详细内容（前10条）

1. ⭐ GSE328448 时空转录组学表征小鼠肝脏衰老过程中的免疫微环境 [空间转录组学]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、aging、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Jiahua Lu ; Yuqian Wang ; Wenxue Zhao ; Zihao Zhao ; Zhaoya Gao ; Jin Gu ; Cheng Li ; Jie ChengSeries Type : OtherOrganism : Mus musculusThe liver is a major metabolic organ, responsible for synthesizing and breaking down diverse metabolites. Recently, the liver’s immunological functions have gradually been unveiled: combating pathogens and maintaining tissue homeostasis. Age-related functional alterations in these immune cells emerge as potential drivers of hepatic dysfunction and age-associated pathologies. However, systematic investigations into spatiotemporal immune cell dynamics during liver aging remain limited. To address this gap, we analyzed young and old mouse livers using single-cell/nuclei and spatial transcriptomics, revealing T cells as the immune cell population with the most pronounced transcriptomic alterations, marked by enrichment of exhausted CD8+ T cells in aged livers. Spatial mapping showed exhausted CD8+ T cells accumulating in portal vein (PV) zone, co-localizing with periportal hepatocytes (PP hepatocytes). Up-regulation of LPIN1 in PP hepatocyte promoted T cell exhaustion. CD8+ T cell exhaustion was tightly associated with disease progression. Therefore, our findings suggest that targeting LPIN1 may alleviate T cell exhaustion, offering potential therapeutic strategies for age-related liver diseases.
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2. ⭐ GSE302660 肠道 LKB1 缺失驱动锯齿状癌症通路上的癌前程序 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、scRNA、pathway、regex:intestin(e|al)
• 📝 描述：Contributors : Susanna F Plugge ; Huying Ma ; Jelte Y van der Vaart ; Joep Sprangers ; Folkert Morsink ; Despina Xanthakis ; Cara Jamieson ; Kirsten Stroot ; Anneloes R Keijzer ; Thanasis Margaritis ; Tito Candelli ; Roy Straver ; Jeroen de Ridder ; Frank Holstege ; Wendy de Leng ; Johan Offerhaus ; Alessandra Merenda ; Madelon M MauriceSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusBackground & AimsHeterozygous inactivating mutations of Serine Threonine Kinase 11 (STK11)/Liver Kinase B1 (LKB1) are causative to the Peutz-Jeghers syndrome (PJS), a hereditary disease characterized by gastrointestinal hamartomatous polyposis and increased cancer susceptibility. While LKB1 loss-induced polyp formation has been ascribed to non-epithelial tissues, how LKB1 deficiency increases cancer risk of patients by altering the phenotypical landscape and hierarchical organization of epithelial tissues remains poorly understood.MethodsUsing CRISPR/Cas9, we generated heterozygous and homozygous Lkb1-deficient mouse small intestinal and human colon organoids. These organoids were characterized by an integrated approach that combines imaging, bulk and single-cell RNA sequencing and growth factor dependency assays. Our findings were validated in human PJS-derived tissues using immunohistochemistry and linked to colorectal cancer profiles using the TCGA cancer database.ResultsOur results reveal that heterozygous Lkb1 loss is sufficient to push intestinal cells into a premalignant transcriptional program associated with serrated colorectal cancer, which is further amplified by loss-of-heterozygosity. This altered epithelial growth state associates with persistent features of regeneration and enhanced EGFR ligand and receptor expression, conferring niche-independent growth properties to Lkb1-deficient organoids. Moreover, our newly generated LKB1-mutant signature is enriched in sporadic serrated colorectal cancer, and synergistic cooperation of Lkb1-deficiency with mutant Kras was experimentally confirmed by assessing organoid growth properties and transcriptomes.ConclusionsHeterozygous loss of LKB1 pushes intestinal cells into a chronic regenerative state which is amplified upon loss-of-heterozygosity. Lkb1-deficiency thereby generates fertile ground for serrated colorectal cancer formation in the intestine, potentially explaining the increased cancer risk observed in PJS.
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3. ⭐ GSE324814 空间转录组学解析PD-1靶向IL15突变体在B16-F10-OVA荷瘤小鼠中的作用机制

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Tessier Julien ; Lee Joon SangSeries Type : OtherOrganism : Mus musculusKD050 is an anti-PD-1/IL-15 bi-functional antibody with strong PD-1 antagonist function, but lower lymphocyte stimulation enabled by a novel mutation on the IL-15. Here, we spatially characterized at RNA level the effect of mKD050 surrogate I in B16-OVA (melanoma) mouse model, in comparison with anti-mPD1 and mouse non-targetKD050 (mntKD050).
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4. ⭐ GSE328225 利用细胞因子信号重编程 CAR 可提高 CAR-T 细胞疗法在实体瘤治疗中的疗效并赋予持久的免疫记忆 [肿瘤浸润 CAR-T 细胞]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune、T cell、cytokine
• 📝 描述：Contributors : Rongchen Sun ; Xue Yang ; Changshuai CheSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensChimeric antigen receptor (CAR) T-cell therapy has shown remarkable efficacy in hematologic malignancies but remains limited in solid tumors because of the immunosuppressive microenvironment, tumor heterogeneity, poor immune-cell infiltration, and progressive T-cell dysfunction. Because cytokine costimulation is critical for maintaining T-cell fitness, we developed a modular engineering strategy, distinct from previous approaches based on direct insertion of large cytokine receptor fragments, in which the intracellular CAR signaling domain was reconstructed to incorporate compact IL-2/IL-15 receptor–derived activation motifs, thereby enabling antigen-dependent coactivation while preserving the overall architecture of the parental CAR. Through systematic screening, we identified S71 as the optimal construct, with significantly greater antitumor activity than other mutants across multiple solid and hematologic tumor targets. Mechanistically, S71 rewired CAR signaling and reprogrammed tumor-induced metabolic responses through a self-sustaining mechanism, improving mitochondrial function and supporting durable T-cell activity. Functionally, S71 promoted enhanced persistence and robust immune memory responses against solid tumors. These findings demonstrate that modular integration of cytokine signaling motifs into CAR intracellular domains can improve CAR-T-cell fitness and antitumor efficacy, and they establish S71 as a promising strategy for overcoming barriers to CAR-T-cell therapy in solid tumors.
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5. ⭐ GSE295237 单细胞空间转录组学研究表明，兴奋性神经元和星形胶质细胞特异性失调和异常相互作用易受 FCDI 影响 [空间转录组学]

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Yaqian Zhang ; Qihang Zou ; Yingying Liu ; Liemin ZhouSeries Type : OtherOrganism : Homo sapiensFocal cortical dysplasia (FCD) is a common neurodevelopmental disorder characterized by malformations of cortical development and is a leading cause of drug-resistant epilepsy. In this study, we employed single-nucleus RNA sequencing (snRNA-seq) and spatial transcriptomics sequencing (ST-seq) to investigate the molecular pathological features of FCD type I (FCDI) brain tissue from both cell type-specific and spatial heterogeneity perspectives. This integrated analysis provides novel theoretical insights into the pathogenesis of FCDI associated epilepsy.
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6. ⭐ GSE295236 兴奋性神经元和星形胶质细胞特异性失调和异常相互作用易受 FCDI 的影响，正如单细胞空间转录组学 [snRNA-seq] 所表明的那样。

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Yaqian Zhang ; Qihang Zou ; Yingying Liu ; Liemin ZhouSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensFocal cortical dysplasia (FCD) is a common neurodevelopmental disorder characterized by malformations of cortical development and is a leading cause of drug-resistant epilepsy. In this study, we employed single-nucleus RNA sequencing (snRNA-seq) and spatial transcriptomics sequencing (ST-seq) to investigate the molecular pathological features of FCD type I (FCDI) brain tissue from both cell type-specific and spatial heterogeneity perspectives. This integrated analysis provides novel theoretical insights into the pathogenesis of FCDI associated epilepsy.
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7. ⭐ GSE302659 肠道 LKB1 缺失驱动锯齿状癌症通路上的癌前程序 [bulkRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、pathway、regex:intestin(e|al)
• 📝 描述：Contributors : Susanna F Plugge ; Huying Ma ; Jelte Y van der Vaart ; Joep Sprangers ; Folkert Morsink ; Despina Xanthakis ; Cara Jamieson ; Kirsten Stroot ; Anneloes R Keijzer ; Thanasis Margaritis ; Tito Candelli ; Roy Straver ; Jeroen de Ridder ; Frank Holstege ; Wendy de Leng ; Johan Offerhaus ; Alessandra Merenda ; Madelon M MauriceSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusBackground & AimsHeterozygous inactivating mutations of Serine Threonine Kinase 11 (STK11)/Liver Kinase B1 (LKB1) are causative to the Peutz-Jeghers syndrome (PJS), a hereditary disease characterized by gastrointestinal hamartomatous polyposis and increased cancer susceptibility. While LKB1 loss-induced polyp formation has been ascribed to non-epithelial tissues, how LKB1 deficiency increases cancer risk of patients by altering the phenotypical landscape and hierarchical organization of epithelial tissues remains poorly understood.MethodsUsing CRISPR/Cas9, we generated heterozygous and homozygous Lkb1-deficient mouse small intestinal and human colon organoids. These organoids were characterized by an integrated approach that combines imaging, bulk and single-cell RNA sequencing and growth factor dependency assays. Our findings were validated in human PJS-derived tissues using immunohistochemistry and linked to colorectal cancer profiles using the TCGA cancer database.ResultsOur results reveal that heterozygous Lkb1 loss is sufficient to push intestinal cells into a premalignant transcriptional program associated with serrated colorectal cancer, which is further amplified by loss-of-heterozygosity. This altered epithelial growth state associates with persistent features of regeneration and enhanced EGFR ligand and receptor expression, conferring niche-independent growth properties to Lkb1-deficient organoids. Moreover, our newly generated LKB1-mutant signature is enriched in sporadic serrated colorectal cancer, and synergistic cooperation of Lkb1-deficiency with mutant Kras was experimentally confirmed by assessing organoid growth properties and transcriptomes.ConclusionsHeterozygous loss of LKB1 pushes intestinal cells into a chronic regenerative state which is amplified upon loss-of-heterozygosity. Lkb1-deficiency thereby generates fertile ground for serrated colorectal cancer formation in the intestine, potentially explaining the increased cancer risk observed in PJS.
• 🔗 查看原文

8. ⭐ GSE328224 利用细胞因子信号重编程 CAR 可提高 CAR-T 细胞疗法在实体瘤治疗中的疗效并赋予其持久的免疫记忆

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、T cell、cytokine
• 📝 描述：Contributors : Rongchen Sun ; Xue Yang ; Changshuai CheSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensChimeric antigen receptor (CAR) T-cell therapy has shown remarkable efficacy in hematologic malignancies but remains limited in solid tumors because of the immunosuppressive microenvironment, tumor heterogeneity, poor immune-cell infiltration, and progressive T-cell dysfunction. Because cytokine costimulation is critical for maintaining T-cell fitness, we developed a modular engineering strategy, distinct from previous approaches based on direct insertion of large cytokine receptor fragments, in which the intracellular CAR signaling domain was reconstructed to incorporate compact IL-2/IL-15 receptor–derived activation motifs, thereby enabling antigen-dependent coactivation while preserving the overall architecture of the parental CAR. Through systematic screening, we identified S71 as the optimal construct, with significantly greater antitumor activity than other mutants across multiple solid and hematologic tumor targets. Mechanistically, S71 rewired CAR signaling and reprogrammed tumor-induced metabolic responses through a self-sustaining mechanism, improving mitochondrial function and supporting durable T-cell activity. Functionally, S71 promoted enhanced persistence and robust immune memory responses against solid tumors. These findings demonstrate that modular integration of cytokine signaling motifs into CAR intracellular domains can improve CAR-T-cell fitness and antitumor efficacy, and they establish S71 as a promising strategy for overcoming barriers to CAR-T-cell therapy in solid tumors.
• 🔗 查看原文

9. ⭐ GSE291782 单细胞转录组学揭示巨噬细胞驱动的内皮间质转化和损伤肌肉修复调控

• ✍️ 作者：未知作者
• 🏷️ 关键词：macrophage、single-cell、transcriptomics
• 📝 描述：Contributors : Filipa Timóteo-Ferreira ; Riccardo Gamberale ; Cristiana Barone ; Mauro Bergamaschi ; Anna Sofia Tascini ; Raffaella Meneveri ; Emanuele Azzoni ; Silvia BrunelliSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThis study investigates the interactions between innate immune cells and vascular-associated cells within the regenerating muscle niche. Specifically, the transcriptomes of Cdh5-CreERT2:R26R-tdTomato mice were analysed following the partial ablation of infiltrating macrophages (MPs) to understand their influence on endothelial cell (EC) behaviour after injury. This work provides a comprehensive transcriptomic signature of the regenerative muscle niche and highlights key molecular interactions between MPs and ECs.
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10. GSE319884 基因组分析旨在识别接受免疫治疗的晚期恶性肿瘤患者中炎症性肿瘤表型的相关因素

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、regex:immuno(logy|therapy|suppression)
• 📝 描述：Contributors : Thomas F Gajewski ; Daniel J OlsonSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThis biomarker study will analyze tissues from patients with cancer who are receiving immunomodulatory treatment (or therapy that could be hypothesized to modulate the immune response), to correlate molecular/genetic features of the tumor cells, the host, and the intestinal microbiome with the immunologic phenotype of the tumor microenvironment. Recent data have suggested that patients with pre-existing T cell infiltration in the tumor microenvironment and/or an “inflamed” gene expression profile in tumor sites have better clinical outcome following treatment with several immunotherapeutic approaches. However, the mechanism by which this spontaneous anti-tumor immune response develops in only a subset of patients is not understood. Potential correlations between mutational patterns in the tumor, germline genetic polymorphisms, peripheral blood immune response parameters, and the composition of intestinal microbiota and the presence or absence of a T cell-infiltrated tumor microenvironment will be sought. Understanding these mechanisms will have important implications for future patient selection for treatment with immunotherapies and highlight new potential pathways for therapeutic development. Mechanisms of secondary resistance to immunotherapies also will be interrogated using tissues obtained at time of recurrence.
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1. Wobble Genomics 将在 2026 年美国癌症研究协会 (AACR) 年会上展示其最新的 mRNA 测序研究成果。

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、genomics
• 📝 描述：RNA sequencing of full-length mRNA from blood supports liquid biopsy approaches for selecting antibody-drug conjugate therapies in breast cancer, improving precision treatment decisions without invasive biopsies…
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2. 科学家震惊：细菌重塑DNA机制，塑造细胞形态

• ✍️ 作者：未知作者
• 🏷️ 关键词：bacteria、regex:bacter(ia|ial|ium)
• 📝 描述：Cyanobacteria—ancient microbes that oxygenated Earth and made complex life possible—are still revealing surprises billions of years later. Scientists have now discovered that a molecular system once used to separate DNA has been repurposed into something entirely different: a structure that shapes the cell itself.
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3. 费城儿童医院的研究人员开发出一种用于诊断罕见疾病的新型RNA测序平台。

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：RNA sequencing using targeted long-read approaches enables detection of disease-causing variants by revealing how genetic changes disrupt full-length RNA molecules…
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4. 健康人肝脏的空间图谱揭示了基因表达的新见解

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial
• 📝 描述：RNA sequencing combined with spatial transcriptomics maps gene activity in the healthy human liver, revealing zonation patterns and early cellular changes linked to steatosis
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5. 这种缺失的维生素或许能阻止癌细胞的扩散。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Cancer cells are known for their “glutamine addiction,” but many can escape this weakness by switching to alternative fuels. Researchers found that vitamin B7 acts like a metabolic “license,” enabling this escape route through a key enzyme. Without biotin, cancer cells lose that flexibility and stop growing. Mutations in a cancer-linked gene can make this vulnerability even stronger, offering a promising new target for therapy.
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• GSE328332 空间分辨的肥胖驱动的早期乳腺癌分子变化
• GSE313676 即时荧光寿命成像显微镜揭示乳腺癌肿瘤周围微环境中基质细胞的机械代谢重编程
• GSE328334 利用高细胞密度生物打印技术在胶质母细胞瘤中形成精确且可重复的低氧肿瘤微环境
• GSE328235 卡非佐米相关HSV-1脑炎小鼠模型的单细胞测序
• GSE328464 靶向 CCR1 介导的巨噬细胞表型转换以缓解间质性膀胱炎的膀胱疼痛和尿功能障碍
• GSE328341 衰老延迟伤口愈合中细胞衰老反应减弱和改变
• GSE310322 绘制自关联染色质枢纽图谱，揭示 Id 蛋白是耗竭 T 细胞命运的关键决定因素
• GSE288427 早衰症DNA修复缺陷小鼠衰老和饮食限制引起的翻译变化
• GSE288421 衰老和饮食限制对早衰症 DNA 修复缺陷小鼠的翻译变化 [Ribo-Seq]
• GSE324714 获得性遗传和细胞状态改变是IDH突变型胶质瘤进展的基础[共培养实验]
• GSE324694 获得性遗传和细胞状态改变是IDH突变型胶质瘤进展的基础 II
• GSE324481 获得性遗传和细胞状态改变是IDH突变型胶质瘤进展的基础
• GSE305298 RNA-seq 数据来自人类 HCT116 野生型细胞、HCT116 DNMT1 低表达型细胞和 HCT116 UHRF1 低表达型细胞。
• GSE328230 ATAC-seq 分析揭示 KLF2 调控 HCC 中的染色质可及性程序
• GSE326327 NanoString nCounter 小鼠泛癌免疫谱分析：体外慢性 PMS2 抑制和体内抗 PD-1 治疗后 CT26 肿瘤的免疫分析
• GSE295220 FABP4介导的脂肪酸转运促进铂耐药卵巢癌细胞的增殖和存活
• GSE264529 格尔塞尼辛破坏了秀丽隐杆线虫的肠道屏障
• GSE230252 产前慢性应激暴露诱导的Th17/Treg细胞失衡与子代PI3K/Akt/NF-κB信号通路的激活有关
• GSE294576 menin 抑制对人类 AML 细胞系 MV4-11 的影响 [ATAC-seq]
• GSE286215 体内B细胞多样化机制的时间映射