详细内容（前10条）

1. ⭐ GSE316752 肿瘤细胞聚集通过调节 H3K36 组蛋白去甲基化酶 KDM2A 增强转移能力 [ChIP-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、ChIP-seq、histone、clustering
• 📝 描述：Contributors : Carolyn Kravitz ; Kiran D Patel ; Emily Wingrove ; Dejian Zhao ; Tang Tang ; Sampada Chande ; Yuchen Huo ; Thomas F Westbrook ; Qin Yan ; Don X NguyenSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensDisseminated tumor cells can form clusters via cell-cell adhesion, which increases their capacity to initiate metastasis. Metastatic clusters are characterized by distinct changes in transcription, suggesting that epigenetic mechanisms underlie their unique phenotypic state. By performingfunctional epigenomic studies in models of non-small-cell lung cancer, we identified the histone H3 lysine 36 (H3K36) demethylase KDM2A as being differentially required for the fitness of metastatic cell clusters. This contextual dependency on KDM2A is predicated by tumor cell-cell aggregation, which specifically induces KDM2A binding to CpG island enriched promoters. At these defined genomic loci, KDM2A maintains H3K36 monomethylation, which preferentially correlates with transcriptional activation. KDM2A directly targets oxidative phosphorylation genes and KDM2A activity is required for optimal mitochondrial respiration and apical cell junction integrity in cell clusters. Consequently, suppressing KDM2A reduces metastatic seeding and colonization in multiple organs, including in the brain. These findings reveal a chromatin regulatory mechanism by which homotypic cell communication instructs the epigenome of disseminated tumor cells to potentiate their metastatic competence.
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2. ⭐ GSE316191 靶向 HMGB2 可作为双重免疫调节剂，通过增强 CD8+ T 细胞功能和抑制肝细胞癌的肿瘤生长发挥作用 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、carcinoma、T cell、ATAC-seq
• 📝 描述：Contributors : Weifeng Qu ; Guiqi Zhu ; Yinghong ShiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusT cell exhaustion is a critical obstacle for durable treatment response in hepatocellular carcinoma (HCC). Developing drugs that control tumor growth and simultaneously bolster immune function is of great significance. The transcriptional regulator high mobility group box 2 (HMGB2) has emerged as a risk factor in prognosis of HCC. However, the role of HMGB2 in HCC tumor microenvironment (TME) is poorly understood. Here, we discovered HMGB2+ CD8+ T cells as being associated with T cell exhaustion and resistance to anti-PD-1 treatment through single-cell RNA sequencing of human and murine HCC tissues. Mechanistically, HMGB2 impaired the mitochondrial oxidative phosphorylation in CD8+ T cells by increasing the ubiquitination of NRF2, thus reduced the antitumor effector function. In tumor cells, HMGB2 inactivated the interferon-γ (IFN-γ) response through TRIM24/STAT1 pathway, inhibiting susceptibility and recruitment to effector T cells. Tannic acid, a specific inhibitor of HMGB2, synergized with PD-1 antibody to attenuate tumor growth and reverse T cell exhaustion. Collectively, this study revealed that HMGB2, a T cell exhaustion associated molecule, contributed to tumor immune escape by dual action on CD8+ T cells and tumor cells. These data also provided translational insight into synergistic treatment strategies.
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3. ⭐ GSE315942 染色体不稳定性通过 cGAS–趋化因子–髓系轴塑造食管腺癌的肿瘤微环境 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、tumor microenvironment、chemokine、RNA-seq
• 📝 描述：Contributors : Bruno Beernaert ; Eileen E ParkesSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensChromosomal instability (CIN), a pervasive feature of esophageal adenocarcinoma (EAC), drives tumor aggressiveness and metastasis. CIN stimulates the cGAS–STING pathway, typically linked to anti-tumor immunity. However, despite the high CIN burden in EAC, the cGAS–STING pathway remains largely intact. To address this paradox, we interrogated multiple esophageal cancer models, discovering myeloid-attracting chemokines – with CXCL8 as a prominent hit – as conserved CIN-driven targets in EAC. Using multiplexed immunofluorescence microscopy, we quantified ongoing CIN in human EAC tumors by measuring cGAS-positive micronuclei, validated by whole-genome sequencing. Coupling in situ CIN detection with single-nucleus RNA sequencing and multiplex immunophenotyping of human EAC, we link CIN to tumor-intrinsic innate immune activation, CXCL8 expression, and myeloid cell-mediated immunosuppression. In EAC patients, CIN-high, myeloid-dominated tumors correlate with poor outcomes and aberrant cGAS–STING signaling. These insights explain the counterintuitive maintenance of cGAS–STING and highlight disruption of the CIN–cGAS–inflammation axis as a potential therapeutic strategy in EAC.
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4. ⭐ GSE316655 Claudins 与 LILRB 免疫抑制受体相互作用，促进癌症中的髓系免疫抑制

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、regex:immuno(logy|therapy|suppression)
• 📝 描述：Contributors : Xiaoye Liu ; Alec Zhang ; Kenian ChenSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe mechanisms underlying tumor cell-myeloid cell interactions within the tumor microenvironment (TME) remain unclear, and predictive biomarkers for patient response to myeloid checkpoint blockade are lacking. This study identified specific binding between tight-junction claudins (CLDNs) and leukocyte immunoglobulin-like receptor subfamily B members LILRB2 and LILRB5. In multiple human cancer cohorts, the spatial proximity of LILRB2⁺ macrophages to CLDN-expressing cancer cells correlated with clinical outcomes, nominating this spatial relationship as a potential biomarker. In syngeneic LILRB2-transgenic and humanized mouse models, CLDN18.2–LILRB2 interaction triggered bidirectional signaling, enhanced the immunosuppressive activity of myeloid cells, and accelerated tumor progression. These effects were reversed by LILRB2 blockade. Mechanistically, the CLDN-LILRB2 axis sustained immunosuppression by regulating NF-κB and STAT signaling pathways. Our findings reveal a novel tight junction protein-mediated mechanism of myeloid cell regulation in the TME, offering a rationale for targeting this pathway in cancer therapy.
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5. ⭐ GSE316127 染色体不稳定性通过 cGAS-趋化因子-髓系轴塑造食管腺癌的肿瘤微环境

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、tumor microenvironment、chemokine
• 📝 描述：Contributors : Bruno Beernaert ; Eileen E ParkesSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensChromosomal instability (CIN), a pervasive feature of esophageal adenocarcinoma (EAC), drives tumor aggressiveness and metastasis. CIN stimulates the cGAS–STING pathway, typically linked to anti-tumor immunity. However, despite the high CIN burden in EAC, the cGAS–STING pathway remains largely intact. To address this paradox, we interrogated multiple esophageal cancer models, discovering myeloid-attracting chemokines – with CXCL8 as a prominent hit – as conserved CIN-driven targets in EAC. Using multiplexed immunofluorescence microscopy, we quantified ongoing CIN in human EAC tumors by measuring cGAS-positive micronuclei, validated by whole-genome sequencing. Coupling in situ CIN detection with single-nucleus RNA sequencing and multiplex immunophenotyping of human EAC, we link CIN to tumor-intrinsic innate immune activation, CXCL8 expression, and myeloid cell-mediated immunosuppression. In EAC patients, CIN-high, myeloid-dominated tumors correlate with poor outcomes and aberrant cGAS–STING signaling. These insights explain the counterintuitive maintenance of cGAS–STING and highlight disruption of the CIN–cGAS–inflammation axis as a potential therapeutic strategy in EAC.
• 🔗 查看原文

6. ⭐ GSE316062 染色体不稳定性通过 cGAS–趋化因子–髓系轴塑造食管腺癌的肿瘤微环境 [snRNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、tumor microenvironment、chemokine
• 📝 描述：Contributors : Bruno Beernaert ; Eileen E ParkesSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensChromosomal instability (CIN), a pervasive feature of esophageal adenocarcinoma (EAC), drives tumor aggressiveness and metastasis. CIN stimulates the cGAS–STING pathway, typically linked to anti-tumor immunity. However, despite the high CIN burden in EAC, the cGAS–STING pathway remains largely intact. To address this paradox, we interrogated multiple esophageal cancer models, discovering myeloid-attracting chemokines – with CXCL8 as a prominent hit – as conserved CIN-driven targets in EAC. Using multiplexed immunofluorescence microscopy, we quantified ongoing CIN in human EAC tumors by measuring cGAS-positive micronuclei, validated by whole-genome sequencing. Coupling in situ CIN detection with single-nucleus RNA sequencing and multiplex immunophenotyping of human EAC, we link CIN to tumor-intrinsic innate immune activation, CXCL8 expression, and myeloid cell-mediated immunosuppression. In EAC patients, CIN-high, myeloid-dominated tumors correlate with poor outcomes and aberrant cGAS–STING signaling. These insights explain the counterintuitive maintenance of cGAS–STING and highlight disruption of the CIN–cGAS–inflammation axis as a potential therapeutic strategy in EAC.
• 🔗 查看原文

7. GSE316732 雷帕霉素逆转肝脏对饮食诱导的代谢应激的反应，这种反应会随着年龄的增长而加剧。

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、metabolic
• 📝 描述：Contributors : Aaron P. Havas ; Adarsh Rajesh ; Xue Lei ; Peter D. AdamsSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAging is associated with increased susceptibility to metabolic stress and chronic liver disease, yet the interactions between age and metabolic stressors and the potential for ameliorating interventions remain incompletely understood. Here, we examined the hepatic response of young (7-month-old) and old (25-month-old) C57BL/6 male mice to a 9-week high-fat diet (HFD) and assessed whether rapamycin, a well-established pro-longevity intervention, could mitigate age-exacerbated effects. While both age groups developed metabolic-associated steatohepatitis (MASH), older mice displayed more severe hepatic steatosis, inflammation, and transcriptional dysregulation. Transcriptomic profiling of whole livers and purified hepatocytes revealed that aging amplifies HFD-induced inflammatory and metabolic gene expression changes, including activation of immune pathways and suppression of metabolic pathways. Notably, treatment of aging mice with rapamycin reversed the majority of HFD-driven transcriptional alterations, including upregulation of pro-inflammatory regulators such as Stat1, and dysregulation of metabolic gene networks. Rapamycin also reduced hepatosteatosis, total body weight, and a tumorigenic transcriptomic signature associated with hepatocellular carcinoma risk. These findings demonstrate that aging intensifies hepatic sensitivity to dietary metabolic stress and identify rapamycin as a promising therapeutic to counteract age-related liver dysfunction and metabolic dysfunction-associated steatotic liver disease (MASLD) progression.
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8. GSE291910 Dnmt3a 依赖的从头 DNA 甲基化增强谱系定向并保持记忆 Th1 和 Tfh 细胞的功能 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、methylation
• 📝 描述：Contributors : Scott Hale ; Bryant PerkinsSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusFollowing acute viral infection, naïve CD4+ T cells differentiate into T follicular helper (Tfh) and T helper 1 (Th1) cells that generate long-lived memory cells. However, it is unclear how memory Tfh and Th1 cells maintain their lineage commitment. We demonstrate that Tfh and Th1 lineages acquire distinct Dnmt3a-dependent de novo DNA methylation programs that are preserved into memory. Dnmt3a deletion impairs lineage commitment and functionality of memory Th1 and Tfh cells, resulting in aberrant Runx1 upregulation that represses germinal center Tfh cell differentiation. In contrast, transient pharmacological DNA methyltransferase inhibition during priming impairs repression of Tfh-associated genes while properly silencing Runx1, and results in enhanced Tfh cell functionality in primary and secondary responses to viral infections. Together, these findings demonstrate that Dnmt3a-mediated epigenetic programing is required to enforce T helper lineage commitment and preserve Tfh and Th1-specific functions during the recall response to infection, and reveal novel strategies to improve long-lived adaptive immunity against infectious diseases.
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9. GSE270117 7种PDA细胞系的单细胞RNA测序

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell
• 📝 描述：Contributors : Pasquale Laise ; Mikko Turunen ; Alvaro C Garcia ; Lorenzo Tomassoni ; H C Maurer ; Ela Elyada ; Bernhard Schmierer ; Jeremy Worley ; Jordan Kesner ; Xiangtian Tan ; Ester C Fernandez ; Xue Yuanqing ; Chen Yining ; Kelly Wong ; Urszula N Wasko ; Somnath Tagore ; Alexander L Wang ; Sabrina Ge ; Alina C Iuga ; Aaron Griffin ; Winston Wong ; Gulam A Manji ; Mariano J Alvarez ; Faiyaz Notta ; David A Tuveson ; Kenneth P Olive ; Andrea CalifanoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensWe performed Single-Cell RNA Sequencing of 7 PDA Cell Lines to characterize and quantify PDA subtypes populations
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10. GSE159921 混合转录因子过表达分析（单细胞RNA测序）

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNAseq、single-cell
• 📝 描述：Contributors : Pasquale Laise ; Mikko Turunen ; Alvaro C Garcia ; Lorenzo Tomassoni ; H C Maurer ; Ela Elyada ; Bernhard Schmierer ; Jeremy Worley ; Jordan Kesner ; Xiangtian Tan ; Ester C Fernandez ; Sue Yuanqing ; Chen Yining ; Kelly Wong ; Urszula N Wasko ; Somnath Tagore ; Alexander L Wang ; Sabrina Ge ; Alina C Iuga ; Aaron Griffin ; Winston Wong ; Gulam A Manji ; Mariano J Alvarez ; Faiyaz Notta ; David A Tuveson ; Kenneth P Olive ; Andrea CalifanoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe aim of this study is to investigate the effect of the combinatorial overexpression of the top GLS MRs in a MOS cell line (at single-cell level).
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1. 用于单细胞RNA测序数据分析摄取和标准化的智能体AI框架

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、single-cell
• 📝 描述：CellAtria uses AI to automate data ingestion and RNA sequencing analysis, making reuse of public single-cell datasets faster, standardized, and accessible without advanced computational skills…
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2. 维生素A可能有助于癌细胞躲避免疫系统的攻击。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune
• 📝 描述：A vitamin A byproduct has been found to quietly disarm the immune system, allowing tumors to evade attack and weakening cancer vaccines. Scientists have now developed a drug that shuts down this pathway, dramatically boosting immune responses and slowing cancer growth in preclinical studies.
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• GSE316818 一种细菌YopJ家族乙酰转移酶通过JAK1的Nε-乙酰化抑制宿主免疫反应
• GSE291819 单细胞 RNA 转录组揭示了氯沙坦减轻氮芥诱导的角膜损伤的潜在机制
• GSE316749 AURKA/PHB2 信号通路驱动 KRAS G12C 突变型非小细胞肺癌对 KRAS G12C 抑制剂产生获得性耐药
• GSE316223 α-突触核蛋白从肠道扩散至大脑的体内模型
• GSE287470 疾病相关小胶质细胞 TLR4-Lyn 激酶是 5XFAD 小鼠模型中神经炎症、Aβ 吞噬作用、神经元损伤和细胞存活的关键调节因子。
• GSE316754 衰老细胞清除疗法增强前列腺癌化疗的免疫原性
• GSE315021 利用DAP-Seq技术分析转录因子RGSV P3的全基因组结合位点
• GSE313496 多组织 DNA 甲基化分析，旨在识别脊柱裂特有的独特神经组织的合适替代组织
• GSE277649 缺乏 PD-1 的干细胞样 CD8+ T 细胞通过降低 TCR 信号传导和自我更新能力来适应慢性刺激 [scRNA-seq]
• GSE277648 缺乏 PD-1 的干细胞样 CD8+ T 细胞通过降低 TCR 信号传导和自我更新能力来适应慢性刺激 [RNA-seq]
• GSE310584 人类 PDA 细胞系：经曲美替尼 (TRAM) 和/或羟氯喹 (HCQ) 治疗后的单细胞 RNA 测序
• GSE303670 提高肾移植中DSA阴性抗体介导排斥反应的组织学检测
• GSE302604 慢性间歇性低氧模拟睡眠呼吸暂停，重塑肝脏昼夜代谢结构
• GSE292402 使用 KP4 PDA 细胞系进行单细胞条形码谱系追踪 - 曲美替尼药物治疗前后
• GSE291914 Dnmt3a依赖的从头DNA甲基化增强谱系定向并维持记忆性Th1和Tfh细胞的功能
• GSE291911 Dnmt3a 依赖的从头 DNA 甲基化增强谱系定向并保持记忆 Th1 和 Tfh 细胞的功能 [WGEM-seq]
• GSE288771 OCI-AML3 中 LTR12C 家族的表观遗传沉默
• GSE280160 体外阵列 OVOL2 在 PDA 细胞系中的过表达（批量 RNA-Seq）
• GSE268441 PATU8988S PDA 细胞系单细胞条形码谱系追踪
• GSE268229 KP4 PDA 细胞系单细胞条形码谱系追踪
• GSE268077 HS766T PDA 细胞系单细胞条形码谱系追踪
• GSE266034 人类胰腺导管腺癌细胞系：正常培养基与无血清培养基中的单细胞RNA测序
• GSE161369 胰腺癌数据集
• GSE161368 TF 过表达分析在 PDA 细胞系中（批量 RNA-Seq）
• GSE160977 来自 PDAC 肿瘤患者来源异种移植模型的单细胞数据。
• GSE159918 六个 PDA 细胞系的测序数据。
• GSE316547 选择性调节小鼠肠道M1和M3毒蕈碱受体表达对特化上皮细胞和体重具有不同的影响
• GSE313846 Notch1胞内结构域（NICD1）的ChIP测序分析
• GSE308855 整合多组学分析揭示微环境重塑是屋尘螨诱发肺癌进展的关键驱动因素
• GSE223225 人类成纤维细胞衰老过程中功能性长链非编码RNA的鉴定和表征