科研日报 2026-04-10

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📅 Daily Report - 2026-04-10

今日筛选出 84 条内容,来自 3 个来源

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🤖 今日AI智能总结

🧬 数据前沿

今日焦点: 单细胞测序技术揭示联合疗法(CDK4/6与PD-1阻断)在去分化脂肪肉瘤中的疗效预测生物标志物。空间转录组学技术进一步阐明了神经母细胞瘤与其免疫微环境的相互作用。

主要方向

  • 探索尼洛沙尼(Niclosamide)在克服肿瘤免疫逃逸中的治疗潜力。
  • 鉴定驱动植物入侵性的B染色体作用机制。
  • 揭示miR-21-5p在口咽鳞状细胞癌放疗抵抗中的作用。
  • 研究三阴性乳腺癌卡铂耐药的克服策略。
  • 阐明NF-κB信号通路在胰腺癌中的表观遗传调控。

技术亮点

  • 10x Genomics Xenium技术实现对胸膜间皮瘤的靶向空间转录组学分析。
  • 整合RNA-seq、ChIP-seq、miRNA-seq、CUT&Tag等多种高通量测序技术,从不同层面深入解析癌症、免疫、发育等复杂生物学过程。

📊 学点生信

今日焦点: Bioconductor 与 R-universe 强强联合,共同开发通用基础设施,旨在提升 R 生物信息学生态系统的质量和可维护性。

主要方向

  • 整合 Bioconductor 的高质量、同行评审的生物信息学工具。
  • 优化 R 包的构建、分发和管理流程。

技术亮点

  • 建立统一的开发和分发标准,促进 R 生物信息学工具的互操作性和复用性。

🧪 博客更新

今日焦点: 新型单细胞及时空测序技术首次绘制出人类毛囊衰老分子图谱,揭示了导致脱发和白发的细胞特异性变化。

主要方向

  • 揭示毛囊衰老过程中的细胞信号通路紊乱及干细胞功能下降机制。
  • 探索脑内硫化氢(H₂S)生成蛋白CSE在阿尔茨海默病中的作用。
  • 发现植物化合物协同增效机制,可将抗炎效果提升百倍。

技术亮点

  • 结合单细胞与时空测序,实现对毛囊衰老的精细分子解析。
  • RNA测序与蛋白质分析联用,精确追踪免疫细胞活动和细胞因子动态。

📚 分类浏览

🧬 数据前沿 (79条)

详细内容(前10条)

1.GSE320497 鉴定尼克酰胺在克服肿瘤微环境中 IFN-γ 依赖性癌症免疫逃逸方面的治疗潜力

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:tumor、cancer、immune、tumor microenvironment
  • 📝 描述:Contributors : Yue Zhang ; En CaiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTumor cells frequently develop immune resistance through interferon-γ (IFN-γ)–induced PD-L1 expression, acquisition of cancer stem cell (CSC)–like features, and adaptation to hypoxia within the tumor microenvironment (TME). Although IFN-γ activates both STAT1 and STAT3, how these pathways interact to regulate immune evasion under hypoxia remains unclear. Using the MC38 murine colorectal cancer model and T cell–tumor spheroid co-culture assays, we examined how IFN-γ signaling through STAT1 and STAT3 regulates PD-L1 expression, CSC plasticity, and cytotoxic T cell function under normoxic and hypoxic conditions. Pharmacologic inhibitors and siRNA-mediated knockdown were used to dissect pathway function, and Niclosamide, an FDA-approved anthelmintic, was evaluated as a dual STAT1/STAT3 inhibitor. We found that IFN-γ primarily induced PD-L1 expression through STAT1 activation, whereas CSC plasticity was associated with STAT3 signaling. STAT1 and STAT3 displayed reciprocal regulation—blocking one enhanced activation of the other. Niclosamide effectively inhibited phosphorylation of both STAT1 and STAT3, resulting in suppressed PD-L1 upregulation and reduced CSC enrichment. In addition, it also partially inhibited hypoxia-induced HIF-1α expression. In co-culture assays, Niclosamide enhanced T cell infiltration and reduced exhaustion under hypoxic conditions, resulting in improved T cell killing. Our findings identified Niclosamide as a potent dual STAT1/3 inhibitor capable of reversing IFN-γ and hypoxia-driven immune evasion. Repurposing Niclosamide may represent a promising strategy to enhance the efficacy of immune checkpoint blockade in solid tumors.
  • 🔗 查看原文

2.GSE320212 鉴定预测去分化脂肪肉瘤联合 CDK4/6 和 PD-1 阻断疗法疗效的衰老和免疫生物标志物:连续肿瘤活检的单细胞 RNA 测序

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:tumor、immune、RNA-seq、single-cell
  • 📝 描述:Contributors : Rosenbaum Evan ; Gularte Mérida Rodrigo ; D’Angelo SandraSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThis dataset comes from an exploratory correlatives sub-study embedded within NCT04438824, a single-arm, open-label phase II trial evaluating the combination of the CDK4/6 inhibitor palbociclib and the PD-1 inhibitor INCMGA00012 in patients with advanced well-differentiated or dedifferentiated liposarcoma. The dbGaP submission is limited to the first 12 patients enrolled on the trial, for whom protocol-mandated tumor biopsies were collected for single-cell RNA sequencing. Single-cell RNASeq was performed to characterize cellular composition and transcriptional states within the tumor microenvironment in this pilot cohort. The dataset includes processed single-cell expression profiles and a restricted set of associated clinical variables such as demographics and response data abstracted from the parent study.
  • 🔗 查看原文

3.GSE295468 Single-cell and spatial transcriptomics uncover the role of B chromosomes in driving plant invasiveness

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:single-cell、spatial、spatial transcriptomics、transcriptomics
  • 📝 描述:Contributors : Cui Wang ; James Ord ; Mengxiao Yan ; Yunfei Cai ; Hongjin Shao ; Lele Lin ; Jarkko Salojärvi ; Lele Liu ; Weihua GuoSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Phragmites australisInvasive plants can significantly disrupt native biodiversity, yet the genetic mechanisms driving their success remain poorly understood. This study investigates the genetic basis of invasiveness in the common reed (Phragmites australis), a resilient grass species that became invasive in North America following its introduction from Europe. By integrating whole-genome sequencing with bulk, single-cell, and spatial transcriptomics, we constructed a comprehensive single-cell atlas of the common reed’s shoot system. UMAP analysis revealed 19 distinct cell clusters within the shoot, which were annotated using Gene Ontology (GO) enrichment to identify key cell types, including mesophyll, epidermal, bundle sheath, differentiating vascular cells, shoot apical meristems, and a cell cycle-associated cluster. We inferred key genes involved in the specification of several tissues, such as epidermal cells and ground meristems. For gene expression analysis, shoot tissues from three individuals of the invasive North American population and three from the native European population were included. Comparative transcriptomic analysis revealed significant upregulation of genes associated with the light-harvesting components of photosynthesis in several tissues of the invasive population, while genes involved in the respiratory burst related to defense responses were notably downregulated.
  • 🔗 查看原文

4.GSE304579 miR-21-5p 激活替代末端连接赋予口腔鳞状细胞癌放射抗性 [SUGH-OSCC 患者肿瘤的 RNA-seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:carcinoma、resistance、RNA-seq
  • 📝 描述:Series Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensMarked heterogeneity in radiosensitivity is a major challenge in the treatment of oral squamous cell carcinoma (OSCC), often resulting in poor outcomes for radioresistant tumors. The underlying molecular drivers of this resistance remain elusive. Here, we identify a novel mechanism in which miR-21-5p promotes radiation resistance by selectively activating the error-prone DNA double-strand break (DSB) repair pathway alternative end-joining (Alt-EJ). Integrative miRNA profiling, multi-omic analyses, and functional assays demonstrate that miR-21-5p upregulation coupled with suppression of its target gene signature increases Alt-EJ dependence for DSB repair. This Alt-EJ reliance enhances genomic instability, increases tumor mutational burden and microhomology-mediated indels, and confers pronounced radiation resistance in OSCC models, while correlating with poor radiotherapy response in patients. Importantly, pharmacological or genetic inhibition of Alt-EJ components, including PARP1 and POLQ, restores radiosensitivity in vitro and in vivo, with PARP1 inhibition specifically reversing miR-21-5p-mediated resistance in a syngeneic mouse model. Further RNA-seq analyses of these mice tumors confirmed that PARP inhibitor induced selective radiosensitization effects for miR-21-5p-overexpressing tumors were accompanied by a pronounced reduction in alt-EJ expression. Collectively, these findings establish the miR-21-5p/Alt-EJ axis as a key driver of radiation resistance in OSCC and support Alt-EJ targeting as a promising approach for precision radiosensitization.
  • 🔗 查看原文

5.GSE304277 miR-21-5p 激活替代末端连接赋予口腔鳞状细胞癌放射抗性 [SCC7 小鼠肿瘤的 RNA-seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:carcinoma、resistance、RNA-seq
  • 📝 描述:Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusMarked heterogeneity in radiosensitivity is a major challenge in the treatment of oral squamous cell carcinoma (OSCC), often resulting in poor outcomes for radioresistant tumors. The underlying molecular drivers of this resistance remain elusive. Here, we identify a novel mechanism in which miR-21-5p promotes radiation resistance by selectively activating the error-prone DNA double-strand break (DSB) repair pathway alternative end-joining (Alt-EJ). Integrative miRNA profiling, multi-omic analyses, and functional assays demonstrate that miR-21-5p upregulation coupled with suppression of its target gene signature increases Alt-EJ dependence for DSB repair. This Alt-EJ reliance enhances genomic instability, increases tumor mutational burden and microhomology-mediated indels, and confers pronounced radiation resistance in OSCC models, while correlating with poor radiotherapy response in patients. Importantly, pharmacological or genetic inhibition of Alt-EJ components, including PARP1 and POLQ, restores radiosensitivity in vitro and in vivo, with PARP1 inhibition specifically reversing miR-21-5p-mediated resistance in a syngeneic mouse model. Further RNA-seq analyses of these mice tumors confirmed that PARP inhibitor induced selective radiosensitization effects for miR-21-5p-overexpressing tumors were accompanied by a pronounced reduction in alt-EJ expression. Collectively, these findings establish the miR-21-5p/Alt-EJ axis as a key driver of radiation resistance in OSCC and support Alt-EJ targeting as a promising approach for precision radiosensitization.
  • 🔗 查看原文

6.GSE327347 利用 10x Genomics Xenium 对胸膜间皮瘤进行靶向空间转录组分析

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:10x、spatial、genomics
  • 📝 描述:Contributors : David T Severson ; Sam Freyaldenhoven ; Ben Wadowski ; William G Richards ; Raphael Bueno ; Matthew B CougarSeries Type : OtherOrganism : Homo sapiensTargeted spatial transcriptomic profiling was performed on seven formalin-fixed paraffin-embedded pleural mesothelioma tumor samples from four cases using the 10x Genomics Xenium platform. The Xenium Human Immuno-Oncology panel supplemented with 100 additional custom genes selected from known pleural mesothelioma biomarkers and single-cell RNA-seq-derived marker genes was used. Raw and processed Xenium files are provided for each sample. To ensure data integrity with downloaded Xenium files, md5 checksums are provided in ‘Xenium_GEO.md5’. This dataset is part of a multi-modality study including matched scRNA-seq, bulk RNA-seq, and Xenium spatial transcriptomics generated from overlapping pleural mesothelioma samples. Related controlled-access sequencing data are available in dbGaP under accession phs004285.
  • 🔗 查看原文

7.GSE309617 治疗协同作用克服三阴性乳腺癌的卡铂耐药性 [批量 RNA 测序]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer、resistance、RNA-seq
  • 📝 描述:Contributors : Julia E Altman ; Emily K Zboril ; Aaron Valentine ; Nina Dashti-Gibson ; David C Boyd ; Rachel K Myrick ; Amy L Olex ; Mikhail G Dozmorov ; Joshua C HarrellSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBackground: Triple-negative breast cancer (TNBC) is an aggressive subtype lacking targeted therapeutic options, where platinum-based chemotherapy such as carboplatin serves as a cornerstone of treatment. Despite initial responses, the rapid emergence of acquired resistance remains a major clinical barrier. Understanding the molecular adaptations that drive platinum resistance is essential to develop strategies to restore sensitivity and identify alternative vulnerabilities. Methods: We generated four isogenic patient-derived xenograft (PDX) pairs (WHIM30, BCM‑2147, BCM‑3887, BCM‑7482) through serial carboplatin exposure to model acquired resistance in TNBC. Bulk RNA sequencing, immunohistochemistry, and histopathological analyses were performed to define transcriptomic and phenotypic changes associated with resistance. Synergistic therapeutic combinations were identified using high-throughput drug screening in carboplatin-resistant (CR) PDX-derived models, followed by in vivo validation in NSG mice. Tumor growth and survival were assessed using mixed-effects modeling, two-way ANOVA, and Welch’s student t-test. Results: The resulting isogenic PDX pairs captured both convergent and model-specific adaptations to carboplatin. CR tumors demonstrated heterogeneous activation of DNA damage repair pathways, including restoration of BRCA1-dependent homologous recombination (BCM‑2147, WHIM30) and compensatory upregulation of mismatch repair (BCM‑3887). In the BRCA1-mutant BCM‑7482 model, resistance correlated with HORMAD1 upregulation, suggesting an alternative HRD-associated mechanism. Morphologically, BCM‑7482CR tumors exhibited a significant increase in nuclear size compared to their sensitive counterpart (p < 0.0001). Drug screening identified mTOR pathway inhibition as a recurrent vulnerability across CR models. Sacituzumab govitecan (SG) combined with Everolimus produced robust synergy in vitro and superior tumor control in vivo compared to single agents in both WHIM30CR and BCM‑2147CR. A second combination, Everolimus + Selinexor (KPT‑330), also reduced tumor burden, achieving statistical significance in an expanded WHIM30CR cohort and suppressing metastatic progression in the intrinsically resistant WHIM2…
  • 🔗 查看原文

8.GSE309616 治疗协同作用克服三阴性乳腺癌的卡铂耐药性 [scRNA-seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer、resistance、scRNA
  • 📝 描述:Contributors : Julia E Altman ; Emily K Zboril ; Aaron Valentine ; Nina Dashti-Gibson ; David C Boyd ; Rachel K Myrick ; Amy L Olex ; Mikhail G Dozmorov ; Joshua C HarrellSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBackground: Triple-negative breast cancer (TNBC) is an aggressive subtype lacking targeted therapeutic options, where platinum-based chemotherapy such as carboplatin serves as a cornerstone of treatment. Despite initial responses, the rapid emergence of acquired resistance remains a major clinical barrier. Understanding the molecular adaptations that drive platinum resistance is essential to develop strategies to restore sensitivity and identify alternative vulnerabilities. Methods: We generated four isogenic patient-derived xenograft (PDX) pairs (WHIM30, BCM‑2147, BCM‑3887, BCM‑7482) through serial carboplatin exposure to model acquired resistance in TNBC. Bulk RNA sequencing, immunohistochemistry, and histopathological analyses were performed to define transcriptomic and phenotypic changes associated with resistance. Synergistic therapeutic combinations were identified using high-throughput drug screening in carboplatin-resistant (CR) PDX-derived models, followed by in vivo validation in NSG mice. Tumor growth and survival were assessed using mixed-effects modeling, two-way ANOVA, and Welch’s student t-test. Results: The resulting isogenic PDX pairs captured both convergent and model-specific adaptations to carboplatin. CR tumors demonstrated heterogeneous activation of DNA damage repair pathways, including restoration of BRCA1-dependent homologous recombination (BCM‑2147, WHIM30) and compensatory upregulation of mismatch repair (BCM‑3887). In the BRCA1-mutant BCM‑7482 model, resistance correlated with HORMAD1 upregulation, suggesting an alternative HRD-associated mechanism. Morphologically, BCM‑7482CR tumors exhibited a significant increase in nuclear size compared to their sensitive counterpart (p < 0.0001). Drug screening identified mTOR pathway inhibition as a recurrent vulnerability across CR models. Sacituzumab govitecan (SG) combined with Everolimus produced robust synergy in vitro and superior tumor control in vivo compared to single agents in both WHIM30CR and BCM‑2147CR. A second combination, Everolimus + Selinexor (KPT‑330), also reduced tumor burden, achieving statistical significance in an expanded WHIM30CR cohort and suppressing metastatic progression in the intrinsically resistant WHIM2…
  • 🔗 查看原文

9.GSE296832 表观遗传背景定义了胰腺癌中经典和非经典 NF-κB 信号通路的转录活性 [RNA-seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer、RNA-seq、epigenetic
  • 📝 描述:Contributors : Joana E Aggrey-Fynn ; Steven A JohnsenSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensNF-κB signaling in pancreatic ductal adenocarcinoma (PDAC) operates through canonical and noncanonical pathways mediated by RELA and RELB, respectively. We show that TNFα selectively activates the canonical RELA pathway, while TWEAK induces noncanonical signaling through RELB. Through integrated transcriptomic, epigenomic, and transcription factor binding analyses, we reveal distinct temporal dynamics and binding patterns, with RELB preferentially occupying AP1-rich, epigenetically active regions. Single-cell RNA-seq and tissue staining highlight pathway-specific crosstalk with the tumor microenvironment. These findings uncover fundamental differences in RELA and RELB regulatory mechanisms and their distinct contributions to PDAC gene regulation.
  • 🔗 查看原文

10.GSE296831 表观遗传背景定义了胰腺癌中经典和非经典 NF-κB 信号通路的转录活性 [ChIP-Seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer、ChIP-seq、epigenetic
  • 📝 描述:Contributors : Joana E Aggrey-Fynn ; Steven A JohnsenSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensNF-κB signaling in pancreatic ductal adenocarcinoma (PDAC) operates through canonical and noncanonical pathways mediated by RELA and RELB, respectively. We show that TNFα selectively activates the canonical RELA pathway, while TWEAK induces noncanonical signaling through RELB. Through integrated transcriptomic, epigenomic, and transcription factor binding analyses, we reveal distinct temporal dynamics and binding patterns, with RELB preferentially occupying AP1-rich, epigenetically active regions. Single-cell RNA-seq and tissue staining highlight pathway-specific crosstalk with the tumor microenvironment. These findings uncover fundamental differences in RELA and RELB regulatory mechanisms and their distinct contributions to PDAC gene regulation.
  • 🔗 查看原文

💡 该来源还有 69 条内容,详见 文末

📊 学点生信 (1条)

详细内容(全部1条)

1. Bioconductor 和 R-universe 在通用基础设施开发方面开展合作

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:Bioconductor
  • 📝 描述:For more than two decades, the Bioconductor project has been a cornerstone of the R ecosystem, providing high-quality, peer-reviewed tools for bioinformatics and computational biology. Its curated repository model, rigorous review standards, and tight… Continue reading: Collaborating between Bioconductor and R-universe on Development of Common Infrastructure
  • 🔗 查看原文
🧪 博客更新 (4条)

详细内容(全部4条)

1.揭示毛发衰老的奥秘:利用单细胞和时空测序技术绘制人类毛囊衰老的分子图谱

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:aging、sequencing、single-cell
  • 📝 描述:RNA sequencing reveals cell-specific changes in hair follicle aging, identifying disrupted signaling and stem cell decline that contribute to hair loss and graying…
  • 🔗 查看原文

2. 新的测序方法揭示了免疫信号传导中隐藏的缺口

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:immune、sequencing
  • 📝 描述:RNA sequencing combined with protein analysis enables detailed tracking of immune cell activity, revealing cytokine dynamics and improving understanding of cancer and immune response timing…
  • 🔗 查看原文

3. 科学家发现香料协同作用可将抗炎效果提升100倍。

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:inflammation
  • 📝 描述:Chronic inflammation often works quietly in the background but can fuel serious diseases like diabetes, heart disease, and cancer. New research reveals that everyday plant compounds—like menthol from mint, cineole from eucalyptus, and capsaicin from chili peppers—can team up inside immune cells to dramatically boost their anti-inflammatory power. While individual compounds showed modest effects, certain combinations amplified results hundreds of times over by activating different cellular pathways at once.
  • 🔗 查看原文

4. 这种“臭鸡蛋”状脑气体可能是对抗阿尔茨海默病的关键。

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:Alzheimer
  • 📝 描述:Scientists have uncovered a surprising new player in Alzheimer’s disease: a protein called CSE that helps produce tiny amounts of hydrogen sulfide gas in the brain. In experiments with genetically engineered mice, removing this protein led to memory loss, brain damage, and other hallmarks of Alzheimer’s, including weakened blood-brain barriers and reduced formation of new neurons. The findings suggest that this “rotten egg” gas, when carefully regulated, may actually protect brain cells and support memory.
  • 🔗 查看原文

📊 关键词统计

关键词出现次数
RNA-seq22
cancer9
resistance8
transcriptome6
metabolic6
immune5
metabolism5
ATAC-seq5
sequencing4
single-cell4
carcinoma4
spatial4
tumor3
pathway3
leukemia3
epigenetic3
scRNA3
ChIP-seq3
transcriptomics2
Alzheimer2

📎 更多内容

🧬 数据前沿 其他内容 (69条)

📅 报告生成时间:2026-04-09 22:01
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