详细内容（前10条）

1. ⭐ GSE233462 泛素D驱动结直肠癌免疫逃逸和对PD-1抗体免疫疗法的耐药性

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、regex:immuno(logy|therapy|suppression)、resistance
• 📝 描述：Contributors : Senlin Zhao ; Jing Zhang ; Zijuan Hu ; Yushuai Mi ; Hong Zhang ; Xuefeng He ; Xinyang Zhong ; Yaxian Wang ; Ye Xu ; Sanjun Cai ; Xinxiang Li ; Ping Wei ; WanJun Chen ; Dawei LiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusUbiquitin D drives colorectal cancer immune evasion and resistance to anti PD1 immunotherapy by suppressing FBXW7 mediaUbiquitin D drives colorectal cancer immune evasion and resistance to anti PD1 immunotherapy by suppressing FBXW7 mediated CD73 degradation [scRNA-seq]The majority of patients with colorectal cancer (CRC) can’t benefit from anti-PD-1 immunotherapy due to an insufficient T cell response in the tumor microenvironment (TME); however, the underlying mechanism remains unknown. Here, we show that ubiquitin D (UBD) in tumor cells inhibits CD8+ T cell‑mediated anti‑tumor responses, and consequently mediates resistance to anti‑PD‑1 immunotherapy in experimental and clinical CRC. Mechanistically, UBD disrupted E3 ligase F‑box and WD repeat domain‑containing 7 (FBXW7)‑induced proteasome degradation of CD73, thereby increasing the concentration of intracellular adenosine, which subsequently suppressed CD8+ T cell function in the TME. Importantly, blockade of CD73 sensitized UBD‑overexpressed cancer cells to anti-PD‑1 immunotherapy by restoring intratumor CD8+ T cell function. We have thus revealed a previously unrecognized mechanism for CRC resistance to anti‑PD‑1 therapy through UBD‑CD73‑adenosine mediated suppression of CD8+ T cells. This new information potentially provides a novel strategy to overcome resistance to PD‑1 blockade in patients with CRC.
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2. ⭐ GSE332984 单细胞 RNA 测序揭示复发性 TFH 淋巴瘤中 FOXP3 阳性调控样状态的获得

• ✍️ 作者：未知作者
• 🏷️ 关键词：lymphoma、sequencing、single-cell
• 📝 描述：Contributors : Tania P Sainz ; Vakul Mohanty ; Yuchen Pan ; Ken Chen ; Francisco VegaSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Nodal T follicular helper cell lymphomas (nTFHLs) are mature T-cell neoplasms characterized by transcriptional and phenotypic features of TFH cells. In this study, we analyzed relapsed TFH lymphoma samples using single-cell RNA sequencing, TCR repertoire analysis, whole-exome sequencing, and viral detection analysis. Single-cell transcriptomic profiling identified a dominant malignant T-cell population expressing canonical TFH-associated genes, with acquisition of a FOXP3-positive regulatory-like transcriptional state at relapse. T-cell receptor clonotype analysis demonstrated oligoclonal expansion within the malignant compartment. Targeted genomic profiling identified recurrent TET2 mutations together with PLCG1 and TP53 alterations. Viral detection analysis identified EBV sequences but no HTLV-1/2 sequences. Processed Seurat objects, cell-level metadata, mutation annotation tables, and viral detection results are provided.
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3. ⭐ GSE332601：Mgmt缺陷小鼠中NDMA诱导的肝损伤的空间转录组学分析（跨性别和时间）。

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributor : Pribyl LeeSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusSpatial transcriptomics (10x Genomics Visium) was performed on fresh-frozen liver tissue (left lobe) from Mgmt-/- mice treated with N-nitrosodimethylamine (NDMA) or saline vehicle during the juvenile period. The study includes male and female mice sacrificed at 10 weeks or 10 months post-birth to characterize spatially resolved transcriptomic changes associated with NDMA-induced liver damage and potential carcinogenesis over time. Mice carried the RaDR+/+; GPT+/+ genotype enabling detection of recombination and mutation events. Tissue sections were processed using the 10x Visium workflow, H&E stained, imaged, permeabilized for spatially barcoded cDNA synthesis, and sequenced on an Illumina NextSeq 500.
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4. ⭐ GSE326950 空间转录组学揭示脊髓性肌萎缩症中神经和非神经组织中失调的程序

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Anne Rietz ; Lokesh Kumari ; Elliot J. AndrophySeries Type : OtherOrganism : Mus musculusSpinal muscular atrophy (SMA) is caused by insufficient levels of the survival motor neuron (SMN) protein and clinically manifests as profound weakness due to motor neuron degeneration. While recent evidence suggests it is a multisystem disorder, the pathological programs in neural and peripheral tissues are poorly understood. We applied spatial transcriptomics to cross-sections from the entire lumbar region of pre-symptomatic SMA and control mice to define early, tissue-wide transcriptional consequences of SMN deficiency. This approach enabled spatially preserved analysis of spinal cord, dorsal root ganglia, muscle, bone, cartilage, bone marrow, adipose, and connective tissues within their native anatomical context. Within the SMA spinal cord, motor neuron associated regions and ventral interneurons exhibited upregulation of neurofilaments, tubulin isoforms, and microtubule transport machinery. Neurofilament changes were largely restricted to motor neurons, and tubulin dysregulation extended broadly across ventral regions. Multiple tissues displayed collagen and extracellular matrix gene dysregulation at post-natal day 4. Skeletal muscle demonstrated fiber type-specific stress responses, including induction of atrophy-associated genes, while bone displayed an osteoclast-dominant transcriptional signature, consistent with accelerated resorption and a pro-osteoporotic state. Bone marrow transcriptomes indicated activation of neutrophil degranulation, innate immune signaling, and osteoclastogenic pathways, identifying bone marrow as an active inflammatory and skeletal regulatory niche in SMA. Adipose tissue exhibited extracellular matrix dysregulation, complement activation, profibrotic TGF-β signaling, and stress-induced lipolysis. These findings reveal that SMN deficiency drives early transcriptional reprogramming across multiple tissues well before motor neuron loss and identify non-neuronal pathological programs that offer therapeutic targets for improving long-term outcomes in SMA.
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5. ⭐ GSE269041 解析急性髓系白血病组织特异性微环境（scRNA-Seq 免疫）

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、immune、scRNA
• 📝 描述：Contributors : Varvara Paraskevopoulou ; Ziyan Lin ; Iannis AifantisSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAcute myeloid leukemia (AML) is a blood cancer with poor survival outcomes. Limited studies have reported lethal complications in patients due to leukemia infiltration into solid tissues such as the lung, but the related mechanisms remain understudied. Here, we map the transcriptional landscape of the mouse lung microenvironment at single-cell resolution in the AML-infiltrated lungs. Our analysis demonstrated a considerable remodeling of the lung microenvironment under leukemia conditions, as indicated by expansion of stromal myofibroblasts and reduction of endothelial capillary aerocytes. Those changes were accompanied by changes in immune resident cells of the lung microenvironment, as supported by reduction of B- and T- cell proportions, and increased frequencies of activated neutrophils and monocyte populations. We show an induction of inflammatory response within the microenvironment of the leukemic lung. We dissect the spatial interplay between AML and the lung microenvironment, and we identify previously unappreciated interactions driven by inflammatory mediators within the leukemic milieu. Of note, we show that Lgals9 (encoding for Galectin-9) mediates most of cell-cell interactions within the microenvironment of the AML-infiltrated lungs. LGALS9 is highly expressed in AML patients and its role in AML remains elusive. Targeting Galectin-9 reduces the AML burden in the lungs and reverses the infiltration phenotype. Combining single-cell, spatial transcriptomics approaches and functional experimentsin vivo, our study is the first to characterize the pulmonary infiltration phenotype in AML, opening the route for novel treatment strategies in acute leukemia.
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6. GSE317244 犬口腔肿瘤样本（CAA、COSCC）的批量 RNA 测序。

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、sequencing
• 📝 描述：Contributors : Jennifer K Grenier ; Santiago PeraltaSeries Type : Expression profiling by high throughput sequencingOrganism : Canis lupus familiarisCanine acanthomatous ameloblastoma (CAA) is a locally invasive benign oral neoplasm. Clinically, differentiating CAA from canine oral squamous cell carcinoma (COSCC) has proven to be difficult as they share many clinical, radiological, and histological features. Molecularly, even though they both have an overactive MAPK pathway in comparison to healthy gingiva tissue, their mutational landscape is distinct. Bulk RNA sequencing (RNA-seq) has uncovered pronounced differences between CAA and COSCC in programs related to, among others, hypoxia, PI3K-AKT signaling, and cell proliferation.
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7. GSE316710 解析急性髓系白血病中的组织特异性微环境 [RNA-Seq anti-IL33]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、RNA-seq
• 📝 描述：Contributors : Varvara Paraskevopoulou ; Ziyan Lin ; Iannis AifantisSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAcute myeloid leukemia (AML) is a blood cancer with poor survival outcomes. Limited studies have reported lethal complications in patients due to leukemia infiltration into solid tissues such as the lung, but the related mechanisms remain understudied. Here, we map the transcriptional landscape of the mouse lung microenvironment at single-cell resolution in the AML-infiltrated lungs. Our analysis demonstrated a considerable remodeling of the lung microenvironment under leukemia conditions, as indicated by expansion of stromal myofibroblasts and reduction of endothelial capillary aerocytes. Those changes were accompanied by changes in immune resident cells of the lung microenvironment, as supported by reduction of B- and T- cell proportions, and increased frequencies of activated neutrophils and monocyte populations. We show an induction of inflammatory response within the microenvironment of the leukemic lung. We dissect the spatial interplay between AML and the lung microenvironment, and we identify previously unappreciated interactions driven by inflammatory mediators within the leukemic milieu. Of note, we show that Lgals9 (encoding for Galectin-9) mediates most of cell-cell interactions within the microenvironment of the AML-infiltrated lungs. LGALS9 is highly expressed in AML patients and its role in AML remains elusive. Targeting Galectin-9 reduces the AML burden in the lungs and reverses the infiltration phenotype. Combining single-cell, spatial transcriptomics approaches and functional experiments in vivo, our study is the first to characterize the pulmonary infiltration phenotype in AML, opening the route for novel treatment strategies in acute leukemia.
• 🔗 查看原文

8. GSE275542 解析急性髓系白血病中的组织特异性微环境 [scRNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、scRNA
• 📝 描述：Contributors : Varvara Paraskevopoulou ; Ziyan Lin ; Iannis AifantisSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAcute myeloid leukemia (AML) is a blood cancer with poor survival outcomes. Limited studies have reported lethal complications in patients due to leukemia infiltration into solid tissues such as the lung, but the related mechanisms remain understudied. Here, we map the transcriptional landscape of the mouse lung microenvironment at single-cell resolution in the AML-infiltrated lungs. Our analysis demonstrated a considerable remodeling of the lung microenvironment under leukemia conditions, as indicated by expansion of stromal myofibroblasts and reduction of endothelial capillary aerocytes. Those changes were accompanied by changes in immune resident cells of the lung microenvironment, as supported by reduction of B- and T- cell proportions, and increased frequencies of activated neutrophils and monocyte populations. We show an induction of inflammatory response within the microenvironment of the leukemic lung. We dissect the spatial interplay between AML and the lung microenvironment, and we identify previously unappreciated interactions driven by inflammatory mediators within the leukemic milieu. Of note, we show that Lgals9 (encoding for Galectin-9) mediates most of cell-cell interactions within the microenvironment of the AML-infiltrated lungs. LGALS9 is highly expressed in AML patients and its role in AML remains elusive. Targeting Galectin-9 reduces the AML burden in the lungs and reverses the infiltration phenotype. Combining single-cell, spatial transcriptomics approaches and functional experimentsin vivo, our study is the first to characterize the pulmonary infiltration phenotype in AML, opening the route for novel treatment strategies in acute leukemia.
• 🔗 查看原文

9. GSE269043 剖析急性髓系白血病中的组织特异性微环境（空间）

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、spatial
• 📝 描述：Contributors : Varvara Paraskevopoulou ; Ziyan Lin ; Manel Esteller ; Iannis AifantisSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAcute myeloid leukemia (AML) is a blood cancer with poor survival outcomes. Limited studies have reported lethal complications in patients due to leukemia infiltration into solid tissues such as the lung, but the related mechanisms remain understudied. Here, we map the transcriptional landscape of the mouse lung microenvironment at single-cell resolution in the AML-infiltrated lungs. Our analysis demonstrated a considerable remodeling of the lung microenvironment under leukemia conditions, as indicated by expansion of stromal myofibroblasts and reduction of endothelial capillary aerocytes. Those changes were accompanied by changes in immune resident cells of the lung microenvironment, as supported by reduction of B- and T- cell proportions, and increased frequencies of activated neutrophils and monocyte populations. We show an induction of inflammatory response within the microenvironment of the leukemic lung. We dissect the spatial interplay between AML and the lung microenvironment, and we identify previously unappreciated interactions driven by inflammatory mediators within the leukemic milieu. Of note, we show that Lgals9 (encoding for Galectin-9) mediates most of cell-cell interactions within the microenvironment of the AML-infiltrated lungs. LGALS9 is highly expressed in AML patients and its role in AML remains elusive. Targeting Galectin-9 reduces the AML burden in the lungs and reverses the infiltration phenotype. Combining single-cell, spatial transcriptomics approaches and functional experimentsin vivo, our study is the first to characterize the pulmonary infiltration phenotype in AML, opening the route for novel treatment strategies in acute leukemia.
• 🔗 查看原文

10. GSE269042 解析急性髓系白血病中的组织特异性微环境（scRNA-Seq Niche）

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、scRNA
• 📝 描述：Contributors : Varvara Paraskevopoulou ; Ziyan Lin ; Iannis AifantisSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAcute myeloid leukemia (AML) is a blood cancer with poor survival outcomes. Limited studies have reported lethal complications in patients due to leukemia infiltration into solid tissues such as the lung, but the related mechanisms remain understudied. Here, we map the transcriptional landscape of the mouse lung microenvironment at single-cell resolution in the AML-infiltrated lungs. Our analysis demonstrated a considerable remodeling of the lung microenvironment under leukemia conditions, as indicated by expansion of stromal myofibroblasts and reduction of endothelial capillary aerocytes. Those changes were accompanied by changes in immune resident cells of the lung microenvironment, as supported by reduction of B- and T- cell proportions, and increased frequencies of activated neutrophils and monocyte populations. We show an induction of inflammatory response within the microenvironment of the leukemic lung. We dissect the spatial interplay between AML and the lung microenvironment, and we identify previously unappreciated interactions driven by inflammatory mediators within the leukemic milieu. Of note, we show that Lgals9 (encoding for Galectin-9) mediates most of cell-cell interactions within the microenvironment of the AML-infiltrated lungs. LGALS9 is highly expressed in AML patients and its role in AML remains elusive. Targeting Galectin-9 reduces the AML burden in the lungs and reverses the infiltration phenotype. Combining single-cell, spatial transcriptomics approaches and functional experimentsin vivo, our study is the first to characterize the pulmonary infiltration phenotype in AML, opening the route for novel treatment strategies in acute leukemia.
• 🔗 查看原文

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1. 对血液样本进行 RNA 测序可以监测免疫反应，并有助于为高危患者量身定制治疗方案。

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、sequencing
• 📝 描述：RNA sequencing of blood samples may help predict immune response to chemoimmunotherapy and support more personalized treatment strategies for high-risk…
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2. 新的基因组学方法揭示了衰老大脑令人惊讶的细胞动态变化

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging
• 📝 描述：Advanced RNA sequencing methods, including IRISeq and EnrichSci, uncover spatial interactions and molecular changes linked to aging in vulnerable brain cell populations…
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3. 科学家发现日常食物中隐藏的致癌化学物质

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Scientists have identified potentially cancer-causing chemicals hiding in many everyday foods, especially those exposed to high heat cooking methods like grilling, roasting, smoking, and frying. The compounds, known as PAHs, can form during cooking or enter foods through contamination, raising concerns about long-term health risks.
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• GSE269040 解析急性髓系白血病中的组织特异性微环境（RNA-Seq VecadAML）
• GSE269039 解析急性髓系白血病（RNA-Seq AML）的组织特异性微环境
• GSE331183 奶牛从出生到成年的血液 DNA 甲基化发育动态：基于酶甲基测序 (EM-seq) 的纵向研究。
• GSE332968 Resf1 是正常胎盘发育和滋养层细胞特异性异染色质形成所必需的 [scRNA-Seq]
• GSE332646 野生型和Mgmt-/-基因型小鼠在多个时间点经NDMA或生理盐水处理后幼鼠肝脏的批量RNA测序
• GSE302028 原发性和转移性乳腺癌细胞中线性RNA图谱的全面分析
• GSE302027 天然、分化和干细胞样状态下原发性和转移性乳腺癌细胞中环状RNA的分布图谱
• GSE276297 建立具有性腺嵌合体的鸡原始生殖细胞系 [scRNA-Seq]
• GSE210746 前列腺癌和293FT细胞中3′UTRCES介导的替代性多聚腺苷酸化（APA）工程的表征
• GSE328788 抑制细胞毒性 CD8+ T 细胞中的程序性细胞死亡-1 会加剧压力超负荷诱导的心脏损伤
• GSE327655 抑制细胞毒性 CD8+ T 细胞中的程序性细胞死亡-1 会通过颗粒酶 B 加剧压力超负荷诱导的心脏损伤
• GSE327544 内源性肽GPR15L通过塑造肠道菌群来对抗结肠炎
• GSE310474 少突胶质细胞前体细胞发育和对癌组蛋白 H3.3 K27M 反应的细胞自主区域差异 [ChIP-Seq]
• GSE310472 少突胶质细胞前体细胞发育和对癌组蛋白 H3.3 K27M 反应的细胞自主区域差异 [ATAC-Seq]
• GSE308630 MLL4复合物在H3K4甲基化和p53依赖性转录激活中的分子机制
• GSE304335 线粒体靶向二甲双胍刺激人和小鼠胰腺肿瘤细胞发生内质网应激介导的细胞凋亡
• GSE290817 少突胶质细胞前体细胞发育和对癌组蛋白 H3.3 K27M 反应的细胞自主区域差异 [scRNA-seq]
• GSE290816 少突胶质细胞前体细胞发育和对癌组蛋白 H3.3 K27M 反应的细胞自主区域差异 [RNA-seq]
• GSE269038 解析急性髓系白血病中的组织特异性微环境（CRISPR）
• GSE161955 对三种小麦基因型小穗中茉莉酸、水杨酸和乙烯响应转录组的发现揭示了茉莉酸信号的快速和保守响应
• GSE332889 喹啉酸代谢可能缓解急性肾损伤向慢性肾病的转化
• GSE331306 小胶质细胞 CD31 通过 SHP2–STAT3–MME 轴调控阿尔茨海默病病理，从而抑制 Aβ 清除
• GSE331294：对5xFAD小鼠全脑进行单核RNA测序分析，这些小鼠存在小胶质细胞特异性CD31敲低。