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1. ⭐ GSE338087 大B细胞淋巴瘤患者肿瘤组织RNA测序分析：axi-cel治疗前肿瘤微环境研究

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、lymphoma、tumor microenvironment、B cell、RNA-seq
• 📝 描述：Contributors : Michael D Jain ; Marco L Davila ; Sae BomSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensWe examined the tumor immune infiltrate and its relationship with clinical outcomes in patients with LBCL receiving Axicabtagene ciloleChimeric antigen receptor (CAR) T cell therapies have revolutionized B cell malignancy treatment, but many patients with large B cell lymphoma (LBCL) experience primary resistance or relapse. To uncover resistance mechanisms, we examined pre-infusion tumor biopsies and observed that increased immunoregulatory macrophages correlate with poor clinical responses. In murine models, CAR T cell-produced interferon-gamma (IFN-) upregulates inducible nitric oxide synthase (iNOS, NOS2) in immunoregulatory macrophages, impairing CAR T cell function. Proteomic profiling revealed that iNOS-expressing macrophages promote apoptosis and cell cycle arrest while downregulating protein synthesis machinery in CAR T cells. Metabolically, CAR T cells exhibit reduced glycolytic intermediates and altered tricarboxylic acid (TCA) cycle activity. Pharmacological inhibition of iNOS enhances CAR T cell treatment efficacy in vivo. Notably, elevated levels of iNOS+CD14+ monocytes in leukaphereses are associated with non-durable responses to CAR T cells. Targeting iNOS in immunoregulatory macrophages, potentially by modulating CAR T-produced IFN-, could improve LBCL outcomes.
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2. ⭐ GSE335480 单细胞追踪揭示黑色素瘤TIL治疗过程中肿瘤反应性T细胞的可塑性

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、T cell、single-cell
• 📝 描述：Contributors : Michael T Sandholzer ; Clara Serger ; Alessia G Liner ; Sarp Uzun ; David Koenig ; Helen Thut ; Reto Ritschard ; Jonas D Fuerst ; Andreas Zingg ; Natalia Rodrigues Mantuano ; Benjamin Kasenda ; Katharina Glatz ; Elisabeth A Kappos ; Matthias Matter ; Andreas Holbro ; Frank Stenner ; Jakob Passweg ; Nina Khanna ; Lukas Jeker ; Mascha Binder ; Alfred Zippelius ; Heinz LaeubliSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensAdoptive cell therapy (ACT) with tumor-infiltrating lymphocytes (TILs) can induce durable responses in metastatic melanoma, yet the clonal and transcriptional dynamics that govern tumor-reactive T cell fate during ex vivo expansion and after transfer remain poorly understood. Here, we performed longitudinal single-cell RNA and T cell receptor (TCR) sequencing across five timepoints, from baseline tumors through a two-phase ex vivo expansion to post-infusion peripheral blood and tumor biopsies, in seven melanoma patients, generating a high-resolution map of both CD8+ and CD4+ tumor-reactive T cell plasticity. During early expansion (preREP), tumor-reactive CD8+ T cells were reinvigorated from an exhausted state and acquired distinct HLA-II-high or KLF2-high transcriptional profiles. In-depth characterization of the CD4+ compartment revealed lineage-dependent reinvigoration. After transfer, both CD8+ and CD4+ tumor-reactive clones acquired stem-like profiles and tissue-homing markers before re-infiltrating tumor lesions. Mechanistically, we identify two processes linked to treatment failure in non-responders: de novo expansion of immunosuppressive regulatory T cells, and co-transfer of Type 17 T cells. These data provide a comprehensive longitudinal framework of T cell plasticity during TIL-ACT.
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3. ⭐ GSE335152 全基因组DNA甲基化谱分析鉴定出电离辐射诱导的低甲基化基因，这些基因在口腔鳞状细胞癌中具有临床意义

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、genome、methylation
• 📝 描述：Contributors : Yu Kyeong Han ; Jihye Park ; Bomin Seol ; Hye Su Han ; Ha Young Park ; So Young Jung ; Ji Won Hyun ; Hae Ryoun Park ; Keunsoo Kang ; Joo Mi YiSeries Type : Methylation profiling by genome tiling arrayOrganism : Homo sapiensBackground: The epigenetic consequences of ionizing radiation (IR), particularly its effects on DNA methylation, remain poorly understood. Here, we investigated whether IR induces genome-wide DNA methylation changes in OSCC cells and examined whether IR-induced hypomethylated candidate genes correspond to epigenetically silenced loci in oral cancer patient tumors, and whether their methylation status influences clinical outcomes.Methods: OSCC cells were treated with IR or 5-aza-2’-deoxycytidine (5-aza-dC) and subjected to genome-wide DNA methylation profiling using the Illumina HumanMethylationEPIC BeadChip. Candidate hypomethylated genes were validated by qRT-PCR and quantitative methylation-specific PCR (qMSP). DNMT1 promoter occupancy was assessed by chromatin immunoprecipitation (ChIP). Clinical relevance was evaluated using the TCGA-HNSCC dataset.Results: IR significantly reduced DNMT1 and DNMT3b protein levels in OSCC cells, indicating IR-induced global DNA hypomethylation. Genome-wide profiling identified three candidate genes, MLPH, BMP4, and MYO5A, showing concordant promoter demethylation and transcriptional upregulation following IR treatment, with ChIP analysis confirming reduced DNMT1 occupancy at their promoters. Importantly, TCGA-HNSCC analysis revealed that BMP4 and MLPH are hypermethylated and transcriptionally silenced in untreated HNSCC tumors, a finding mechanistically complementary to our experimental data, suggesting that IR reverses tumor-associated epigenetic silencing through DNMT1-mediated passive demethylation. Consistently, BMP4 hypermethylation was associated with poor overall survival, and BMP4-hypermethylated patients receiving radiotherapy survived longer than those receiving chemotherapy.Conclusions: This study provides the first evidence that IR induces genome-wide DNA hypomethylation in OSCC through DNMT1 and DNMT3b downregulation, reactivating epigenetically silenced genes including MLPH, BMP4, and MYO5A. These findings suggest that IR-induced epigenetic reactivation of tumor-silenced genes may represent a clinically meaningful mechanism of radiotherapy response, and that BMP4 methylation status may serve as a potential predictive biomarker in oral cancer.
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4. GSE338088 单羧酸转运蛋白 2 (MCT2) 通过塑造免疫微环境减轻肺肿瘤进展 [snRNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune
• 📝 描述：Contributors : Yen On Chan ; Zhuanhong Qiao ; Trupti Joshi ; David Gozal ; Abdelnaby KhalyfaSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusMonocarboxylate transporter 2 (MCT2; SLC16A7) is a high-affinity pyruvate transporter implicated in cancer metabolism. However, its role in lung cancer progression and the tumor microenvironment remains unclear. This study examined the effects of MCT2 loss on tumor growth and cell type-specific transcriptional changes within the tumor microenvironment. MCT2 loxP/loxP mice were crossed with mCre-Tg mice, and MCT2 deletion was induced by tamoxifen. Control (CO) mice received vehicle treatment. TC1 cells (100,000 cells/mouse) were injected subcutaneously, and tumors were harvested after 24 days. Single-nucleus RNA sequencing (snRNA-seq) was performed on isolated tumor nuclei (4,000 nuclei/sample; n = 3 per group) using the 10x Genomics Chromium platform. Data were processed with Cell Ranger v3.0.2 and Seurat v5.2.1, followed by differential expression and pathway enrichment analyses integrated with macrophage bulk RNA-seq data. MCT2-deficient tumors grew significantly faster than control tumors, supporting a tumor-suppressive role for MCT2. Transcriptomic analysis generated high-quality profiles from 7,840 CO and 10,175 KO nuclei. Clustering identified 10 cellular populations, including nine annotated cell types. MCT2 deficiency altered pathways involved in glycolysis, the tricarboxylic acid cycle, oxidative phosphorylation, and fatty acid metabolism across multiple populations. Macrophages showed prominent transcriptional changes, including enrichment of MAPK, PI3K-Akt, IgSF-CAM, and cell adhesion molecule signaling pathways. These findings were supported by macrophage bulk RNA-seq data. MCT2 deficiency enhances tumor growth and induces widespread transcriptional remodeling of the tumor microenvironment. Altered metabolic and immune-related pathways, particularly in macrophages, may contribute to lung cancer progression and represent potential therapeutic targets.
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5. GSE338086 单羧酸转运蛋白 2 (MCT2) 通过塑造免疫微环境减轻肺肿瘤进展 [bulk RNA]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune
• 📝 描述：Contributors : Yen On Chan ; Zhuanhong Qiao ; Trupti Joshi ; David Gozal ; Abdelnaby KhalyfaSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusMonocarboxylate transporter 2 (MCT2; SLC16A7) is a high-affinity pyruvate transporter implicated in cancer metabolism. However, its role in lung cancer progression and the tumor microenvironment remains unclear. This study examined the effects of MCT2 loss on tumor growth and cell type-specific transcriptional changes within the tumor microenvironment. MCT2 loxP/loxP mice were crossed with mCre-Tg mice, and MCT2 deletion was induced by tamoxifen. Control (CO) mice received vehicle treatment. TC1 cells (100,000 cells/mouse) were injected subcutaneously, and tumors were harvested after 24 days. Single-nucleus RNA sequencing (snRNA-seq) was performed on isolated tumor nuclei (4,000 nuclei/sample; n = 3 per group) using the 10x Genomics Chromium platform. Data were processed with Cell Ranger v3.0.2 and Seurat v5.2.1, followed by differential expression and pathway enrichment analyses integrated with macrophage bulk RNA-seq data. MCT2-deficient tumors grew significantly faster than control tumors, supporting a tumor-suppressive role for MCT2. Transcriptomic analysis generated high-quality profiles from 7,840 CO and 10,175 KO nuclei. Clustering identified 10 cellular populations, including nine annotated cell types. MCT2 deficiency altered pathways involved in glycolysis, the tricarboxylic acid cycle, oxidative phosphorylation, and fatty acid metabolism across multiple populations. Macrophages showed prominent transcriptional changes, including enrichment of MAPK, PI3K-Akt, IgSF-CAM, and cell adhesion molecule signaling pathways. These findings were supported by macrophage bulk RNA-seq data. MCT2 deficiency enhances tumor growth and induces widespread transcriptional remodeling of the tumor microenvironment. Altered metabolic and immune-related pathways, particularly in macrophages, may contribute to lung cancer progression and represent potential therapeutic targets.
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6. GSE316851 SETDB1 介导的 RhoB 抑制促进前列腺癌的 EMT 和转移进展 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq
• 📝 描述：Contributors : Fong ka wing ; Jinpeng Liu ; Ryan GoettlSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensMetastatic castration-resistant prostate cancer (CRPC) remains a clinical challenge, and epithelial–mesenchymal transition (EMT) contributes to metastatic progression and reduced response to therapy. However, the upstream epigenetic mechanisms that sustain EMT programs in advanced prostate cancer (PCa) are not fully defined. We identify the histone H3 lysine 9 (H3K9) methyltransferase SET domain bifurcated 1 (SETDB1) as a key regulator of EMT and metastasis through direct repression of the small GTPase RhoB. SETDB1 is genomically amplified and transcriptionally upregulated in metastatic CRPC, and SETDB1 depletion reduces cell migration, invasion, and metastatic dissemination. Integrated chromatin profiling and transcriptomic analyses demonstrate that SETDB1 occupies the RhoB promoter and mediates its transcriptional silencing through H3K9 methylation. Restoration of RhoB reverses EMT gene expression and suppresses invasive behavior, whereas RhoB knockdown rescues the effects of SETDB1 depletion, establishing RhoB as a critical downstream effector of SETDB1 function. Androgen signaling inhibitor-resistant PCa models exhibit RhoB loss and EMT activation, linking this axis to therapy-resistant phenotypes. Finally, antisense oligonucleotide-mediated SETDB1 silencing restores RhoB expression and suppresses EMT and invasion in CRPC cell models. Together, these findings define a SETDB1-RhoB epigenetic pathway that promotes EMT and metastatic progression in PCa and may be therapeutically targeted in advanced disease.
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7. GSE337003 长读测序揭示哺乳动物胚胎合子基因组激活过程中转座元件衍生的嵌合转录本

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、genome
• 📝 描述：Contributors : Saki Kawakami ; Koichi Kitao ; Shuntaro Ikeda ; Shinnosuke HondaSeries Type : Expression profiling by high throughput sequencingOrganism : Bos taurus ; Mus musculusWe performed long-read RNA-seq using mouse late 2-cell and bovine 8-16 cell embryos for constructing transposable element (TE)-driven chimeric mRNA library.
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8. GSE309183 乳酸诱导的H3K4me3组蛋白修饰促进PLOD1驱动的前列腺癌侵袭

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、histone
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensProstate cancer (PCa) progression is strongly influenced by the metabolites available in the tumor microenvironment (TME), including lactic acid (LA), which is actively imported by PCa cells to boost mitochondrial metabolism and drive de novo collagen synthesis, sustaining survival and malignancy. LA exploitation promotes the unbalance of tricarboxylic acid (TCA) cycle intermediates, particularly succinate and fumarate, well-known epigenetic modifiers for histone (de)methylation. Here, we show that the LA-induced increase in succinate levels affects the transcriptionally activating H3K4me3 methylation mark in PCa cells, promoting a pro-invasive phenotype. Notably, pharmacological targeting of H3K4me3 using OICR-9429 reduces LA-enhanced PCa cell invasiveness. Moreover, LA-induced H3K4me3 enrichment regulates the expression of procollagen-Lysine,2-Oxoglutarate 5-Dioxygenase 1 (PLOD1), a key enzyme involved in collagen maturation. Genetic impairment of PLOD1 reduces the LA-driven invasive potential of PCa cells, thereby highlighting PLOD1 as a crucial epigenetically regulated mediator of tumor invasion. Overall, our findings uncover a LA-fuelled metabolic-epigenetic axis that promotes the H3K4me3-mediated PLOD1 upregulation, thereby enhancing PCa aggressiveness and revealing potential vulnerability that could be exploited for targeted therapy.
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9. GSE316850 SETDB1 介导的 RhoB 抑制促进前列腺癌的 EMT 和转移进展 [CUT&Run]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Contributors : Fong ka wing ; Jinpeng Liu ; Ryan GoettlSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensMetastatic castration-resistant prostate cancer (CRPC) remains a clinical challenge, and epithelial–mesenchymal transition (EMT) contributes to metastatic progression and reduced response to therapy. However, the upstream epigenetic mechanisms that sustain EMT programs in advanced prostate cancer (PCa) are not fully defined. We identify the histone H3 lysine 9 (H3K9) methyltransferase SET domain bifurcated 1 (SETDB1) as a key regulator of EMT and metastasis through direct repression of the small GTPase RhoB. SETDB1 is genomically amplified and transcriptionally upregulated in metastatic CRPC, and SETDB1 depletion reduces cell migration, invasion, and metastatic dissemination. Integrated chromatin profiling and transcriptomic analyses demonstrate that SETDB1 occupies the RhoB promoter and mediates its transcriptional silencing through H3K9 methylation. Restoration of RhoB reverses EMT gene expression and suppresses invasive behavior, whereas RhoB knockdown rescues the effects of SETDB1 depletion, establishing RhoB as a critical downstream effector of SETDB1 function. Androgen signaling inhibitor-resistant PCa models exhibit RhoB loss and EMT activation, linking this axis to therapy-resistant phenotypes. Finally, antisense oligonucleotide-mediated SETDB1 silencing restores RhoB expression and suppresses EMT and invasion in CRPC cell models. Together, these findings define a SETDB1-RhoB epigenetic pathway that promotes EMT and metastatic progression in PCa and may be therapeutically targeted in advanced disease.
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10. GSE315101 端粒缩短诱导的衰老小胶质细胞分泌的可溶性 DLK1 会损害少突胶质细胞功能并改变神经元活动 [DLK1_snRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：Neuronal
• 📝 描述：Contributors : Bangyan Liu ; Maria Telpoukhovskaia ; Matthew Mahoney ; Yilin Feng ; Alice Maria Giani ; Eileen Ruth Torres ; Lihong Zhan ; Pearly Ye ; Jingjie Zhu ; Nessa R Foxe ; Daphne Zhu ; Xinran Tong ; Deepak Srivastava ; Christine V. Theodoris ; Shiaoching Gong ; Mingrui Zhao ; Li Fan ; Li GanSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiens ; Mus musculusAging is a predominant risk factor of neurodegenerative disorders such as Alzheimer’s and Parkinson’s disease. Here, we investigated the impact of telomere shortening, a physiological hallmark of aging, on brain function. Telomere-shortened mice exhibited cognitive decline and exacerbated lipofuscinosis, accompanied by the emergence of senescent microglia with a senescence-associated secretory phenotype and oligodendrocyte lineage cells with impaired maturation. Using iPSC-derived microglia with shortened telomeres, we identified DLK1 as a novel senescence-associated ligand secreted by senescent microglia. Elevated soluble DLK1 was detected in the cerebrospinal fluid of both telomere-shortened and physiologically aged mice, and this increase was abolished by microglial depletion, confirming its microglial origin. Functionally, AAV-mediated expression of sDLK1 in mouse brains induced hypomyelination and disrupted oligodendrocyte differentiation in vivo. In human iPSC-derived systems, sDLK1 impaired late-stage oligodendrocyte maturation and disrupted neuronal calcium signaling. Together, these findings establish replicative microglial senescence as a pathological feature of telomere shortening and identify sDLK1 as one key effector linking senescent microglia to oligodendrocyte dysfunction and neuronal dysregulation during brain aging.
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1. 单细胞核RNA测序发现罕见鼻窦癌的新治疗靶点

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：RNA sequencing reveals distinct cellular programs and therapeutic targets in rare sinonasal carcinomas, supporting precision oncology approaches tailored to specific tumor subtypes…
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2. 研究揭示肾脏如何在损伤后重建免疫防御

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune
• 📝 描述：RNA sequencing reveals how kidney macrophages and epithelial cells coordinate tissue repair, providing new insights into recovery after acute kidney injury…
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• GSE315100 端粒缩短诱导的衰老小胶质细胞分泌的可溶性 DLK1 会损害少突胶质细胞功能并改变神经元活动（ipsc_cell）
• GSE261042：突变型异柠檬酸脱氢酶1 (IDH1) 胶质瘤中自噬上调揭示新的治疗靶点
• GSE244761 MLL-AF9 淋巴母细胞对化疗敏感和耐药的转录组
• GSE338073 血浆多 miRNA 模型对阿尔茨海默病、帕金森病和路易体痴呆进行分类
• GSE337525 扩展Pol III转录组图谱：POLR3A的eCLIP和ROPE-seq
• GSE323968 转录特征表明 RB 功能可能预测子宫内膜癌对 CDK4/6 抑制剂的反应
• GSE317450 果蝇幼虫脂肪细胞中 abd-A 和 Abd-B 的转录调控 [RNA-Seq]
• GSE307980 ClC-Kb 缺乏抑制肾小管的增殖和线粒体代谢
• GSE302426 CDK8 抑制作用将 Med1 隔离在 EWS-FLI 增强子处 [ChIP-seq]
• GSE302424 CDK8 抑制作用将 Med1 隔离在 EWS-FLI 增强子处 [ATAC-seq]
• GSE337700 不愈合骨折的单细胞RNA测序数据
• GSE337663 治疗持续性白血病对通过靶向 KHSRP 恢复 SLC23A1 具有选择性敏感性（AML 患者样本）
• GSE337641：Wfdc2缺陷小鼠肺的单细胞转录组分析及其对阿米洛利治疗的反应
• GSE335511 单细胞测序数据支持“IL-4/C1q激活的星形胶质细胞衍生的细胞外囊泡通过募集外周白细胞促进中风梗死恢复”
• GSE304126 CDK8 抑制作用将 Med1 隔离在 EWS-FLI 增强子处 [RNA-Seq]
• GSE302269 GID泛素连接酶对代谢转变的双向调控
• GSE301941 非诺贝特通过调节 PTPN14/MARK/Hippo 信号通路抑制肿瘤增殖和进展
• GSE301876 活动性肺结核患者肺泡和肉芽肿区域的空间转录组分析
• GSE281077 种子内生细菌在入侵植物遭受胁迫前诱导其产生类似干旱胁迫的转录组启动状态
• GSE288064 RNA测序研究了HUVEC、HCMEC和人原代骨骼肌细胞在体外机械负荷作用下的反应