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1. ⭐ GSE343928 微卫星稳定型结直肠肿瘤来源的SEMA3A通过抑制TCF1驱动CD8⁺ T细胞衰老和免疫治疗耐药

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、T cell、regex:immuno(logy|therapy|suppression)、resistance
• 📝 描述：Series Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusMicrosatellite-stable (MSS) colorectal cancers (CRC) display inherent insensitivity to immune checkpoint blockade, and the pivotal mechanisms responsible for this immunotherapeutic resistance have not been fully clarified. Here, we demonstrate that MSS CRC elicit CD8⁺ T cell senescence to mediate immune evasion, which distinguishes them from microsatellite-instable (MSI) CRC. We further identify SEMA3A, a secreted protein markedly upregulated in MSS CRC, as a crucial mediator that directly drives CD8⁺ T cell senescence. Mechanistically, SEMA3A engages neuropilin-1 (NRP1) to hijack JAK1 signaling, which blunts cytokine-triggered STAT3 phosphorylation and ultimately reduces TCF1 expression. At the molecular level, TCF1 directly binds to and transcriptionally represses senescence-associated genes. The loss of TCF1 in CD8⁺ T cells infiltrating MSS CRC tumors abolishes this transcriptional repression, thereby inducing CD8⁺ T cell senescence and conferring refractoriness to PD-L1 blockade. In syngeneic murine models of MSS CRC, dual neutralization of SEMA3A and PD-L1 restores TCF1 expression, rescues CD8⁺ T cells from senescence, and significantly improves immunotherapy efficacy. Clinical data corroborate that SEMA3A expression is positively correlated with CD8⁺ T cell senescence and serves as a reliable prognostic biomarker for inferior immunotherapy responses in patients with MSS CRC. Collectively, this study delineates a SEMA3A/NRP1-JAK1-STAT3-TCF1 signaling axis that governs CD8⁺ T cell senescence and tumor immune evasion in MSS CRCs, validating SEMA3A as a promising predictive biomarker and druggable therapeutic target for this immunotherapy-refractory MSS CRC.
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2. ⭐ GSE343811 微卫星稳定型结直肠肿瘤来源的 SEMA3A 通过抑制 TCF1 驱动 CD8⁺ T 细胞衰老和免疫治疗耐药

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、T cell、regex:immuno(logy|therapy|suppression)、resistance
• 📝 描述：Contributor : Huihui YaoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusMicrosatellite-stable (MSS) colorectal cancers (CRC) display inherent insensitivity to immune checkpoint blockade, and the pivotal mechanisms responsible for this immunotherapeutic resistance have not been fully clarified. Here, we demonstrate that MSS CRC elicit CD8⁺ T cell senescence to mediate immune evasion, which distinguishes them from microsatellite-instable (MSI) CRC. We further identify SEMA3A, a secreted protein markedly upregulated in MSS CRC, as a crucial mediator that directly drives CD8⁺ T cell senescence. Mechanistically, SEMA3A engages neuropilin-1 (NRP1) to hijack JAK1 signaling, which blunts cytokine-triggered STAT3 phosphorylation and ultimately reduces TCF1 expression. At the molecular level, TCF1 directly binds to and transcriptionally represses senescence-associated genes. The loss of TCF1 in CD8⁺ T cells infiltrating MSS CRC tumors abolishes this transcriptional repression, thereby inducing CD8⁺ T cell senescence and conferring refractoriness to PD-L1 blockade. In syngeneic murine models of MSS CRC, dual neutralization of SEMA3A and PD-L1 restores TCF1 expression, rescues CD8⁺ T cells from senescence, and significantly improves immunotherapy efficacy. Clinical data corroborate that SEMA3A expression is positively correlated with CD8⁺ T cell senescence and serves as a reliable prognostic biomarker for inferior immunotherapy responses in patients with MSS CRC. Collectively, this study delineates a SEMA3A/NRP1-JAK1-STAT3-TCF1 signaling axis that governs CD8⁺ T cell senescence and tumor immune evasion in MSS CRCs, validating SEMA3A as a promising predictive biomarker and druggable therapeutic target for this immunotherapy-refractory MSS CRC.
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3. ⭐ GSE255118 口腔癌肿瘤免疫细胞的单细胞RNA测序

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、sequencing、single-cell
• 📝 描述：Contributors : S S Jiang ; K P Chang ; S C LiuSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThis data is mainly used to investigate the tumor micro-environment of head and neck cancer. A total of 9,894 immune cells were isolated from 8 oral tumor tissues with OSCC patients by analyzing single-cell RNA seq.
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4. ⭐ GSE343063 小细胞肺癌中空间分辨的细胞间通讯揭示巨噬细胞驱动的免疫逃逸机制

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、macrophage、spatially
• 📝 描述：Contributors : Tingxiao Gao ; Jalal M Kazan ; Fatema Zohora ; Javier Ruiz-Ramirez ; Troy Ketela ; Danielle B Sacdalan ; Michael Cabanero ; Vivek Philip ; Michael M Hoffman ; Ming S Tsao ; Tracy L McGaha ; Gregory W Schwartz ; Benjamin H LokSeries Type : OtherOrganism : Homo sapiensSmall cell lung cancer (SCLC) exhibits poor responses to immunotherapy despite abundant immune infiltration. We performed single-cell spatial transcriptomic profiling of more than 2.5 million cells from six surgically resected limited-stage SCLC tumors using the 10x Genomics Xenium In Situ platform (5K Human Pan Tissue & Pathways Panel). Spatially resolved cell-cell communication analysis identified macrophages as the dominant communicating immune population and revealed distinct spatial macrophage states associated with differential T-cell phenotypes and immune evasion programs.
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5. ⭐ GSE239297 致癌 KRAS 通过转录后调控的 KRAS 诱导颗粒 (KGs) 促进胰腺导管腺癌 (PDAC) [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：regex:onco(logy|logist|gene|genic)、RNA-seq、KRAS
• 📝 描述：Contributors : Zoey Ziyue Yang ; Mara Cardenas ; Angelina BortolettoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiens ; Mus musculusOver 90% of pancreatic ductal adenocarcinoma (PDAC) tumors harbor mutations in KRAS which promote many hallmark characteristics of cancer. How a single driver mutation causes the malignant properties observed in PDAC is poorly understood. We discovered that oncogenic KRAS suppresses miRNA biogenesis and function, thus increasing the stability and translation efficiency of miRNA targets. Defective miRNA function causes an accumulation of mRNA, and drives the localization of components of the mRNA degradation machinery into novel post-transcriptional condensates termed KRAS-induced granules (KGs). Mechanistically, we find that KG formation depends on the phosphorylation of Argonaute2 at tyrosine393 and requires EGFR, but not MEK or PI3K signaling. Using in vivo and in vitro models, we find that genetic ablation of KGs leads to decreased proliferation and migration, delayed tumorigenesis, and reduced tumor angiogenesis and innervation. Our findings reveal an essential and therapeutically targetable role for altered post-transcriptional regulation in PDAC tumorigenesis.
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6. ⭐ GSE332885 宿主 MTDH 对肝脏和免疫轴的多器官协调作用促进全身肿瘤进展 [ATAC-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune、ATAC-seq
• 📝 描述：Contributors : Yong Tang ; Yong Wei ; Yibin KangSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusCancer progression is systemically influenced by distant organ dysfunction induced by primary tumors, yet the mechanisms linking long distance tumor-organ crosstalk to antitumor immunity remain unclear. Here, we identify host Metadherin (MTDH) as a critical regulator of tumor-induced immunosuppression and metabolic reprogramming via tumor-liver interactions. Using Mtdh knockout (KO) mouse models, we show that concurrent MTDH loss in hepatocytes and CD8⁺ T cells enhances effector T cell function and suppresses tumor growth and metastasis. Mechanistically, tumor-derived extracellular vesicles (EVPs) activate Kupffer cells to secrete TNFα and TGF-β, which suppress hepatic PPARα-mediated lipid oxidation via NF-κB signaling. MTDH loss restores hepatic lipid catabolism and promotes mitochondrial metabolic reprogramming in CD8⁺ T cells in response to a lipid-reduced environment , thereby boosting anti-tumor immunity. Genetic or pharmacological targeting of MTDH synergizes with anti-PD-1 therapy in murine cancer models. These findings establish host MTDH as key modulator of tumor-liver crosstalk through metabolic and immune interactions, driving systemic cancer progression.
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7. ⭐ GSE315470 人类跟腱空间转录组学

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Lingling Hu ; Matthew GreenblattSeries Type : OtherOrganism : Homo sapiensWe used 10x Genomics Xenium spatial profiling to map gene expression across sections of human fetal Achilles tendons. By combining genetic data with spatial coordinates and histology images, we identified specific cell types—including tendon stem cells, various mature tendon cells, and cartilage cells—and characterized different types of immune cells (macrophages) within the tissue structure.
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8. GSE343561 m6A 缺失减弱巨噬细胞 I 型干扰素反应 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：macrophage、RNA-seq
• 📝 描述：Contributors : Edward M Courvan ; Cody J Hecht ; Frederick Longshore-Neate ; Luisa M Vasconcelos ; Roy R ParkerSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensMacrophages play an important role in coordinating the antiviral response. Post-transcriptional regulation of mRNA is important for inflammatory gene expression that supports the defense against viral pathogens. N-6 methyladenosine (m6A) deposition on mRNA by METTL3 constitutes one such post-transcriptional event which facilitates a cascade of downstream regulation via RNA decay and translation. We were surprised to find that in both THP1-derived and peripheral blood macrophages, m6A depletion with the METTL3 inhibitor STM2457 leads to a defective type I interferon response and enhanced proliferation of the human coronavirus OC43. Using TimeLapse-seq to simultaneously measure changes in abundance, RNA decay and transcription, we find that STM2457 downregulates the interferon response at the receptor level and via reduction in the potency of the first wave of transcription. We conclude that macrophages depend on m6A to support expression of interferon sensing machinery and in m6A’s absence, fail to mount as strong of a type I interferon response.
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9. GSE341212 多模态空间分析揭示了髓系定义的 ENKTL 亚组的不同特征以及预后炎症微环境中的肿瘤-髓系协同作用 [ENKTL_GeoMx_Protein]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、spatial
• 📝 描述：Contributors : Lichang Deng ; Siok-Bian Ng ; Min Liu ; Reagan LintonSeries Type : Expression profiling by arrayOrganism : Homo sapiensExtranodal NK/T-cell lymphoma (ENKTL) is an aggressive Epstein–Barr virus (EBV)-associated malignancy with a heterogeneous tumor microenvironment, yet macrophage heterogeneity and tumor-macrophage crosstalk remain poorly defined. Here, we integrate spatial transcriptomic and proteomic profiling with single-cell spatial molecular imaging of ENKTL samples and identify two subgroups defined by distinct macrophage programs. Subgroup 1 is enriched for inflammatory macrophages exhibiting IFN-α/γ responses and immune-regulatory molecules including IDO1 and CD274, whereas Subgroup 2 is immune-quiescent and macrophage-sparse, with its macrophage compartment skewed towards STAB1 macrophages with scavenging features. Notably, an NF-κB-activated and EBV-associated tumor subset is specifically enriched in Subgroup 1, displaying concurrent immunostimulatory and immunoregulatory features that parallel the co-enriched myeloid states and showing reproducible sample-level associations with these myeloid states across datasets. Spatial neighborhood analysis further delineates an inflammation niche where NF-κB tumor cells physically co-localize with these inflammatory macrophages, accompanied by enhanced tumor-myeloid and myeloid-myeloid signaling, implicating a process of tumor-associated myeloid recruitment followed by CCL- and IL1-mediated myeloid self-reinforcement. Critically, higher abundance of this niche correlates with improved survival across independent cohorts, revealing contrasting spatial tumor-immune architectures with prognostic relevance. Together, our study provides a spatially resolved framework for understanding ENKTL biology and guiding immunotherapeutic strategies.
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10. GSE339338 多模态空间分析揭示了髓系定义的 ENKTL 亚组的不同以及预后炎症微环境中的肿瘤-髓系合作 [ENKTL_GeoMx_WTA]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、spatial
• 📝 描述：Contributors : Lichang Deng ; Siok-Bian Ng ; Min Liu ; Reagan LintonSeries Type : OtherOrganism : Homo sapiensExtranodal NK/T-cell lymphoma (ENKTL) is an aggressive Epstein–Barr virus (EBV)-associated malignancy with a heterogeneous tumor microenvironment, yet macrophage heterogeneity and tumor-macrophage crosstalk remain poorly defined. Here, we integrate spatial transcriptomic and proteomic profiling with single-cell spatial molecular imaging of ENKTL samples and identify two subgroups defined by distinct macrophage programs. Subgroup 1 is enriched for inflammatory macrophages exhibiting IFN-α/γ responses and immune-regulatory molecules including IDO1 and CD274, whereas Subgroup 2 is immune-quiescent and macrophage-sparse, with its macrophage compartment skewed towards STAB1 macrophages with scavenging features. Notably, an NF-κB-activated and EBV-associated tumor subset is specifically enriched in Subgroup 1, displaying concurrent immunostimulatory and immunoregulatory features that parallel the co-enriched myeloid states and showing reproducible sample-level associations with these myeloid states across datasets. Spatial neighborhood analysis further delineates an inflammation niche where NF-κB tumor cells physically co-localize with these inflammatory macrophages, accompanied by enhanced tumor-myeloid and myeloid-myeloid signaling, implicating a process of tumor-associated myeloid recruitment followed by CCL- and IL1-mediated myeloid self-reinforcement. Critically, higher abundance of this niche correlates with improved survival across independent cohorts, revealing contrasting spatial tumor-immune architectures with prognostic relevance. Together, our study provides a spatially resolved framework for understanding ENKTL biology and guiding immunotherapeutic strategies.
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1. 使用 knitr 引擎创建用于渲染 Quarto 文档的独立 R 脚本——这要归功于新的 R 包管理器 ir 和 uvr。

• ✍️ 作者：未知作者
• 🏷️ 关键词：R package
• 📝 描述：Introduction In previous posts I have described how to use the self-contained Python scripts feature in the uv Python package manager to create virtual environments to render Quarto documents using the Jupyter nbstata kernel and the python3 kernel. I… Continue reading: Creating self-contained R scripts for rendering Quarto documents using the knitr engine – courtesy of the new R package managers ir and uvr
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1. ⭐ 让奶酪味道鲜美的细菌也可能对你的肠道有益。

• ✍️ 作者：未知作者
• 🏷️ 关键词：bacteria、regex:bacter(ia|ial|ium)、gut、regex:gut(-?microbiome)?
• 📝 描述：Scientists studying three artisan British cheeses found that the microbes responsible for their distinctive flavors may also offer surprising benefits for gut health. As the cheeses matured, helpful bacteria transformed their aromas and textures while potentially producing compounds linked to reduced inflammation, cholesterol regulation, and appetite control.
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2. 新的RNA测序模型改进了UMI转录组学的测序深度规划

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、transcriptomics
• 📝 描述：RNA sequencing model NB-Lib predicts sequencing depth requirements from shallow pilot data while accounting for library complexity, amplification differences, and molecular recovery…
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3. 科学家揭示驱动乳腺癌的隐藏神经网络

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Researchers have uncovered a surprising way triple-negative breast cancer may turn the body against itself. Tumors appear to recruit macrophages—immune cells normally involved in healing and fighting infection—and use them to release a protein called BDNF that draws nerves into the tumor. Those nerves may then help the cancer grow, resist treatment, and potentially spread.
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• GSE339304 多模态空间分析揭示了髓系定义的 ENKTL 亚组的不同以及预后炎症微环境中的肿瘤-髓系合作 [ENKTL_CosMx6x]
• GSE315384 免疫检查点 ENPP1 抑制棕色脂肪细胞衍生的细胞外 cGAMP，以防止全身代谢功能障碍。
• GSE315247 免疫检查点 ENPP1 抑制棕色脂肪细胞来源的细胞外 cGAMP 以抵抗全身代谢功能障碍
• GSE285095 致癌 KRAS 通过转录后调控的 KRAS 诱导颗粒 (KGs) 促进胰腺导管腺癌 (PDAC) [Ribo eCLIP]
• GSE285093 致癌 KRAS 通过转录后调控的 KRAS 诱导颗粒 (KGs) 促进胰腺导管腺癌 (PDAC) [AGO2 嵌合 eCLIP]
• GSE281227 致癌 KRAS 通过转录后调控的 KRAS 诱导颗粒 (KGs) 促进胰腺导管腺癌 (PDAC) [SLAM-seq]
• GSE239309 致癌 KRAS 通过转录后调控的 KRAS 诱导颗粒 (KGs) 促进胰腺导管腺癌 (PDAC) [miRNA-seq]
• GSE343545 RAF/MEK胶对RAF的空间调控使得全剂量联合泛RAF抑制剂和强效RAS突变肿瘤选择性MAPK及生长抑制剂成为可能
• GSE337145 巨噬细胞衍生的 CCL13 通过 SIX1-SPP1 信号通路在表达 CCR1 的成纤维细胞中驱动子宫纤维化 [scRNA-seq]
• GSE343958：用 5-氟尿嘧啶或奥拉帕尼处理的 HCT116 结直肠癌 3D 球体的批量 RNA 测序
• GSE343274 小鼠支气管肺泡灌洗液细胞的单细胞RNA测序
• GSE288238：单核细胞中通过 cGAS-STING 通路调控 I 型干扰素诱导的基因网络的全基因组图谱
• GSE310802 对整块切除的非肌层浸润性膀胱癌进行形态学和单细胞分析，揭示三级淋巴结构的结构和功能破坏
• GSE294169 研究发现，小鼠 Lig4 基因功能减弱突变易导致 Th1 型肠道炎症。
• GSE343885 多梳抑制复合物 2 驱动血流敏感性内皮状态，而这种状态是血管炎症和疾病的基础。
• GSE343559 m6A 耗竭减弱巨噬细胞 I 型干扰素反应 [延时测序]
• GSE336540 通过复制和转录维持核小体组织可抵消活性染色质的异常融合 [Hi-C]
• GSE329488 利用转基因调控优先考虑哮喘中的核心基因和通路 [Th2 RNA-Seq]
• GSE329487 利用转基因调控优先研究哮喘中的核心基因和通路 [RNA-Seq]
• GSE326957 卵巢细胞外基质力学调控女性生殖衰老过程中卵母细胞-卵泡的相互作用
• GSE287761 通过复制和转录维持核小体组织可抵消活性染色质的异常融合 [ChIP-seq]
• GSE344027 自噬抑制可增强高级别突变型 IDH1 胶质瘤的放射治疗反应 [CUT&Run]
• GSE341910 NRAS 敲低逆转单核细胞状态并使耐药的 FLT3-AML 细胞对吉瑞替尼重新敏感 [原发性 AML RNA-Seq]
• GSE341909 NRAS 敲低逆转单核细胞状态并使耐药的 FLT3-AML 细胞对吉瑞替尼重新敏感 [RNA-Seq]
• GSE341230 破坏 BRD4-BD1–p62 相互作用可恢复保护性自噬 [RNA-seq]
• GSE341228 破坏 BRD4-BD1–p62 相互作用可恢复保护性自噬 [ChIP-seq]
• GSE336036 巨噬细胞衍生的 CCL13 通过 CCR1 表达成纤维细胞中的 SIX1-SPP1 信号通路驱动子宫纤维化
• 东非木薯花叶病毒感染木薯的GSE328300 RNA测序
• GSE277384 延伸因子 P 控制鼠伤寒沙门氏菌抗菌素耐药基因的核糖体移码。
• GSE277383 延伸因子 P 控制鼠伤寒沙门氏菌抗菌素耐药基因的核糖体移码 [efp]
• GSE277235 延伸因子 P 控制鼠伤寒沙门氏菌抗菌素耐药基因 [ugtL] 的核糖体移码
• GSE343704：FDX1敲低在MOLM13急性髓系白血病细胞中的转录组分析
• GSE343698 MCF-7乳腺癌细胞中UBE2C缺失和过表达的转录组分析
• GSE343565 CircKif26b 恢复通过稳定 MOB4 和抑制 Hippo 通路挽救与年龄相关的血管生成障碍
• GSE305825：高尔卡度胺联合CD20 T细胞衔接器通过增强T细胞活化和迁移，延长淋巴瘤模型患者的生存期。
• GSE343853 双重打击机制引发自身免疫性脱发 [scRNA-seq]
• GSE288621 脾脏中Notch2和RBPJ缺陷型单核吞噬细胞的比较单细胞RNA测序