科研日报 2026-07-28
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📅 Daily Report - 2026-07-28
今日筛选出 29 条内容,来自 1 个来源
🤖 今日AI智能总结
🧬 数据前沿
今日焦点: 新研究揭示JAK抑制剂可能激活MAPK通路导致皮肤鳞状细胞癌进展,并重塑肿瘤微环境,为癌症治疗提供新思路;单细胞测序技术在解析免疫细胞图谱、疾病机理及开发新型治疗策略方面展现巨大潜力。
主要方向:
- 肿瘤免疫微环境与癌症治疗:通过RNA-seq、单细胞测序等技术,深入解析JAK抑制剂对皮肤癌的影响,以及PRMT5介导的内含子滞留与免疫激活的关联,为癌症治疗提供新靶点和策略。
- 免疫细胞功能与疾病机制:利用单细胞测序,阐明膜性肾病、动脉粥样硬化中免疫细胞的特征,以及牛奶过敏与肠道菌群失调的关系。
- 神经科学与干细胞研究:通过类器官模型,研究阿尔茨海默病相关蛋白、微胶质细胞与神经元相互作用,并开发先进的干细胞分化和共培养技术。
技术亮点:
- 单细胞RNA测序 (scRNA-seq):广泛应用于解析复杂疾病(如肾病、动脉粥样硬化、阿尔茨海默病)中的细胞异质性,并用于开发新型治疗方法。
- AI赋能的生物分子设计:AI技术在靶向癌细胞表面蛋白的迷你结合物设计和优化方面取得进展。
📚 分类浏览
🧬 数据前沿 (29条)
详细内容(前10条)
1. ⭐ GSE278530 JAK 抑制通过 MAPK 通路激活导致侵袭性皮肤鳞状细胞癌,并塑造肿瘤免疫微环境,从而创造新的治疗机会 [RNA-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:tumor、carcinoma、immune、RNA-seq、pathway
- 📝 描述:Contributors : Hélène Pasquer ; Lina Benajiba ; Camille Lobry ; Emmanuelle LatourSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusSecondary malignancies are the most feared adverse effects of cancer therapies. In this study, we explore the oncogenic effects of the JAK inhibitor ruxolitinib on the skin. First, we demonstrate an epidemiological association between ruxolitinib exposure and development of aggressive cutaneous squamous cell carcinoma (cSCC), by conducting a disproportionality analysis on international pharmacovigilance data and a large local cohort study. We next demonstrate the causal link between ruxolitinib treatment and cSCC development, using in vitro and in vivo models. Mechanistically, we reveal that ruxolitinib induces transformation of pre-malignant keratinocytes into aggressive cSCC by activating the MAPK pathway through the COT kinase. Intriguingly, ruxolitinib also reshapes the immune microenvironment of cSCC resulting in T regulatory cells reduction and T CD8+ cells increase. Ruxolitinib-mediated immune microenvironment effects create new therapeutic opportunities by enhancing anti-PD1 treatment efficacy in cSCC and other immunotherapy resistant cancer types such as pancreatic cancer and acute myeloid leukemia.
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2. ⭐ GSE341102 单细胞测序揭示原发性膜性肾病患者外周血单核细胞的免疫细胞图谱
- ✍️ 作者:未知作者
- 🏷️ 关键词:immune、sequencing、single-cell
- 📝 描述:Contributors : Wenjun Shan ; Qiyu LiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensPrimary membranous nephropathy (PMN) stands as the predominant pathological subtype of primary nephrotic syndrome in adults. Approximately one-third of patients diagnosed with primary membranous nephropathy will eventually progress to end-stage renal disease (ESRD), carrying a poor prognosis. Our study employed single-cell RNA sequencing to investigate PMN, with the objectives of characterizing immune cell phenotypes, deciphering intercellular interaction patterns, and elucidating the potential mechanisms implicated in PMN pathogenesis.
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3. GSE339602 人iPSC来源的前脑类器官经β-淀粉样蛋白42处理、小胶质细胞共培养和马拉维罗克处理后的单细胞RNA测序
- ✍️ 作者:未知作者
- 🏷️ 关键词:sequencing、single-cell
- 📝 描述:Contributor : Yilin FengSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensHuman induced pluripotent stem cell (iPSC)-derived forebrain organoids were used to model Alzheimer’s disease-associated pathology and investigate the effects of microglia co-culture and CCR5 inhibition. Day 60 forebrain organoids were assigned to four experimental groups: untreated control, amyloid-β42 (Aβ42)-treated, Aβ42-treated followed by co-culture with mature human iPSC-derived microglia, and Aβ42-treated followed by maraviroc treatment and co-culture with mature human iPSC-derived microglia. Single-cell RNA sequencing was performed using the MGI DNBelab C-TaiM4 platform to characterize transcriptional changes and cellular composition across the four experimental conditions.
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4. GSE335789 动脉粥样硬化中生物物理分离的免疫细胞的单细胞RNA测序
- ✍️ 作者:未知作者
- 🏷️ 关键词:immune、scRNA
- 📝 描述:Contributor : Cenk O GurdapSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensWe developed new method to profile biophysical properties of immune cells. We performed this technique to healthy and atherosclerosis individuals. We selected very healthy and diseases 4 individuals for each catergory based on biophysics and performed 10x genomics.
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5. GSE311690 利用嵌入式负二项分布对肿瘤细胞低计数RNA测序数据进行反卷积
- ✍️ 作者:未知作者
- 🏷️ 关键词:tumor、sequencing
- 📝 描述:Contributors : Matthew Montierth ; Kinga Nemeth ; Wenyi Wang ; George CalinSeries Type : Non-coding RNA profiling by high throughput sequencingOrganism : Homo sapiensA major challenge in studying tumor heterogeneity is the presence of mixed signals in gene expression data, especially when working with sparse count datasets such as microRNA and spatial transcriptomics. Estimating tumor-specific transcript proportions can provide critical insights into tumor heterogeneity and cell plasticity. However, current methods often require comprehensive single-cell reference data, which is not always obtainable, and may suffer from technical biases. To overcome these issues, we introduce DeMixNB, a semi-reference-based deconvolution method designed specifically for estimating transcript proportions from sparse expression matrices using a negative binomial model, without the reliance on high-quality external reference data. Through simulations and analyses of real microRNA sequencing and spatial transcriptomics data from breast and lung cancers, we demonstrate that DeMixNB accurately estimates tumor-specific transcript proportions and provides meaningful biological insights from real-world datasets.
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6. GSE303756 牛奶过敏表型中耐受性的丧失与过敏原特异性 CD4+ T 细胞亚群过度增殖和微生物菌群失调有关
- ✍️ 作者:未知作者
- 🏷️ 关键词:T cell、regex:micro(b|be|bial|organism)
- 📝 描述:Contributors : Tracy Augustine ; Asmma Doudin ; Nicholas Van PanhuysSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensCow milk allergy (CMA) is the most prevalent pediatric food allergy, presenting in IgE and non-IgE mediated forms. Currently, the CD4+ T cell inflammatory responses underlying non-IgE CMA remain poorly characterized. By applying an allergen-reactive CD4+ T cell sorting and differential gene expression analysis approach, we characterized the CD4+ T cell subsets associated with both IgE and non-IgE mediated CMA endotypes and assessed their associations with gut bacterial compositions. Analysis of conventional (Tcon) and regulatory (Treg) CD4+ T cells revealed an expansion of inflammatory Tcon in CMA subjects, coincident with TH-like subset polarization and alterations in Treg signaling pathways. TH2-skewing was dominant in IgE mediated allergies, whereas subjects with non-IgE mediated allergies exhibited a CD4+ T cell compartment dominated by a novel TH response. Microbial dysbiosis was observed across all CMA endotypes, and network mapping revealed significant associations between a decrease in butyrate producing bacteria and the presence of inflammatory TH-like subsets. These insights link the composition of the allergen-reactive Tcon/Treg compartment to CMA pathology and identifies differences in bacterial dysbioses associated with specific disease endotypes.
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7. GSE333486 CAR 设计赋予多种免疫细胞独特的抗原特异性激活身份
- ✍️ 作者:未知作者
- 🏷️ 关键词:immune、antigen
- 📝 描述:Contributors : Satoshi Yamazaki ; Takaharu Kimura ; Takao Yogo ; Ayano Sugiyama-FinnisSeries Type : Other ; Expression profiling by high throughput sequencingOrganism : Homo sapiensHaematopoietic stem and progenitor cells (HSPCs) are multipotent cells, capable of generating all haematopoietic lineages, representing a powerful platform for regenerative immunotherapy. In parallel, CAR-engineering has extended beyond T cells, which have achieved success in treating B cell malignancies, to broader immune cell types alongside cell type-specific CAR design. However, how CAR architecture modulates activation phenotypes across immune lineages remains poorly understood. Here, we systematically compared previously validated, immune cell-optimised CARs across immune cell types using a human HSPC-derived multilineage CAR-immune cell platform. HSPC-derived T, NK and myeloid cells demonstrated immune activation across different CAR designs whereas cell-specific activation showed CAR design dependency in B cells. Hallmark pathway analysis revealed that immune lineage was the dominant determinant of activation-induced transcriptional states while CAR design modulated signalling programmes within lineage constrained programmes, notably proliferation, inflammation and cytokine responses. Single cell InTraSeq highlights differential activation of signalling pathways depending on CAR design and lineage identity with links to downstream transcriptional programmes across T, B and myeloid cells. Although exploratory and performed with limited sample sizes, this demonstrates the activated phenotypes and pathways mediated by CAR design and lineage identity that may inform the development of next-generation CAR-immune cells with tailored activation-induced characteristics.
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8. GSE327671 PRMT5介导的内含子保留触发针对癌症的先天性和适应性免疫
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、immunity
- 📝 描述:Contributors : Wiktoria Blaszczak ; Wojciech Barczak ; Chuyue Zhang ; Garret Rochford ; Annalisa Nicastri ; Claire Hutchings ; Anastasia Samsonova ; Alexander Kanapin ; Nicola Ternette ; Paul Klenerman ; Nicholas B La ThangueSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensPRMT5 is expressed at high levels in many cancers, where it regulates diverse cellular pathways that contribute to oncogenesis. Here, we have defined a new role for PRMT5 in regulating and coordinating the interplay between the innate and adaptive immune response. This occurs through the influence of PRMT5 on RNA splicing and the presence of retained introns (RIs). We found that RIs, which occur upon PRMT5 inhibition, have a propensity to form double-stranded RNA structures which activate the innate immune response. Furthermore, many RIs contain cryptic open reading frames which can be translated and then processed into small peptides that assemble with the MHC class I complex. Significantly, RI-derived peptides are highly immunogenic and a murine cancer vaccine, carrying a string of antigenic RI peptides, delayed tumour growth and enhanced survival. RIs are present in human tumour cells, and we identified T lymphocytes in cancer patients with antigen specificity for RI-derived peptides that killed human tumour cells in vitro. Regulating intron retention thus offers a new therapeutic approach to regulate tumour immunogenicity.
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9. GSE302789 线粒体 ROS 诱导代谢适应和适应不良,从而差异性地调节肝细胞对铁死亡的敏感性
- ✍️ 作者:未知作者
- 🏷️ 关键词:metabolic
- 📝 描述:Contributors : Somesh Banerjee ; Matthew R Smith ; Yining I Wang ; Michael Wang ; Derrik Gratz ; Gregory K Tharp ; Peijian HeSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusFerroptosis mediates the pathogenesis of a plethora of diseases. Mitochondrial reactive oxygen species (mtROS) plays a critical role in ferroptosis induction, but the precise mechanism by which mtROS promotes lipid peroxidation-dependent ferroptosis remains poorly understood. Herein, we employed hepatocytes and iron-induced ferroptosis as models to identify the specific mtROS-mediated redox and metabolic changes that modulate ferroptosis sensitivity. Iron overload induced the activation of multiple antioxidative mechanisms, including altered transport and metabolism of redox-active metals, small Maf (sMaf)-mediated activation of transcription factor nuclear factor erythroid 2-related factor 2 (NRF2), and an increased potential of glutathione biosynthesis. Iron also induced mtROS-dependent suppression of fatty acid oxidation, the activities of citric acid cycle and mitochondrial respiration, protecting against ferroptosis. We further identified that mtROS signaling potentially impairs the biosynthesis of coenzyme Q10 (CoQ) by attenuating the expression of genes in the mevalonate pathway and CoQ8A, a stabilizer of CoQ complex. Importantly, elevating CoQ8A expression mitigated, whereas silencing CoQ8A expression enhanced, the vulnerability of hepatocytes to ferroptosis. The mtROS-mediated downregulation of CoQ8A was dependent on farnesoid X receptor (FXR) and retinoid X receptors (RXRs). Our study demonstrated, for the first time, that mtROS induces impaired CoQ biosynthesis as a maladaptive change that promotes ferroptosis.
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10. GSE341155 CHI3L1促进卵巢癌细胞的增殖和转移
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer
- 📝 描述:Series Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensAdipocyte-tumor interaction plays a critical role in tumor microenvironment. Typically, high-grade serous ovarian carcinoma (HGSOC) preferentially metastasizes to the omentum, an adipocyte-rich tissue, and obesity correlates with worse patient prognosis. However, the underlying mechanisms remain poorly understood. Here, we identify a bidirectional adipocyte–cancer cell axis in which HGSOC cells stimulate lactate metabolism in adjacent adipocytes, leading to hypoxia-inducible factor 1α (HIF-1α) activation and subsequent secretion of chitinase 3-like 1 (CHI3L1). On the one hand, CHI3L1 acts as an inflammatory factor that promotes the secretion of additional cytokines, perpetuating omental inflammation, driving CD8⁺ T cell exhaustion, and shaping an immunosuppressive microenvironment that favors tumor metastasis. On the other hand, CHI3L1 binds to and stabilizes protein arginine methyltransferase 5 (PRMT5) in tumor cells, thereby enhancing its methyltransferase activity. This upregulation suppresses dual-specificity phosphatase 1 (DUSP1), a phosphatase of mitogen-activated protein kinase (MAPK), and sustains oncogenic MAPK signaling across multiple tumor models. Obesity amplifies this pathway by heightening HIF-1α activity and elevating CHI3L1 levels in adipose tissue, which drives both tumor progression and resistance to anti-angiogenic therapy. Pharmacological inhibition of CHI3L1 disrupts this signaling loop and restores therapeutic sensitivity, while also alleviating immune exhaustion in the tumor microenvironment. Collectively, our findings establish CHI3L1 as a key mediator of a unified mechanism that drives omental tropism and obesity-associated aggressive phenotypes, highlighting its potential as a prognostic biomarker and therapeutic target to improve anti-angiogenic therapy.
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💡 该来源还有 19 条内容,详见 文末
📊 关键词统计
| 关键词 | 出现次数 |
|---|---|
| RNA-seq | 6 |
| cancer | 5 |
| sequencing | 4 |
| immune | 4 |
| single-cell | 3 |
| immunity | 3 |
| scRNA | 2 |
| tumor | 2 |
| metabolic | 1 |
| genome | 1 |
| Neuronal | 1 |
| macrophage | 1 |
| T cell | 1 |
| regex:micro(b | be |
| antigen | 1 |
| transcriptome | 1 |
| cardiac | 1 |
| carcinoma | 1 |
| pathway | 1 |
| ATAC-seq | 1 |
📎 更多内容
🧬 数据前沿 其他内容 (19条)
- GSE341147 厚朴酚通过调节 ETS2/SLC7A11/GPX4 信号通路诱导三阴性乳腺癌细胞发生铁死亡
- GSE339558 多物种全基因组 CRISPR 筛选鉴定出保守的冷诱导细胞死亡抑制因子
- GSE339528 人类干细胞衍生小胶质细胞和神经元网络长期共成熟方案的开发和验证
- GSE339488 BYSL 敲低对 MDA-MB-231 人乳腺癌细胞转录组的影响
- GSE339457 利用 RNA 指纹图谱绘制细胞扰动字典的转录反应图谱 [scRNA-Seq]
- GSE339360:结核分枝杆菌感染期间野生型和EZH2缺陷型Hoxb8衍生巨噬细胞的双宿主-病原体RNA测序
- GSE326254 鼻内接种ΔNS1-86减毒活疫苗可对哺乳动物适应性H5N1病毒产生完全免疫力
- GSE311875 RNA-Seq 分析了过表达全长 NELFA、MERVL-NELFA 和 IDR 缺失突变体 (NELFA-IDR-Del) 的 mESC 系中的 2C 基因。
- GSE311873 RNA-Seq 分析报告 mESC 系中 2C 基因,无论是否用 pladienolide B 处理。
- GSE311871 RNA-Seq 分析野生型小鼠胚胎干细胞中 MERVL-NELFA 过表达后 2C 基因的变化
- GSE311870 RNA-Seq 分析在 H2AX WT 或 H2AX KO mESCs 中过表达 Nelfa 后 2C 基因的变化
- GSE308210 高血压应激诱导的巨噬细胞重编程是射血分数保留型非肥胖性心力衰竭发病机制的基础
- GSE278745 精制碳水化合物对全身免疫的影响:一项随机对照喂养试验的结果
- GSE338543 人工智能驱动的靶向癌细胞表面蛋白的微型结合剂的发现和生化优化
- GSE326582 胰腺炎中胰周脂肪组织的转录组谱
- GSE304575 LMNA p.H222P 突变通过损害线粒体钙摄取导致人类心脏层粘蛋白病中的收缩功能障碍
- GSE301771 人类肝窦γδ T细胞在人类巨细胞病毒潜伏感染背景下的单细胞图谱
- GSE277921 染色质可及性分析揭示 hESC 衍生肾脏类器官的调控动态 [ATAC-seq]
- GSE277920 染色质可及性分析揭示 hESC 衍生肾脏类器官的调控动态 [RNA-seq]
📅 报告生成时间:2026-07-27 22:31
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