✍️ 作者：未知作者
• 🏷️ 关键词：inflammation
• 📝 描述：A specially formulated tomato-soy juice packed with natural plant compounds may help calm inflammation linked to obesity, according to a new clinical study. Healthy adults with obesity who drank the juice daily for four weeks saw significant reductions in several key inflammatory proteins in their blood, while a control tomato juice did not produce the same effect.
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• GSE333536 MEK抑制剂曲美替尼可导致小鼠心脏线粒体损伤并诱导先天免疫反应
• GSE333470 从菟丝子体外吸器和拟南芥侧翼宿主茎中富集小RNA的跨界、快速、经济的RISC纯化（TraPR）
• GSE331212 钙代谢紊乱是唐氏综合征唾液分泌减少和微生物菌群失调的根本原因
• GSE330327 基于DISE诱导的短RNA开发泛癌疗法
• GSE326449 共生菌来源的乙酰胆碱增强黏膜免疫教育
• GSE326448 共生菌来源的乙酰胆碱增强粘膜免疫教育 [PRESTO_salsa_screen_acetonitrile_methanol_water_extracted_in_vitro_metabolomes]
• GSE326301 共生菌来源的乙酰胆碱增强粘膜免疫教育 [PRESTO_Salsa_screen_InVio_Bu_corrected]
• GSE326298 共生菌来源的乙酰胆碱增强粘膜免疫教育 [PRESTO-Salsa_screen_InVivo_Ea_corrected]
• GSE326286 共生菌来源的乙酰胆碱增强粘膜免疫教育 [PRESTO_salsa_screen_ethylacetate_extracted_in_vitro_metabolome]
• GSE326280 共生菌来源的乙酰胆碱增强粘膜免疫教育 [PRESTO_salsa_screen_butanol_extracted_in_vitro_metabolome]
• GSE326271 共生菌来源的乙酰胆碱增强粘膜免疫教育 [PRESTO_Salsa_screen_acetonitrile_methanol_water_extracted_in_vivo_metabolome]
• GSE326266 共生菌来源的乙酰胆碱增强粘膜免疫教育 [mouse_lamina_propria_bulk_RNA-seq]
• GSE326264 共生菌来源的乙酰胆碱增强粘膜免疫教育 [小鼠回肠固有层单细胞RNA测序]
• GSE326262 共生菌来源的乙酰胆碱增强粘膜免疫教育 [Citrobacter_portucalensis_RNA-seq]
• GSE231496 一种支持精确空间域识别的掩码生成图表示学习框架
• GSE331144 人类肺成纤维细胞的转录和空间分析表明，CTHRC1+细胞是纤维化中的成纤维信号枢纽
• GSE329287 胚胎植入前外源性雌激素暴露会扰乱胚胎运输，并对小鼠输卵管和子宫的转录组产生不同的影响
• GSE305215 睾丸发育的单细胞多组学分析
• GSE333263 SoFIC 协调物理屏障和代谢稳态以对抗噬菌体感染
• GSE333210 ZEB1 K80R抑制NF-κB/EMT轴和肿瘤促炎基因表达
• GSE331503 组蛋白变体 MacroH2A1 在 K134 位点的乳酸化调控骨髓间充质干细胞的成骨分化 [ATAC]
• GSE329731 单核 RNA 测序阐明了 mimeCM 对阿霉素诱导的心脏毒性的保护作用
• GSE308534 RNA-seq 分析了链脲佐菌素 (STZ) 诱导的伴有焦虑样行为的糖尿病性疼痛性神经病变小鼠模型中室旁丘脑 (PVT) 和后岛叶皮层 (pIC) 的 RNA 序列
• GSE298695 内皮细胞 Piezo1 的机械感知通过 ATF2-ID1-Wnt2 通路促进部分肝切除术后的肝脏再生
• GSE298573 CMPortal：一个面向社区、数据驱动的资源，旨在为利用人类多能干细胞构建心脏模型提供方案设计信息
• GSE297972 山梨酸通过 I 类 HDAC 的非经典活性诱导赖氨酸山梨酰化，从而调节炎症基因的表达。
• GSE292214 机械压缩对 HEI-286 雪旺细胞和胰腺癌细胞 MiaPaCa-2 和 Panc01 中基因表达的影响
• GSE264443 动态基因表达分析揭示 COVID-19 中免疫和细胞失调的不同严重程度阶段
• GSE39069 Ikaros影响造血发育中的多个谱系[RNA-Seq]
• GSE38920 Ikaros 在成熟 IgM+ B 细胞中的作用：IkZnF1-/- 和 IkZnF4-/- 突变小鼠的研究 [RNA-seq]
• GSE292835 病毒包含的单核 RNA 测序揭示了传染性鲑鱼贫血症中两种不同的内皮反应模式。