科研日报 2026-04-29
📅 Daily Report - 2026-04-29
今日筛选出 62 条内容,来自 2 个来源
🤖 今日AI智能总结
🧬 数据前沿
今日焦点: 文章揭示了IDH-突变胶质瘤中DNA甲基化改变驱动疾病进展的新机制,以及EZH2抑制剂在重塑三维染色质结构、诱导小细胞肺癌免疫原性表型方面的潜力。
主要方向:
- 肿瘤微环境与免疫治疗:研究IL1RAP作为胰腺癌化学免疫治疗的靶点,以及SIRPα和CD47信号通路在T细胞耗竭和抗肿瘤免疫抑制中的作用。
- 肠道微生物与疾病:探索Rothia mucilaginosa通过重塑肠道菌群和激活神经通路缓解便秘,以及微塑料在炎症性肝病中的影响。
- 发育与疾病机制:解析DNA甲基化在IDH-突变胶质瘤进展中的作用,以及Prop1基因敲入斑马鱼在早期垂体发育单细胞转录组学研究中的应用。
技术亮点:
- 空间转录组学:在小鼠T细胞转移性结肠炎、犬骨肉瘤和微塑料诱导的肝脏炎症中应用,精细解析细胞空间异质性。
- 多组学整合:结合RNA-seq、ATAC-seq和甲基化测序,深入揭示基因调控网络和表观遗传机制。
🧪 博客更新
今日焦点: 新型RNA测序方法实现RNA结合蛋白靶点高精度定位,重大研究揭示农药暴露显著提升癌症风险。
主要方向:
- 基因调控机制研究
- 环境因素与癌症风险评估
技术亮点:
- 基于RNA测序的新型高精度蛋白靶点定位技术
- 复杂农药混合物对癌症风险影响的量化研究
📚 分类浏览
🧬 数据前沿 (60条)
详细内容(前10条)
1. ⭐ GSE236890 小鼠T细胞转移性结肠炎的纵向空间转录组学
- ✍️ 作者:未知作者
- 🏷️ 关键词:T cell、spatial、spatial transcriptomics、transcriptomics
- 📝 描述:Contributors : Jennifer Fransson ; Chiara Sorini ; Eduardo J VillablancaSeries Type : OtherOrganism : Mus musculusIn order to describe in detail the processes involved in chronic colitis, we performed scRNA-seq at multiple time points in a CD45RBhi T cell transfer colitis mouse model. These data were compared to bulk RNAseq and scRNAseq results from the same mice within the same study. Spatial trancriptomics were analyzed by performing NMF to identify spatial patterns of gene expression.
- 🔗 查看原文
2. ⭐ GSE319612 粘液罗氏菌通过重塑肠道菌群和激活神经活性通路缓解便秘
- ✍️ 作者:未知作者
- 🏷️ 关键词:pathway、gut、regex:gut(-?microbiome)?
- 📝 描述:Contributors : Peishi Jiang ; Xiaoqing Yang ; Chenghao Zhang ; Zhiyue Guo ; Yuwei Li ; Chen XuSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusConstipation affects approximately 15% of the global population, and gut microbiota dysbiosis is implicated in its pathogenesis. Rothia mucilaginosa, a commensal bacterium with established anti-inflammatory properties, has not been previously investigated for its effects on intestinal function. In this study, we evaluated the therapeutic potential of R. mucilaginosa in a loperamide-induced constipation mouse model using multiomics approaches. Twenty-six SPF male C57BL/6 mice were divided into normal control (NC, n=8), constipation model control (MC, n=8), and R. mucilaginosa-treated (RG, n=10) groups. R. mucilaginosa intervention significantly improved fecal output and induced gut microbiota remodeling, including enrichment of Akkermansia muciniphila and Alistipes finegoldii. To characterize host molecular responses, RNA-seq was performed on colon tissues to identify differentially expressed genes and pathways associated with constipation alleviation, with particular focus on neuroactive pathway activation.
- 🔗 查看原文
3. ⭐ GSE310710 事后试验和临床前数据表明,IL1RAP 是肿瘤微环境的脆弱性因素,可提高胰腺癌化疗免疫疗法的敏感性
- ✍️ 作者:未知作者
- 🏷️ 关键词:tumor、cancer、tumor microenvironment
- 📝 描述:Contributors : Erin M Dickey ; Harper M Marsh ; Camilla Rydberg Millrud ; Haleh Amirian ; Karthik Rajkumar ; Manan Patel ; Andrew Adams ; Nipun B Merchant ; Anna Bianchi ; Peter J Hosein ; David Lidberg ; Jashodeep DattaSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusINTRODUCTION: Pancreatic ductal adenocarcinoma (PDAC) remains highly resistant to chemotherapy and immunotherapy due to a tumor microenvironment (TME) dominated by myeloid-stromal immunosuppressive circuitries and T-cell dysfunction. Key mediators of this chemoimmunoresistance are interleukin-1 (IL-1) family cytokines (IL-1α/β, IL-33, IL-36), which converge on IL-1 receptor accessory protein (IL1RAP) signaling to reinforce a tolerogenic, pro-inflammatory TME. We hypothesized that IL1RAP-expressing myeloid-stromal compartments sustain a therapeutic barrier in PDAC, and that disrupting this via pharmacologic IL1RAP inhibition could reprogram the TME to enhance chemoimmunotherapy efficacy. METHODS: Chemoresistance in PDAC samples from Human Tumor Atlas Network (HTAN) was stratified by cell-type IL1RAP expression. Clinical outcomes in patients treated with anti-IL1RAP Ab nadunolimab (Nadu)+gemcitabine+nab-paclitaxel (GnP) in Phase II CANFOUR trial (NCT03267316) were stratified by immune and stromal IL1RAP expression; paired PDAC biopsies pre-/post-treatment were analyzed by mIF. Preclinical studies were conducted in the IL1RAPhi stromatogenic Ptf1aCre/+;LSL-KrasG12D;Tgfbr2fl/fl (PKT) murine model. Nadu surrogate Ab-treated tumors were analyzed by scRNAseq, flow cytometry, and histology. Combination Nadu, GnP, and anti-PD1 therapy was tested in survival \ studies. RESULTS: In HTAN dataset, IL1RAP expression was elevated across multiple TME compartments—myeloid, cancer-associated fibroblast (CAF), and tumor cells; notably, IL1RAP was selectively enriched in chemotherapy-resistant (vs sensitive) samples, predominantly in myeloid and CAF/stromal transcriptomes. Stratification of evaluable specimens from CANFOUR trial revealed correlation between high stromal/CAF (p=0.0058) and myeloid (p=0.014) IL1RAP expression and prolonged duration of response to Nadu+GnP. In PKT mice, Nadu treatment reduced tumor volume (p=0.019) and stromal fibrosis. Flow cytometry showed reduced trafficking/persistence (p=0.0077) and increased T-cell abundance (p=0.0033), which were corroborated by mIF in paired human PDAC biopsies pre/post Nadu treatment, showing diminished CD11b+CD14+/CD1…
- 🔗 查看原文
4. ⭐ GSE292130 IDH突变型胶质瘤DNA甲基化的纵向变化通过改变细胞状态分化促进疾病进展[scRNA-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:glioma、scRNA、methylation
- 📝 描述:Contributors : Masashi Nomura ; Ramya Ravirum ; Joshua S. Schiffman ; Dan A. Landau ; Mario L. SuvàSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensIDH-mutant gliomas are initially slow-growing but invariably progress to fatal disease. Major gaps remain in our understanding of the molecular underpinnings and cellular dynamics that drive IDH-mutant evolution. To address this, we integrated joint-capture multi-omic single-cell profiling of DNA methylation, transcriptome and genotype in a longitudinal cohort of 35 IDH-mutant gliomas. Transcriptional and epigenetic comparisons of cell states during glioma progression revealed increased stem-like states, decreased differentiation and identified potential cell states regulators. Single-cell DNA methylation analysis demonstrated methylation loss in progressed tumors, however global DNA methylation was similar between different malignant cells states within individual tumors. This suggests that lower DNA methylation is not due to a change in cell state composition, but rather that it may alter cell state landscapes. To address whether decreased methylation in progressed tumors affects cellular dynamics, we applied a quantitative framework to directly measure cell state heritability and plasticity based on transcriptional annotation of high-resolution phylogenetic trees in clinical samples. Our analysis suggested that decreased methylation reshapes cellular architecture to increased heritability of stem-like states and decreased differentiation. Our study provides insight into the functional impact of DNA methylation on glioma evolution, integrating transcriptional cancer cell states with epigenetic encoding and cell state transition dynamics during cancer progression.
- 🔗 查看原文
5. ⭐ GSE299494 新鲜冷冻犬骨肉瘤肿瘤样本的空间转录组测序
- ✍️ 作者:未知作者
- 🏷️ 关键词:tumor、sequencing、spatial
- 📝 描述:Contributors : Rebecca Nance-Richey ; Rowan J Milner ; Leah AckermanSeries Type : OtherOrganism : Canis lupus familiarisOsteosarcoma (OSA) is a highly aggressive and heterogeneous bone cancer in dogs and humans, with limited treatment advances over decades. Using the 10x Genomics Visium spatial transcriptomics platform, this study analyzed 14 canine OSA tumors to map gene expression patterns within the tumor microenvironment and correlate them with patient outcomes. Spatial and integrated analyses revealed conserved transcriptional clusters and immune cell infiltration patterns, including macrophage-associated regions in long-term survivors. Deconvolution with single-cell RNA-seq data identified co-localizing immune cell populations such as mast cells with osteoclasts and NKT cells with regulatory dendritic cells. These findings provide insight into tumor heterogeneity and immune landscapes, offering potential targets for future therapies in both species.
- 🔗 查看原文
6. ⭐ GSE256234 小鼠IL10KO结肠炎的纵向空间转录组学
- ✍️ 作者:未知作者
- 🏷️ 关键词:spatial、spatial transcriptomics、transcriptomics
- 📝 描述:Contributors : Jennifer Fransson ; Chiara Sorini ; Eduardo J VillablancaSeries Type : OtherOrganism : Mus musculusIn order to describe in detail the processes involved in chronic colitis, we performed spatial transcriptomics at multiple time points in a IL10KO colitis mouse model. These data were compared to bulk RNAseq and scRNAseq (GSE255423) results from the same mice within the same study.
- 🔗 查看原文
7. GSE329205 EZH2 抑制重塑 3D 染色质结构,诱导小细胞肺癌的免疫原性表型 [RNA-Seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、RNA-seq
- 📝 描述:Contributors : Sana Parveen ; Victor X Jin ; Hui-Zi ChenSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensEZH2, the enzymatic core of the Polycomb Repressive Complex 2 (PRC2), is overexpressed in small cell lung cancer (SCLC). Previous studies have shown that EZH2 enforces epigenetic silencing of immune and DNA repair genes, including Class I MHC molecules (HLA‑A/B/C) and SLFN11. To investigate how EZH1/2 inhibition reshapes the 3D chromatin landscape and its relationship to transcriptional regulation, we performed multi‑omic profiling of a neuroendocrine SCLC cell line (NCI‑H146) treated with the dual EZH1/2 inhibitor valemetostat for 9 days. We employed Micro‑C sequencing for high‑resolution 3D genome mapping, ATAC‑sequencing for chromatin accessibility profiling, and RNA‑sequencing for whole‑transcriptome analysis. This is the RNA‑sequencing dataset.
- 🔗 查看原文
8. GSE329204 EZH2 抑制重塑 3D 染色质结构,诱导小细胞肺癌的免疫原性表型 [ATAC-Seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、ATAC-seq
- 📝 描述:Contributors : Sana Parveen ; Victor X Jin ; Hui-Zi ChenSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensEZH2, the enzymatic core of the Polycomb Repressive Complex 2 (PRC2), is overexpressed in small cell lung cancer (SCLC). Previous studies have shown that EZH2 enforces epigenetic silencing of immune and DNA repair genes, including Class I MHC molecules (HLA‑A/B/C) and SLFN11. To investigate how EZH1/2 inhibition reshapes the 3D chromatin landscape and its relationship to transcriptional regulation, we performed multi‑omic profiling of a neuroendocrine SCLC cell line (NCI‑H146) treated with the dual EZH1/2 inhibitor valemetostat for 9 days. We employed Micro‑C sequencing for high‑resolution 3D genome mapping, ATAC‑sequencing for chromatin accessibility profiling, and RNA‑sequencing for whole‑transcriptome analysis. This is the ATAC sequencing dataset.
- 🔗 查看原文
9. GSE325884 构建prop1敲入斑马鱼可实现早期垂体发育的单细胞转录组学研究
- ✍️ 作者:未知作者
- 🏷️ 关键词:single-cell、transcriptomics
- 📝 描述:Contributors : Julian Martinez Mayer ; Maria Ines Perez MillanSeries Type : Expression profiling by high throughput sequencingOrganism : Danio rerioThe adenohypophyseal placode is a developmental structure that is conserved among vertebrates and gives rise to the anterior pituitary. The earliest steps of its formation remain poorly understood. Here, we present a powerful new genetic tool: a zebrafish GAL4 knockin reporter line for prop1. The targeted integration disrupts prop1 function, generating the first prop1-/- zebrafish, which exhibits dwarfism, impaired sexual maturation, and pigmentation defects. The generation of this new reporter line enabled the study of early pituitary development at single cell resolution, using both scRNA-seq and live imaging. We identified epcam/Epcam as a conserved epithelial marker of the adenohypophysis in both zebrafish and mouse. We further mapped transcriptional programs underlying endocrine lineage specification, discovering several previously unrecognized markers for hormone producing lineages, including tfcp2l1, as a likely regulator of lactotrope differentiation. Cell–cell interaction analyses revealed Notch, Fgf, and Slit/Robo signaling as key regulators of progenitor maintenance and differentiation. Overall, this work provides the first single cell atlas of early zebrafish pituitary development, a robust new genetic tool to study fundamental mechanistic insights into pituitary lineage specification and differentiation
- 🔗 查看原文
10. GSE319206 肿瘤内源性信号调节蛋白α (SIRPα) 表达有助于抑制抗肿瘤免疫反应 [RNA_CD172KO]
- ✍️ 作者:未知作者
- 🏷️ 关键词:tumor、immune
- 📝 描述:Contributors : Chien-Huan Weng ; Levi MangarinSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusSignal regulatory protein α (SIRPα) is a well-characterized inhibitory receptor expressed on myeloid immune cells. We and others have recently discovered that human and mouse melanoma cells express high levels of SIRPα. However, whether and how melanoma-intrinsic SIRPα contributes to tumor progression and anti-tumor immunity remains underexplored. Here, we identify a novel role of tumor-intrinsic SIRPα in suppressing anti-tumor immune recruitment and activation. Genetic deletion of SIRPα in melanoma cells enhanced tumor control and increased infiltration of immune cells into the tumor. Transcriptomic analysis revealed that loss of melanoma cell-intrinsic SIRPα leads to upregulation of C-X-C motif chemokine 10 (CXCL10) expression in both human and mouse melanoma cells. Notably, knockdown of Cxcl10 in SIRPα-deficient melanoma cells partially rescued tumor growth and reduced CD8+ T cell infiltration, recapitulating the phenotype observed in SIRPα-expressing tumors. These findings indicate that tumor cell-intrinsic SIRPα suppresses anti-tumor immunity by inhibiting Cxcl10 expression, thereby compromising T cell recruitment to the tumor sites. Thus, our work uncovers a previously unrecognized mechanism by which melanoma cell-intrinsic SIRPα suppresses anti-tumor immunity and highlights the therapeutic potential of silencing SIRPα to enhance anti-tumor immune cell infiltration and promote T cell-mediated tumor control. We envision that SIRPα silencing as a therapeutic strategy that could be applied to other cancer types that express SIRPα.
- 🔗 查看原文
💡 该来源还有 50 条内容,详见 文末
🧪 博客更新 (2条)
详细内容(全部2条)
1. RNA测序方法能够以更高的精度绘制RNA结合蛋白图谱。
- ✍️ 作者:未知作者
- 🏷️ 关键词:sequencing
- 📝 描述:RNA sequencing enables precise mapping of RNA binding protein targets, improving detection of low-abundance interactions and advancing understanding of gene regulation…
- 🔗 查看原文
2. 一项大型研究表明,接触农药会使患癌风险增加150%。
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer
- 📝 描述:A major new study finds that living in pesticide-heavy environments could raise cancer risk by up to 150%, even when the chemicals are considered “safe” on their own. The research suggests these mixtures may silently damage cells years before cancer appears.
- 🔗 查看原文
📊 关键词统计
| 关键词 | 出现次数 |
|---|---|
| cancer | 16 |
| RNA-seq | 10 |
| glioma | 7 |
| sequencing | 5 |
| transcriptomics | 5 |
| tumor | 5 |
| T cell | 4 |
| scRNA | 4 |
| spatial | 4 |
| ATAC-seq | 3 |
| immune | 3 |
| leukemia | 3 |
| methylation | 3 |
| cardiac | 3 |
| metabolic | 2 |
| single-cell | 2 |
| regex:intestin(e | al) |
| spatial transcriptomics | 2 |
| genome | 1 |
| pathway | 1 |
📎 更多内容
🧬 数据前沿 其他内容 (50条)
- GSE319205 血小板反应蛋白-1:CD47 信号传导促进癌症中 T 细胞耗竭的发生 [scRNA_CD172KO]
- GSE319183 T细胞急性淋巴细胞白血病中CD9蛋白的动态表达[批量RNA测序]
- GSE310994 SW620 结直肠癌细胞的 RNA-seq:对照组 (sh-control) 与 ANO1 (TMEM16A) 敲低组 (sh-ANO1)
- GSE308520 解读壶腹癌的单细胞分子图谱:一种罕见的胃肠道恶性肿瘤
- GSE292025 研究发现,IDH 突变型胶质瘤中 DNA 甲基化的纵向变化通过改变细胞状态分化促进疾病进展。
- GSE291885 IDH突变胶质瘤中DNA甲基化的纵向变化通过改变细胞状态分化促进疾病进展[Smart-seq2]
- GSE288156 Wnt信号通路耗竭导致肠道肿瘤细胞可塑性增强、Myc激活和Lgr5+肿瘤干细胞谱系定向丧失
- GSE318096 DDX3X介导的结构化心脏mRNA翻译对女性心脏发育至关重要[RNA-Seq]
- GSE294180 利用空间单细胞转录组学评估微塑料对炎症性肝病的影响
- GSE329270 磷酸化 DEK 通过促进 PBX3 驱动的转录重编程来维持白血病干细胞 [ATAC-seq 2]
- GSE328950 骨桥蛋白将获得性低氧诱导抗血管生成药物耐药性与乳腺癌抗PD-L1药物耐药性联系起来
- GSE328540 大鼠腹主动脉原代内皮细胞全长转录组测序
- GSE294165 叶酸驱动代谢重编程以减轻弓形虫抗原诱导的血管损伤
- GSE236889 小鼠T细胞转移性结肠炎的纵向单细胞RNA测序
- GSE236385 小鼠T细胞转移性结肠炎的纵向批量RNA测序
- GSE329206 EZH2 抑制重塑 3D 染色质结构,诱导小细胞肺癌的免疫原性表型 [microC]
- GSE328799 动态乙酰化/去乙酰化决定 TRIM27 核质定位与癌症进展 [CUT&Tag II]
- GSE328704 MERVL驱动的Pcgf5在植入前胚胎中抑制合子基因组激活方面起着关键作用
- GSE328543 动态乙酰化/去乙酰化决定 TRIM27 核质定位与癌症进展 [CUT&Tag]
- GSE327790 PDHA1 巴豆酰化对于正常妊娠中子宫内膜代谢重编程和蜕膜化至关重要
- GSE327188 动态乙酰化/去乙酰化决定TRIM27的核质定位,进而影响癌症进展
- GSE315867 EBNA1 抑制剂揭示 CDC7 和 POU2F1 是 EBV+ 上皮癌的直接功能靶点 [RNA-Seq]
- GSE308140 丛枝菌根共生的时空调控在细胞分辨率下的研究[RNA-seq]
- GSE296466 PU.1 是去势抵抗性前列腺癌相关反应性基质反应的介质
- GSE287227 瞬时 SP140 抑制可解锁人类多能干细胞的造血干细胞命运 [scRNA-seq]
- GSE287217 瞬时 SP140 抑制可解锁人类多能干细胞的造血干细胞命运 [bulk RNA-seq]
- GSE287211 瞬时 SP140 抑制可解锁人类多能干细胞的造血干细胞命运 [ATAC-seq]
- GSE329284 整合表型和转录组分析表明 ONC212 在雄激素非依赖性前列腺癌模型中是一种领先的伊米普利酮类药物
- GSE325597 成年期 Integrator 的缺失通过缺陷的 pre-mRNA 加工延长寿命和健康寿命 [ChIP-seq]
- GSE325594 成年期 Integrator 的缺失通过缺陷的前体 mRNA 加工延长寿命和健康寿命 [RNA-seq]
- GSE324878 Elongin B 在 H3K27M 突变型弥漫性中线胶质瘤中调控染色质和转录程序 [XIII_ELOB_CUTandRUN]
- GSE324875 Elongin B 在 H3K27M 突变型弥漫性中线胶质瘤中调控染色质和转录程序 [XIII_ELOBKO_chIP_ELOB_RNAPII]
- GSE324874 Elongin B 在 H3K27M 突变型弥漫性中线胶质瘤中调控染色质和转录程序 [XIII_ELOBKO_RNAseq]
- GSE324873 Elongin B 在 H3K27M 突变型弥漫性中线胶质瘤中协调染色质和转录程序 [XIII_K27MKO_CUTandRUN]
- GSE318098 DDX3X介导的结构化心脏mRNA翻译对女性心脏发育至关重要[Ribo-Seq]
- GSE318097 DDX3X介导的结构化心脏mRNA翻译对女性心脏发育至关重要[eCLIP-seq]
- GSE311394 染色体不稳定性驱动首批非洲裔加勒比乳腺癌细胞系中的细胞外基质重塑和药物敏感性
- GSE311069 消除肌强直可改善肌强直营养不良症肌肉盲敲除模型中的肌病:对股四头肌进行深度 RNA 测序,以评估肌强直依赖的转录表达和剪接变化。
- GSE311013 消除肌强直可改善肌强直营养不良症肌肉盲敲除模型中的肌病:Mbnl1 敲除、外显子 7a 缺失和 ADR 小鼠肌肉中 Clcn1 转录本的长读测序。
- GSE272095 ATM缺陷型胰腺癌中可药物靶向的TGF-β介导的基质编程轴
- GSE329274 磷酸化 DEK 通过促进 PBX3 驱动的转录重编程来维持白血病干细胞 [CUT&Tag 2]
- GSE328951 特定部位关节炎的胚胎起源;用 TNF 和 IL1b 刺激的 CD34+(Pi16+) 成纤维细胞的批量 RNA 测序。
- GSE328885 肠道特异性SIRT1敲除小鼠部分肝切除术后肝脏转录组反应
- GSE296725 无偏倚的微环境标记图谱揭示了骨转移中免疫排斥的微环境
- GSE283429 糖尿病肌层巨噬细胞数量的变化
- GSE263383 无偏倚的微环境标记图谱揭示了骨转移中免疫排斥的微环境
- GSE328481 利用立体XCR测序揭示肺腺癌中肿瘤反应性淋巴细胞启动的异位生发中心样微环境
- GSE323377 鸡胚单细胞转录组学揭示苗勒氏管分化的新见解
- GSE260595 小鼠 Il10KO 结肠炎的纵向批量 RNA 测序
- GSE255423 小鼠 Il10KO 结肠炎的纵向单细胞 RNA 测序
📅 报告生成时间:2026-04-28 22:28
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