详细内容（前10条）

1. ⭐ GSE315361 Smyd5 介导 IL-4 表观遗传控制巨噬细胞抗原呈递，从而驱动协同 T 细胞介导的肿瘤抑制 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、T cell、macrophage、antigen、RNA-seq、epigenetic
• 📝 描述：Contributors : Buyun Dang ; Yuling Hong ; Qingxiang Gao ; Shih-Chin ChengSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusIL-4 is classically associated with “M2” macrophages considered tumor-immunosuppressive, yet marker-based labels poorly reflect macrophage function in tumors. Reports of a non-canonical, IL-4–imprinted macrophage state (M2inf) with trained-immunity features prompted us to test whether such imprinting contributes to antitumor immunity in vivo. Here we show that, in B16F10 melanoma, IL-4 programs macrophages through the lysine methyltransferase Smyd5 to deposit promoter-proximal H3K36me3, increase MHC class II, and potentiate T cell activation. Myeloid Il4ra deletion increased tumor burden and reduced MHC class II and intratumoral T cell activation, whereas co-transfer of IL-4–primed macrophages suppressed tumors and expanded activated CD4 and CD8 T cells. Antitumor benefit required adaptive lymphocytes and macrophage-intrinsic MHC class II, as Rag1 deficiency or macrophage Rfx5 deletion abrogated tumor suppression. These findings identify a non-canonical, IL-4–imprinted macrophage program that enables antigen presentation and cooperative T cell immunity in this tumor context.
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2. ⭐ GSE315255 Smyd5 介导 IL-4 表观遗传控制巨噬细胞抗原呈递，从而驱动协同 T 细胞介导的肿瘤抑制 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、T cell、macrophage、antigen、scRNA、epigenetic
• 📝 描述：Contributors : Buyun Dang ; Yuling Hong ; Qingxiang Gao ; Shih-Chin ChengSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusIL-4 is classically associated with “M2” macrophages considered tumor-immunosuppressive, yet marker-based labels poorly reflect macrophage function in tumors. Reports of a non-canonical, IL-4–imprinted macrophage state (M2inf) with trained-immunity features prompted us to test whether such imprinting contributes to antitumor immunity in vivo. Here we show that, in B16F10 melanoma, IL-4 programs macrophages through the lysine methyltransferase Smyd5 to deposit promoter-proximal H3K36me3, increase MHC class II, and potentiate T cell activation. Myeloid Il4ra deletion increased tumor burden and reduced MHC class II and intratumoral T cell activation, whereas co-transfer of IL-4–primed macrophages suppressed tumors and expanded activated CD4 and CD8 T cells. Antitumor benefit required adaptive lymphocytes and macrophage-intrinsic MHC class II, as Rag1 deficiency or macrophage Rfx5 deletion abrogated tumor suppression. These findings identify a non-canonical, IL-4–imprinted macrophage program that enables antigen presentation and cooperative T cell immunity in this tumor context.
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3. ⭐ GSE315253 Smyd5 介导 IL-4 表观遗传控制巨噬细胞抗原呈递，从而驱动协同 T 细胞介导的肿瘤抑制 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、T cell、macrophage、antigen、ATAC-seq、epigenetic
• 📝 描述：Contributors : Buyun Dang ; Yuling Hong ; Qingxiang Gao ; Shih-Chin ChengSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusIL-4 is classically associated with “M2” macrophages considered tumor-immunosuppressive, yet marker-based labels poorly reflect macrophage function in tumors. Reports of a non-canonical, IL-4–imprinted macrophage state (M2inf) with trained-immunity features prompted us to test whether such imprinting contributes to antitumor immunity in vivo. Here we show that, in B16F10 melanoma, IL-4 programs macrophages through the lysine methyltransferase Smyd5 to deposit promoter-proximal H3K36me3, increase MHC class II, and potentiate T cell activation. Myeloid Il4ra deletion increased tumor burden and reduced MHC class II and intratumoral T cell activation, whereas co-transfer of IL-4–primed macrophages suppressed tumors and expanded activated CD4 and CD8 T cells. Antitumor benefit required adaptive lymphocytes and macrophage-intrinsic MHC class II, as Rag1 deficiency or macrophage Rfx5 deletion abrogated tumor suppression. These findings identify a non-canonical, IL-4–imprinted macrophage program that enables antigen presentation and cooperative T cell immunity in this tumor context.
• 🔗 查看原文

4. ⭐ GSE315363 Smyd5 介导 IL-4 表观遗传控制巨噬细胞抗原呈递，从而驱动协同 T 细胞介导的肿瘤抑制 [Crispr 筛选]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、T cell、macrophage、antigen、epigenetic
• 📝 描述：Contributors : Buyun Dang ; Yuling Hong ; Qingxiang Gao ; Shih-Chin ChengSeries Type : OtherOrganism : Mus musculusIL-4 is classically associated with “M2” macrophages considered tumor-immunosuppressive, yet marker-based labels poorly reflect macrophage function in tumors. Reports of a non-canonical, IL-4–imprinted macrophage state (M2inf) with trained-immunity features prompted us to test whether such imprinting contributes to antitumor immunity in vivo. Here we show that, in B16F10 melanoma, IL-4 programs macrophages through the lysine methyltransferase Smyd5 to deposit promoter-proximal H3K36me3, increase MHC class II, and potentiate T cell activation. Myeloid Il4ra deletion increased tumor burden and reduced MHC class II and intratumoral T cell activation, whereas co-transfer of IL-4–primed macrophages suppressed tumors and expanded activated CD4 and CD8 T cells. Antitumor benefit required adaptive lymphocytes and macrophage-intrinsic MHC class II, as Rag1 deficiency or macrophage Rfx5 deletion abrogated tumor suppression. These findings identify a non-canonical, IL-4–imprinted macrophage program that enables antigen presentation and cooperative T cell immunity in this tumor context.
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5. ⭐ GSE306374 小肠和结肠化生潘氏细胞的空间转录组学遗传谱

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics、regex:intestin(e|al)
• 📝 描述：Contributors : Tomohiro Muto ; Go ItoSeries Type : OtherOrganism : Homo sapiensMetaplasia is an epithelial alteration that appears in chronic inflammatory diseases. In ulcerative colitis, Paneth cell metaplasia (PCM) is a well-recognized feature, but its role in the inflamed epithelium remains unclear. Using spatial transcriptomics, we characterized the gene expression profile of PCM, elucidated its regulatory mechanisms, and clarified its functional role in the inflamed colonic epithelium.
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6. ⭐ GSE298564 多组学分析揭示鼻窦鳞状细胞癌的分子图谱和异质性肿瘤微环境 [RPMI 2650 批量 ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、carcinoma、tumor microenvironment、ATAC-seq
• 📝 描述：Contributors : Chaelin You ; Junho Noh ; Jiheui Kim ; Kyuho KangSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensSinonasal squamous cell carcinoma (SNSCC) is a rare and aggressive malignancy with limited treatment options. Here, we conduct a comprehensive multi-omic analysis, integrating bulk and single-cell transcriptomics, epigenomics, and DNA methylation profiling. Our study identifies distinct gene signatures, cellular compositions, and regulatory mechanisms that drive SNSCC pathogenesis. Epigenetic alterations reveal a regulatory landscape underlying transcriptional changes, and we characterize heterogeneous tumor cell populations with unique molecular profiles. Hypoxia-related cells emerge as key drivers of angiogenesis and disease progression. Notably, we uncover a critical interaction between hypoxic tumor cells and endothelial tip cells, mediated by factors such as adrenomedullin (ADM), highlighting a pivotal mechanism in tumor development. These findings provide valuable insights into the tumor microenvironment (TME) of SNSCC and suggest potential therapeutic targets to improve treatment strategies for this challenging malignancy.
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7. ⭐ GSE298563 多组学分析揭示鼻窦鳞状细胞癌的分子图谱和异质性肿瘤微环境 [RPMI2650 批量 RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、carcinoma、tumor microenvironment、RNA-seq
• 📝 描述：Contributors : Chaelin You ; Junho Noh ; Jiheui Kim ; Kyuho KangSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensSinonasal squamous cell carcinoma (SNSCC) is a rare and aggressive malignancy with limited treatment options. Here, we conduct a comprehensive multi-omic analysis, integrating bulk and single-cell transcriptomics, epigenomics, and DNA methylation profiling. Our study identifies distinct gene signatures, cellular compositions, and regulatory mechanisms that drive SNSCC pathogenesis. Epigenetic alterations reveal a regulatory landscape underlying transcriptional changes, and we characterize heterogeneous tumor cell populations with unique molecular profiles. Hypoxia-related cells emerge as key drivers of angiogenesis and disease progression. Notably, we uncover a critical interaction between hypoxic tumor cells and endothelial tip cells, mediated by factors such as adrenomedullin (ADM), highlighting a pivotal mechanism in tumor development. These findings provide valuable insights into the tumor microenvironment (TME) of SNSCC and suggest potential therapeutic targets to improve treatment strategies for this challenging malignancy.
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8. ⭐ GSE278145 多组学分析揭示鼻窦鳞状细胞癌的分子图谱和异质性肿瘤微环境 [批量 RNA 测序]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、carcinoma、tumor microenvironment、RNA-seq
• 📝 描述：Contributors : Chaelin You ; Jihwan Park ; Keunsoo Kang ; Jaewoo Park ; Jungyeon Jang ; Myeongsang Yu ; Yoosam Chung ; Jiheui Kim ; Kyuho KangSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensSinonasal squamous cell carcinoma (SNSCC) is a rare and aggressive malignancy with limited treatment options. Here, we conduct a comprehensive multi-omic analysis, integrating bulk and single-cell transcriptomics, epigenomics, and DNA methylation profiling. Our study identifies distinct gene signatures, cellular compositions, and regulatory mechanisms that drive SNSCC pathogenesis. Epigenetic alterations reveal a regulatory landscape underlying transcriptional changes, and we characterize heterogeneous tumor cell populations with unique molecular profiles. Hypoxia-related cells emerge as key drivers of angiogenesis and disease progression. Notably, we uncover a critical interaction between hypoxic tumor cells and endothelial tip cells, mediated by factors such as adrenomedullin (ADM), highlighting a pivotal mechanism in tumor development. These findings provide valuable insights into the tumor microenvironment (TME) of SNSCC and suggest potential therapeutic targets to improve treatment strategies for this challenging malignancy.
• 🔗 查看原文

9. ⭐ GSE278138 多组学分析揭示鼻窦鳞状细胞癌的分子图谱和异质性肿瘤微环境[DNA甲基化]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、carcinoma、tumor microenvironment、methylation
• 📝 描述：Contributors : Chaelin You ; Jihwan Park ; Keunsoo Kang ; Jaewoo Park ; Jungyeon Jang ; Myeongsang Yu ; Yoosam Chung ; Jiheui Kim ; Kyuho KangSeries Type : Methylation profiling by genome tiling arrayOrganism : Homo sapiensSinonasal squamous cell carcinoma (SNSCC) is a rare and aggressive malignancy with limited treatment options. Here, we conduct a comprehensive multi-omic analysis, integrating bulk and single-cell transcriptomics, epigenomics, and DNA methylation profiling. Our study identifies distinct gene signatures, cellular compositions, and regulatory mechanisms that drive SNSCC pathogenesis. Epigenetic alterations reveal a regulatory landscape underlying transcriptional changes, and we characterize heterogeneous tumor cell populations with unique molecular profiles. Hypoxia-related cells emerge as key drivers of angiogenesis and disease progression. Notably, we uncover a critical interaction between hypoxic tumor cells and endothelial tip cells, mediated by factors such as adrenomedullin (ADM), highlighting a pivotal mechanism in tumor development. These findings provide valuable insights into the tumor microenvironment (TME) of SNSCC and suggest potential therapeutic targets to improve treatment strategies for this challenging malignancy.
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10. ⭐ GSE288091 对经 SOT101 处理的 TC-1 和 TRAMP-C 小鼠的肿瘤、脾脏、淋巴结中的 RNA 样本进行 Nanostring 分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、lymph、regex:lymph(o|atic)?
• 📝 描述：Contributor : Lenka P JelinkovaSeries Type : OtherOrganism : Mus musculusNanrilkefusp alfa (nanril; SOT101) is an interleukin (IL)-15 receptor βγ superagonist that stimulates natural killer (NK) and CD8+ T cells, thereby promoting an innate and adaptive anti-tumor inflammatory microenvironment in mouse tumor models either in monotherapy or combined with an anti-programmed cell death protein 1 (PD-1) antibody. In cynomolgus monkeys, a clinical schedule was identified, which translated into the design of a phase 1/1b clinical trial, AURELIO-03 (NCT04234113). In 51 patients with advanced/metastatic solid tumors, nanril increased the proportions of CD8+ T cells and NK cells in peripheral blood and tumors. It had a favorable safety profile when administered subcutaneously on days 1, 2, 8 and 9 of each 21-day cycle as monotherapy (0.25-15 μg/kg) or combined (1.5-12 μg/kg) with the anti-PD-1 pembrolizumab (200 mg). The most frequent treatment-emergent adverse events were pyrexia, injection site reactions and chills. Furthermore, early clinical efficacy was observed, including in immune checkpoint blockade-resistant/refractory patients.
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1. ⭐ 为什么慢性肠道炎症会发展成结肠癌

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、inflammation、gut、regex:gut(-?microbiome)?
• 📝 描述：A newly uncovered immune chain reaction in the gut may explain why people with inflammatory bowel disease face a much higher risk of colorectal cancer. Researchers found that a powerful inflammatory signal flips on specialized gut immune cells, which then call in waves of white blood cells from the bone marrow and rewire them in ways that help tumors grow. This process appears to damage DNA in the gut lining and create a tumor-friendly environment.
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2. 阿尔茨海默病可能会欺骗大脑，使其抹去自身的记忆。

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：Alzheimer’s may destroy memory by flipping a single molecular switch that tells neurons to prune their own connections. Researchers found that both amyloid beta and inflammation converge on the same receptor, triggering synapse loss. Surprisingly, neurons aren’t passive victims—they actively respond to these signals. Targeting this receptor could offer a new way to protect memory beyond current amyloid-focused drugs.
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• GSE280209 VAMP7依赖的内质网和线粒体蛋白的晚期内体分泌影响肿瘤微环境和巨噬细胞的参与
• GSE277797 多组学分析揭示鼻窦鳞状细胞癌的分子图谱和异质性肿瘤微环境 [snMultiome-seq]
• GSE312103 RNA-seq 揭示外源性血红素治疗加速 CD8+ T 细胞耗竭
• GSE312102 ATAC-seq 揭示血红素调节驱动 CD8⁺ T 细胞耗竭的转录因子的转录活性
• GSE312100 单细胞 RNA 测序揭示，具有非活性血红素结合位点的 Bach2 维持 CD8+ T 细胞的干性
• GSE263465 猪背根神经节神经元的空间转录组分子特征[Visium]
• GSE317235 SAGA/ATAC复合物维持弥漫性中线胶质瘤中异常的染色质调控和代谢程序
• GSE311597 分层 Rorc(γt) 顺式调控级联协调 RORγt⁺ 先天免疫细胞的分化 [ChIP-seq]
• GSE311595 分层 Rorc(γt) 顺式调控级联协调 RORγt⁺ 先天免疫细胞的分化 [ATAC-seq]
• GSE302249 肺癌中肿瘤相关巨噬细胞状态与非保守性lncRNA的关联
• GSE304308 阿尔茨海默病小鼠的脑脂质谱和少突胶质细胞基因表达对高脂饮食的反应不一致。
• GSE317178 纳米荧光素酶-CD63标记揭示了小鼠导管原位癌导管内模型中细胞外囊泡的动力学
• GSE317110 利用16S rRNA测序对大鼠粪便样本中的对照组、放射性肠炎模型组和治疗组进行微生物组分析
• GSE317084 异恶唑苯和PEP3联合处理后拟南芥幼苗的转录组分析
• GSE316845 RNA-Seq结果，来自假手术组、脓毒症诱导心肌病组和AAV-GATA4组小鼠的心脏
• GSE315074 人类单核细胞来源的巨噬细胞中过表达TRIM21、NFATc3或ASK1的差异表达基因
• GSE313641 RNA-seq 分析骨膜蛋白刺激的人鼻上皮细胞
• GSE311856 对 MHC I 类分子伴侣 tapasin 的一种变体 tapasin 进行深度突变扫描
• GSE311596 分层 Rorc(γt) 顺式调控级联协调 RORγt⁺ 先天免疫细胞的分化 [ChIL-seq]
• GSE309067 细胞特异性转录组学和基因沉默揭示水通道蛋白在禾本科植物气孔运动中的功能
• GSE293843 药物或基因 PIKFYVE 抑制对 GEP-NET 的影响 [RNA-Seq]
• GSE254518 DNAJB1表达降低导致黑质衰老：来自单核RNA测序的启示
• GSE223837 SOX6诱导的细胞衰老与衰老细胞清除疗法的联合应用可提高宫颈癌的化疗敏感性