详细内容（前10条）

1. ⭐ GSE316356 体内四价CAR-巨噬细胞作为细胞疫苗，可通过抗原扩散抑制实体瘤并克服肿瘤异质性

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、vaccine、macrophage、antigen
• 📝 描述：Contributors : Shaolong Zhang ; Hengxing Lu ; Hailing Zhang ; Qixin Wu ; Xizhong DingSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Mus musculusWe designed a quadrivalent in vivo CAR-engineered macrophage for treating solid tumors by the LNP-mRNA system. Mechanically, we found that in vivo engineered CAR macrophages can promote the formation of T-cell immune memory against neoantigens through antigen spreading. To further elucidate this phenomenon, we treated orthotopic HCC model mice with PBS, LNP-GPC3 CAR, or LNP-GPC3 CAR-Super IL-2 and subsequently collected splenocytes from these three groups for transcriptomic and TCR sequencing analyses. Based on data from transcriptome and TCR sequencing, we propose a two-signal model for T-cell activation: the GPC3 CAR provides the primary signal by recognizing and presenting tumor antigens, while the secreted Super IL-2 supplies the additional signal necessary for robust T-cell clonal expansion. These findings provide novel mechanistic insights into the anti-tumor activity of in vivo engineered CAR macrophages.
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2. ⭐ GSE302642 IDH突变型胶质瘤起源于携带初始驱动突变的胶质祖细胞（相关登录号：GSE275791）——空间转录组学数据集

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Jung Won Park ; Jeong Ho LeeSeries Type : OtherOrganism : Homo sapiensDiscovering the cell-of-origin harboring the initial driver mutation provides a fundamental basis for understanding tumor evolution and development of new treatments. For isocitrate dehydrogenase (IDH)-mutant gliomas–the most common malignant primary brain tumors in adults under 50–the cell-of-origin remains poorly understood. Here, using patient brain tissues and genome-edited mice, we identified glial progenitor cells (GPCs), including oligodendrocyte progenitor cells (OPCs), as the glioma-originating cell type harboring the IDH mutation as the initial driver mutation. We conducted comprehensive deep sequencing, including droplet digital PCR and deep panel and amplicon sequencing to 142 tissues from 70 patients (32 IDH-mutant gliomas and 38 IDH-negative controls) comprising tumors, histologically normal peritumoral regions or subventricular zones (SVZs), and blood. Surprisingly, low-level IDH mutation was found in the normal peritumor away from the tumor in 37.9% (11 of 29) of IDH-mutant glioma patients, whereas no IDH mutation was detected in the SVZ. Integrating cell-type–specific mutations analysis, the direction of clonal evolution, spatial transcriptomics from patient brains and a novel IDH-mutant glioma mouse model arising from mutant OPCs, we determined that GPCs, including OPCs, harboring the initial driver mutation are responsible for the development and evolution of IDH-mutant gliomas. In summary, our results demonstrate that GPCs containing the IDH mutation are the cells-of-origin harboring the initial driver mutation in IDH-mutant gliomas.
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3. ⭐ GSE314261 圣裘德终生队列中儿童癌症幸存者治疗和生命历程暴露与不良健康结局的全基因组DNA甲基化谱分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、epigenome、methylation
• 📝 描述：Series Type : Methylation profiling by genome tiling arrayOrganism : Homo sapiensLong-term survivors of childhood cancer experience treatment-related cardiotoxicity among a broad spectrum of chronic health conditions, which may be further aggrevated by suboptimal life-course social/behavioral/environmental exposures. Epigenetic mechanisms, particularly DNA methylation (DNAm), provide a potential link through which these exposures become biologically embedded and subsequently influence long-term health outcomes. Epigenome-wide association studies (EWAS) identified DNAm signatures associated with both treatment effects as well as life-course exposures. In parallel, DNAm variations were also evaluated in relation to cardiometabolic risk factors, cardiovascular diseases, and other chronic health conditions, revealing individual CpG sites or genes/geomic regions where these CpGs reside linked to clinically relevant phenotypes. Together, these findings support DNAm as a molecular interface connecting diverse exposures to adverse health outcomes. In addition, epigenetic age acceleration, assessed using DNAm-based aging biomarkers, was observed among survivors exposed to cancer treatments. Epigenetic age acceleration mediated a substantial proportion of the associations between cancer treatment exposures and cardiometabolic risk factors or cardiovascular diseases, supporting accelerated biological aging as a key pathway linking cancer treatment to long-term morbidity. Lifestyle and health behaviors, as well as social vulnerability and psychosocial stress, were also associated with variations in epigenetic age acceleration, highlighting the potential modifiability of aging-related pathways in ameliorating late-effects among childhood cancer survivors. In conclusion, these findings establish DNAm—captured through EWAS signatures and epigenetic age acceleration—as central molecular mechanisms linking treatment effects and life-course exposures to cardiotoxicity along with other chronic health conditions in childhood cancer survivors. This integrative epigenetic framework supports the use of DNAm-based biomarkers for risk stratification and nominates modifiable pathways as potential intervention targets to improve long-term survivorship outcomes.
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4. ⭐ GSE315828 9-PAHSA 调控 TCR-T 细胞命运以增强抗肿瘤免疫力

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immunity、T cell
• 📝 描述：Contributor : Xiaozhen ZhangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusWe identify the endogenous lipid 9-PAHSA as a potent enhancer of T cell anti-tumor function and stemness, validated in murine models and a clinical trial. Mechanistically, we identify ICAM2 as a direct surface sensor for 9-PAHSA and delineate a downstream signaling axis whereby the ICAM2-Ezrin-mTORC2 cascade drives FOXO1 O-GlcNAcylation at S318, facilitating its nuclear translocation to enact a stem-like transcriptional program. Translating this discovery, we engineered armored human TCR-T cells with potentiated ICAM2 expression, which achieve superior tumor control through their enhanced intrinsic efficacy and a remarkable ability to ignite a coordinated and durable host anti-tumor immune response. Our work establishes a new paradigm of metabolite-sensing in T cell biology and provides a compelling therapeutic strategy to potentiate cellular immunotherapy for intractable cancers.
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5. GSE316069 单细胞分析揭示溃疡性结肠炎中γδ T细胞亚群的多样性

• ✍️ 作者：未知作者
• 🏷️ 关键词：T cell、single-cell
• 📝 描述：Contributor : Jakob ArnoldSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Homo sapiensγδ T cells maintain intestinal immune homeostasis, but their contributions to human ulcerative colitis (UC) are poorly understood. We characterized γδ T cells in intestinal biopsies obtained from patients with UC and healthy donors using single-cell RNA sequencing, T cell receptor profiling, and mass cytometry. UC reduced CD103+Vγ4Vδ1+ intraepithelial γδ lymphocytes (γδ IELs) and increased γδ T cell subsets with stem-like phenotypes expressing T cell factor-1 (TCF-1) and programmed cell death receptor 1 (PD-1), or effector-like phenotypes expressing granzyme B, perforin, and T-box expressed in T cells (T-bet). γδ T cell composition changes in UC correlated with decreased expression of epithelial BTNL3 and BTNL8 and increased BTN3A1 and BTN3A3 , suggesting altered recruitment and activation . Clinical improvement recovered γδ IELs and reduced inflammation-associated subsets. Inflammation-associated changes were observed in peripheral blood γδ T cells. Thus, distinct γδ T cell subsets in different niches exert protective or pathogenic functions in UC.
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6. GSE315883 同源重组功能正常的列腺癌中 AR 靶向治疗与 PARP 抑制之间缺乏协同作用 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、ATAC-seq
• 📝 描述：Contributors : Nicole A Traphagen ; Myles BrownSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensRecent clinical trials have explored the combination of androgen receptor (AR) pathway inhibitors and poly (ADP-ribose) polymerase (PARP) inhibitors as a potential treatment for castration-resistant prostate cancer. This combination treatment is based on the premise that AR directly regulates expression of DNA repair genes, leading to synergy between PARP and AR inhibition. Despite some promising preclinical evidence, this combination therapy has shown limited efficacy in patients with homologous recombination (HR)-proficient tumors. To investigate this discrepancy between preclinical and clinical results, we profiled the effects of PARP inhibition in prostate cancer models in the presence or absence of AR inhibition. Surprisingly, AR inhibition impaired response to PARP inhibitors in castration-sensitive cells and had no effect on response in castration-resistant cells. AR inhibition also did not regulate DNA repair in either the castration-resistant or castration-sensitive setting. Instead, we find that cell cycle progression is required for response to PARP inhibition in homologous-recombination proficient prostate cancer.
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7. GSE308003 DAXX 指导精子发生过程中 H3.4 到 H3.3 组蛋白的替换 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、histone
• 📝 描述：Contributors : Satoshi H Namekawa ; Yu-Han YehSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusDuring spermatogenesis, extensive chromatin remodeling and histone replacement reshape the male germline epigenome. While HIRA is known to mediate transcription-coupled incorporation of histone variant H3.3, we identify DAXX as a key histone chaperone directing genome-wide, transcription-dependent replacement of H3.4 (H3T) with H3.3 on autosomes during male meiosis. Simultaneously, DAXX also directs transcription-independent H3.4-to-H3.3 replacement on the sex chromosomes during meiotic sex chromosome inactivation (MSCI). These distinct, chromosome-specific modes of DAXX-mediated H3.3 deposition are essential for epigenomic integrity in the male germline. Loss of DAXX disrupts this process, leading to widespread transcriptional dysregulation in haploid round spermatids and male infertility.
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8. GSE297836 ROR1-PI3K/AKT信号通路驱动TP53突变卵巢癌对细胞周期阻滞的适应性耐药

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、resistance
• 📝 描述：Contributors : Frida Rantanen ; Alice Dini ; Harlan Barker ; Daniela UngureanuSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensWe developed long-term resistant (lt-res, several months) pre-clinical models to adavosertib (ADA) and paclitaxel (PTX). We identified distinct transcriptomic and morphological changes in the ovarian cancer lt-res models. ADA resistance involves signaling pathway alterations that allow cells to maintain unchecked proliferation, while PTX resistance primarily stems from structural changes within the cell, affecting microtubules and drug efflux. Upregulation of receptor tyrosine kinases, such as ROR1, was observed in both ROR1-positive ADA and PTX lt-res models. Targeting ROR1 with zilovertamab-vedotin, a monoclonal antibody-drug conjugate, resulted in enhanced cytotoxicity, demonstrating a new approach against recurrent drug-resistant ovarian cancer.
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9. GSE316347 巨噬细胞免疫活性结肠组装体用于神经炎症诱导的结肠运动障碍的功能研究

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、macrophage
• 📝 描述：Contributors : Claudia Collier ; Karla Ortega Sandoval ; Aelita Salikhova ; Shrinarayanee Rengarajan ; Anvitha Tharakesh ; Alana Aristimuno Millan ; Shanthi Srinivasan ; Shreya A RaghavanSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusFunctional gastrointestinal disorders (FGIDs) affect ∼40% of the global population and are frequently characterized by colonic dysmotility. Symptomatic manifestations of colonic dysmotility significantly reduce quality of life in inflammatory bowel disease (IBD), diabetes, and Gulf War Illness (GWI). Current in vitro models lack the integration of functional physiology with immune and neuronal complexity required to establish causal links between neuroinflammation and dysmotility. Here, an immune-competent bioengineered colon assembloid is introduced that integrates multiple cell types of the external colonic wall, along with functional readouts of motility. Within bioengineered colon assembloids, various inflammatory insults resulted in enteric neuroinflammation, cascading to changes in colonic motility. Key mechanisms of dysmotility following inflammatory insult within the bioengineered colon assembloids included impaired neuronal regeneration, and aberrant smooth muscle remodeling. The bioengineered colon assembloid model mimicked diverse aspects of enteric neuroinflammation. Ultimately, the platform offers a physiologically relevant avenue to interrogate neuroimmune crosstalk and dissect mechanisms of colonic dysmotility, paving the way to new therapeutic strategies to improve colonic motility.
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10. GSE312264 通过非典型蛋白激酶C优化肠道葡萄糖张力效应

• ✍️ 作者：未知作者
• 🏷️ 关键词：kinase、regex:intestin(e|al)
• 📝 描述：Contributors : Chan Woo Kang ; Zhen-Yu Hong ; Hyeonuk Jeon ; Sungsoon Fang ; Insuk Sohn ; Cheol Ryong KuSeries Type : Expression profiling by high throughput sequencingOrganism : Rattus norvegicusIntestinal glucotonic transformation, defined as increased intestinal serum glucose uptake and secretion into the lumen, influences bariatric surgery-associated glycermic control. This study aims to identify downstream molecules that mediate the function of the identified target as an effective intestinjal glucotonic activator. Altered transcriptomes were evaluated in variable intestinal glucotonic models and big data-based drug discovery systems. Protein kinase C (PKC) activation mimicked transcriptome alterations observed during intestinal glucotonic transformation. Among the PKC subfamilies, atypical PKC (aPKC) promoted glucose transporter 1 (GLUT1)-mediated intestinal glucotonic transformation without inducing oncogenic proliferation. Intestinal aPKC activation via a transposon expression vector induced serum glucose uptake into intestinal tissues and excretion into the lumen. Prostratin, a non-tumorigenic phorbol ester, activated aPKC and induced a similar glucotonic effect. Collectively, we identified the prostratin and aPKC/GLUT1 signaling pathways as effective targets for treating diabetes, providing insights into the future development of antidiabetic and weight loss drugs.
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1. 西奈山的研究人员帮助创建了多发性骨髓瘤患者骨髓中规模最大的免疫细胞图谱

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune
• 📝 描述：Single-cell RNA sequencing maps nearly 1.5 million bone marrow immune cells in multiple myeloma, revealing immune dysfunction patterns that may help predict relapse risk…
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2. RNA-MosaicHunter——从批量RNA测序数据中精确检测体细胞单核苷酸变异

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq
• 📝 描述：RNA-MosaicHunter leverages RNA sequencing to accurately detect somatic single-nucleotide variants, revealing elevated mutation burdens in Alzheimer’s cortex and offering insights into variant roles across tissues…
• 🔗 查看原文

• GSE277396 原代小胶质细胞脂质代谢（scRNA-Seq）
• GSE271037 脾脏和脊髓T细胞的单细胞RNA测序
• GSE316044 通过 RNA-seq 分析，研究了在含血清培养基和添加小分子的无血清培养基中培养的牛肌肉干细胞的转录组谱。
• GSE306747 RHOA 控制侵袭性淋巴瘤中的致癌 B 细胞受体信号传导
• GSE315878 同源重组功能正常的列腺癌中AR靶向治疗与PARP抑制剂之间缺乏协同作用
• GSE312061 肝脏特异性递送MDM2反义寡核苷酸可对抗饮食诱导的代谢功能障碍相关的脂肪肝疾病
• GSE308667 DAXX 指导精子发生过程中 H3.4 向 H3.3 组蛋白的替换
• GSE308004 DAXX 指导精子发生过程中 H3.4 到 H3.3 组蛋白的替换 [Cut & Run]
• GSE297435 基于 dCas9 的 DNA 甲基化编辑系统的特异性和稳定性的系统比较 [RNAseq_secondRun]
• GSE297432 基于 dCas9 的 DNA 甲基化编辑系统的特异性和稳定性的系统比较 [亚硫酸氢盐测序（简化表示）_TMS2]
• GSE297430 基于 dCas9 的 DNA 甲基化编辑系统的特异性和稳定性的系统比较 [RNAseq_firstRun]
• GSE297389 基于 dCas9 的 DNA 甲基化编辑系统的特异性和稳定性的系统比较 [亚硫酸氢盐测序（简化表示）_TMS1]
• GSE297385 基于 dCas9 的 DNA 甲基化编辑系统的特异性和稳定性的系统比较 [EPIC]
• GSE296999 用于研究体内高危 BRAFV600E 驱动的结直肠癌的新型同源细胞系 [RNA-seq_organoids]
• GSE296998 用于研究体内高危 BRAFV600E 驱动的结直肠癌的新型同源细胞系 [RNA-seq_NaJa]
• GSE296978 H4K16 酰化作用微调对短链酰基辅酶A脱氢酶缺乏的转录反应（RNA-seq）
• GSE296977 H4K16酰化作用微调对短链酰基辅酶A脱氢酶缺乏的转录反应（ChIP-seq）
• GSE296976 H4K16 酰化作用微调对短链酰基辅酶A脱氢酶缺乏的转录反应（ATAC-seq）
• GSE275791 IDH突变型胶质瘤起源于携带初始驱动突变的胶质祖细胞
• GSE274605 突触核蛋白病模型中能量代谢改变和昼夜节律紊乱的分子特征
• GSE202762 受体酪氨酸激酶在信号响应基因处磷酸化 RNA 聚合酶 II [RNA-seq]
• GSE202761 受体酪氨酸激酶在信号响应基因处磷酸化 RNA 聚合酶 II [ChIP-seq]
• GSE312072 等位基因染色质结构是印记域的普遍特征，并与 Mest-Copg2 位点的顺式作用长链非编码 RNA 协同发挥作用 [RNA-seq]
• GSE312071 等位基因染色质结构是印记域的普遍特征，并与 Mest-Copg2 位点的顺式作用长链非编码 RNA 协同作用 [Capture Hi-C]
• GSE312069 等位基因染色质结构是印记域的普遍特征，并与 Mest-Copg2 位点的顺式作用长链非编码 RNA 协同发挥作用 [ATAC-seq]
• GSE308063 弥漫性低级别和高级别胶质瘤细胞系生物样本库的特征分析
• GSE306737 转录因子 Etv3 控制树突状细胞的耐受功能（来自混合骨髓嵌合体的 Etv3 KO migDC 的 RNA-seq）
• GSE306682 转录因子 Etv3 控制树突状细胞的耐受功能（Etv3 KO GM-DC 的 RNA-seq）
• GSE306680 转录因子 Etv3 控制树突状细胞的耐受功能（Etv3 KO Tregs 的 RNA-seq）
• GSE306414 探索弥漫性低级别星形细胞瘤细胞系 LGG275 中静止期 (P27+) 和有丝分裂期 (P27-) 胶质瘤细胞的分子特征和特性
• GSE305451 揭示低级别胶质瘤细胞系LGG275中星形胶质细胞样细胞和少突胶质细胞样细胞的分子特征
• GSE300165 高通量测序法对肌球蛋白VI进行表达谱分析
• GSE286157：培养6天未照射或经20mGy照射的LT-HSC的HSPC转录组分析
• GSE281655 遗传性内质网应激损害线粒体代谢，导致低剂量照射造血干细胞耗竭 [RREMseqHSC]
• GSE281654 遗传性内质网应激损害线粒体代谢，导致低剂量照射造血干细胞耗竭 [ATACseqHSC]
• GSE277426 染色质组织对 I 型干扰素反应的调控（KO HoxB8-FL 细胞的 ATAC-seq）
• GSE277425 染色质组织对 I 型干扰素反应的调控（IRF8 KO 脾脏 pDC 的 ATAC-seq）
• GSE277424 染色质组织对 I 型干扰素反应的调控（SMC3 KO pDC 激活的 RNA-seq）
• GSE277423 染色质组织对 I 型干扰素反应的调控（L929 成纤维细胞 +/- SEV 的 RNA-seq）
• GSE277422 染色质组织对 I 型干扰素反应的调控（IFN-I TB2/TB4 DKO FL-BMDC 激活的 RNA-seq）
• GSE277289 黏连蛋白介导的染色质重塑控制传统树突状细胞的分化和功能（Hoxb8-FL 分化的 RAD21 和 CTCF ChIP-seq）
• GSE277288 染色质组织对 I 型干扰素反应的调控（L929 成纤维细胞 +/- SEV 的 ATAC-seq）
• GSE277287 染色质组织对 I 型干扰素反应的调控（L929 成纤维细胞的 Hi-C +/- SEV）
• GSE277284 黏连蛋白介导的染色质重塑控制传统树突状细胞的分化和功能（HoxB8-FL 分化的 Hi-C）
• GSE277283 黏连蛋白介导的染色质重塑控制传统树突状细胞的分化和功能（SMC3 KO FL-BMDC 的 Hi-C）
• GSE271283 黏连蛋白介导的染色质重塑控制传统树突状细胞的分化和功能（SMC3 KO 脾脏 cDC 的 RNA 测序）
• GSE271282 黏连蛋白介导的染色质重塑控制传统树突状细胞的分化和功能（IRF8 KO HoxB8-FL DCs 的 RNA-seq）
• GSE270821 染色质组织对 I 型干扰素反应的调控（HoxB8-FL pDC 激活的 ATAC-seq）
• GSE270816 黏连蛋白介导的染色质重塑控制传统树突状细胞的分化和功能（SMC3 KO FL-BMDC 分化和激活的 RNA-seq）
• GSE316074 免疫抑制和细胞功能障碍的转录组特征可区分树突状细胞中潜伏型和转录活跃型 HIV-1 感染
• GSE306618 淋巴系统紊乱是肺移植纤维化的驱动因素
• GSE304876 Ramalin 通过靶向 BACE1、HDAC6 和 MAPK 通路改善阿尔茨海默病病理
• GSE303990 培养的小鼠视网膜祖细胞的表观遗传学和转录组学分析
• GSE276936 原代小胶质细胞的脂质代谢
• GSE316149 单核细胞衍生的IL-10驱动疼痛持续时间的性别差异
• GSE316046 包含从对照组和 DHEA 处理组小鼠中分离的 CD8+ T 细胞的单细胞 RNA 测序数据
• GSE316039 研究发现 MGST3 下调促进结直肠癌进展
• GSE315814 NONO-HOXA1-Wnt轴在心肌细胞分化中的关键作用[scRNA-seq]
• GSE312736 转录组学揭示了在逐渐氮缺乏条件下紫球藻的代谢重编程和胞外多糖合成