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1. ⭐ 氨基酸代谢热度不减：最新生信发文，靶向谷氨酰胺代谢增加免疫治疗疗效！

• ✍️ 作者：东晓生物
• 🏷️ 关键词：免疫、代谢、生信
• 🔗 查看原文

2. ⭐ Nature|文献解读：巨噬细胞靠GSDMD孔道狂送"修复激素"促组织修复！单细胞+代谢组学揭秘肌肉再生新机制, 思路值得学习

• ✍️ 作者：生信小博士
• 🏷️ 关键词：代谢、代谢组、单细胞
• 📝 描述：最近这篇Nature看得我直拍大腿！GSDMD孔道是个"代谢物输送机"，专门递送小分子脂质11,12-EET激活肌肉干细胞。
• 🔗 查看原文

3. ⭐ Cell ｜ 复旦大学季彤教授：破解癌痛与免疫逃逸迷局，肿瘤竟用神经“高速路”逃逸免疫？

• ✍️ 作者：图灵基因
• 🏷️ 关键词：肿瘤、免疫、神经
• 📝 描述：肿瘤如何“遥控”远隔部位的器官或组织，实现系统层面的免疫抑制？近年来兴起的“癌症神经科学”将目光投向了神经系统这一器官间通信的“高速信息网络”。
• 🔗 查看原文

4. 最新8+生信，多组学识别三级淋巴结构（TLS）结构并进行针对性分析。预测预后及免疫治疗疗效，值得借鉴！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：免疫、生信
• 📝 描述：点击查看详情
• 🔗 查看原文

5. 10月最新26+生信，多组学空间免疫谱分析确定了三级淋巴结构（TLS）的亚群并进行深入分析，建议收藏！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：免疫、生信
• 📝 描述：点击查看详情
• 🔗 查看原文

6. STM：隔山打牛！日本科学家发明鼻内疫苗，借用黏膜免疫系统打击HPV感染，有望为宫颈癌治疗带来非侵入性新疗法

• ✍️ 作者：奇点肿瘤探秘
• 🏷️ 关键词：免疫、疫苗
• 📝 描述：鼻腔给药，远狙宫颈癌！
• 🔗 查看原文

7. 文献分享 | Nature:突破极限：iPEX技术实现微米级深度空间蛋白质组学，揭示阿尔茨海默病早期新机制

• ✍️ 作者：王永成Lab
• 🏷️ 关键词：空间组学、蛋白质组
• 🔗 查看原文

8. Nature | 雷群英团队发现乙酰辅酶A作为信号分子调控线粒体自噬及其介导KRAS抑制剂耐药的代谢机制

• ✍️ 作者：人体蛋白质组导航计划
• 🏷️ 关键词：代谢、耐药
• 🔗 查看原文

9. ScIsoX：测量单细胞中异构体水平转录组复杂性

• ✍️ 作者：BMELab
• 🏷️ 关键词：单细胞、转录组
• 📝 描述：ScIsoX：测量单细胞中异构体水平转录组复杂性
• 🔗 查看原文

10. 突破性发现！中山大学肿瘤防治中心高益军/王峰/廖雯婷/赵齐揭示KRAS突变结直肠癌耐药机制，设计三重靶向治疗突破耐药新策略

• ✍️ 作者：转化医学网
• 🏷️ 关键词：肿瘤、耐药
• 📝 描述：这一发现不仅解释了临床治疗中耐药性产生的根源，更提出了通过联合靶向FGFR3来克服耐药性的全新三重靶向治疗策略，对结直肠癌未来的精准治疗具有一定的指导意义。
• 🔗 查看原文

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1. ⭐ GSE235714 炎症性呼吸道鼻腔的免疫上皮相互作用和组织重塑 [NanoString GeoMx 空间转录组学]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributor : Jayakar V NayakSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Homo sapiensChronic rhinosinusitis (CRS) is a common inflammatory disease of the nasal cavity and sinuses that affects millions of individuals worldwide. The complex pathophysiology of CRS remains poorly understood, with emerging evidence implicating diverse immune and epithelial cell types in the disease process. We employed NanoString GeoMx spatial transcriptomics in both intact tissues to investigate the cellular and molecular heterogeneity of CRS with and without nasal polyps.
• 🔗 查看原文

2. ⭐ GSE307990 人类内嗅皮层在不同阿尔茨海默病风险中的空间和单细胞转录组学研究 [Visium]

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer、spatial、Visium、transcriptomics
• 📝 描述：Contributors : Louise A Huuki-Myers ; Heena R Divecha ; Svitlana V Bach ; Madeline R Valentine ; Nicholas J Eagles ; Bernard Mulvey ; Rahul A Bharadwaj ; Ruth Zhang ; James R Evans ; Melissa Grant-Peters ; Ryan A Miller ; Joel E Kleinman ; Shizhong Han ; Thomas M Hyde ; Stephanie C Page ; Daniel R Weinberger ; Keri Martinowich ; Mina Ryten ; Kristen R Maynard ; Leonardo Collado-TorresSeries Type : OtherOrganism : Homo sapiensWe present the first spatially-resolved transcriptomics and single-nucleus RNA-sequencing integrated dataset from the entorhinal cortex (ERC) of postmortem human brain donors. ERC is implicated in early progression of Alzheimer’s Disease (AD) and we chose this brain region to study gene expression changes associated with AD risk by comparing APOE E2 and E4 allele carriers. Donors with no AD diagnosis or widespread neurodegeneration were exclusively selected. As AD risk is increased in African Ancestry in contrast to European Ancestry backgrounds, and AD risk is also increased in women compared to men, our dataset included donors from these different backgrounds. We identified a pre-myleinating oligodendrocyte sub-cluster with transcriptomic changes strongly associated with APOE E4 carriers. These changes were present in both ancestry backgrounds, although they were more pronounced in African Ancestry donors. To facilitate future studies based on this dataset, we provided the raw and processed data, and created interactive web applications.
• 🔗 查看原文

3. ⭐ GSE293968 利用激光捕获核仁显微切割测序 (scRNA-Seq) 分析单个核仁中的基因组结构

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、scRNA、genome
• 📝 描述：Contributors : Kaivalya Walavalkar ; Raffaella SantoroSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe three-dimensional architecture of the eukaryotic genome is a critical determinant in the regulation of gene expression programs. Repressive chromatin regions are localized either at the nuclear lamina or the nucleolus. While the role of the nuclear lamina in genome organization has been widely studied, the role of the nucleolus has only recently come under investigation. Here, we present a new method called nucleolus architecture mapping (NAM) for identifying nucleolus-associated genomic domains (NADs) at a single nucleolus resolution. NAM combines laser capture microdissection and DNA sequencing. We applied NAM to embryonic stem cells (ESCs) and neural progenitor cells and observed a distinct pattern of nucleolus-to-nucleolus heterogeneity for NADs. NAM not only identified characteristic features of NADs, such as high levels of H3K9me2, depletion of H3K27me3, low active histone marks, and repressed gene expression but also revealed that the genomic domains seen in cell population studies to contact both nucleoli and nuclear lamina (NAD/LAD regions) can contact the nucleolus in one cell and the NL in another cell, but rarely both nucleolus and NL in the same cell. Additionally, we found that ribosomal protein (RP) genes are frequently associated with the nucleolus, suggesting a potential direct crosstalk between the nucleolus and the regulation of RP genes, and hence ribosome biogenesis. We also performed NAM upon perturbation of the nucleolus structure by inhibiting PolI transcription with Actinomycin D. This showed a loss of mostly NADs from the nucleolus other than the chromosomes containing rRNA genes, demonstrating that nucleolar integrity is required for genomic contacts with the nucleoli. Additionally, NAM applied to hybrid ESCs demonstrates a predominantly monoallelic distribution of NADs in single cells. We identify parental-specific NADs exhibiting a non-uniform distribution across different chromosomes. Our findings underscore NAM as an invaluable tool for investigating nucleolar organization in individual cells and, potentially, genome organization in other large phase-separated organelles in the future.
• 🔗 查看原文

4. ⭐ GSE292363 p53 驱动与乳腺癌管腔细胞特性相关的表观遗传程序 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq、epigenetic
• 📝 描述：Contributors : Yael Aylon ; Noa Furth ; Efrat Shema ; Moshe OrenSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBreast cancer is one of the most commonly diagnosed cancers among women and the leading cause of death in women under 50. The majority of breast cancers are estrogen receptor α-positive (ER+). Historically, these cancers are treated with therapies, such as tamoxifen, that inhibit ER activity. The TP53 tumor suppressor gene, encoding the p53 protein, is the most frequently mutated gene in breast cancer, and TP53 mutations are associated with diminished tamoxifen response and worse prognosis. Here, we report that in breast cancer cells p53 and ER cooperate to regulate the expression of a set of genes encoding chromatin modifiers. The net result is a global increase in H3K4me3 and decrease in H3K9me3 chromatin marks. The resultant “open” chromatin is associated with increased transcription of luminal cell identity genes and augmented tamoxifen sensitivity. Conversely, diminished p53 control of these chromatin modulators is associated with the evolution of tamoxifen resistance and cancer stem cell properties.
• 🔗 查看原文

5. ⭐ GSE292361 p53 驱动与乳腺癌管腔细胞特性相关的表观遗传程序 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、ATAC-seq、epigenetic
• 📝 描述：Contributors : Yael Aylon ; Noa Furth ; Efrat Shema ; Moshe OrenSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensBreast cancer is one of the most commonly diagnosed cancers among women and the leading cause of death in women under 50. The majority of breast cancers are estrogen receptor α-positive (ER+). Historically, these cancers are treated with therapies, such as tamoxifen, that inhibit ER activity. The TP53 tumor suppressor gene, encoding the p53 protein, is the most frequently mutated gene in breast cancer, and TP53 mutations are associated with diminished tamoxifen response and worse prognosis. Here, we report that in breast cancer cells p53 and ER cooperate to regulate the expression of a set of genes encoding chromatin modifiers. The net result is a global increase in H3K4me3 and decrease in H3K9me3 chromatin marks. The resultant “open” chromatin is associated with increased transcription of luminal cell identity genes and augmented tamoxifen sensitivity. Conversely, diminished p53 control of these chromatin modulators is associated with the evolution of tamoxifen resistance and cancer stem cell properties.
• 🔗 查看原文

6. ⭐ GSE275698 花粉单核甲基胞嘧啶和转录组测序揭示 MBD5/6 和 MBD7 在转录调控中的拮抗作用 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、RNA-seq、transcriptome
• 📝 描述：Contributors : Lucia Ichino ; Colette L Picard ; Brandon A Boone ; Tyler Buckley ; Jaewon Yun ; Kevin Abuhanna ; Yi Zhang ; Noah J Behrendt ; Chongyuan Luo ; Steven E JacobsenSeries Type : Expression profiling by high throughput sequencingOrganism : Arabidopsis thalianaMBD5, MBD6, and MBD7 are CG-specific methyl-readers with opposite functions: MBD5 and MBD6 (MBD5/6) redundantly repress methylated loci in pollen vegetative nuclei (VN), while MBD7 prevents transgene silencing, possibly by promoting DNA demethylation. Here we show that transcriptional derepression in mbd5/6 pollen is rescued by loss of MBD7, suggesting that MBD5/6 counteract MBD7 activity. By simultaneously profiling DNA methylation and gene expression in single pollen nuclei, we found that CG methylation is lost at MBD5/6 targets specifically in the early post-mitotic VN of mbd5/6. This loss precedes mbd5/6 transcriptional derepression and is largely restored in mbd5/6/7 triple mutants. Altering MBD6 to recruit the MBD7 complex instead of its normal interactors caused demethylation and upregulation of MBD5/6 targets, turning MBD6 from a repressor into an activator. We propose that in VN, where chromatin is decondensed, MBD5/6 are required to protect accessible DNA from demethylation and derepression by the MBD7 complex.
• 🔗 查看原文

7. ⭐ GSE269199 利用激光捕获核仁显微切割测序 (ChIP-Seq) 分析单个核仁中的基因组结构

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、ChIP-seq、genome
• 📝 描述：Contributors : Kaivalya Walavalkar ; Raffaella SantoroSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusThe three-dimensional architecture of the eukaryotic genome is a critical determinant in the regulation of gene expression programs. Repressive chromatin regions are localized either at the nuclear lamina or the nucleolus. While the role of the nuclear lamina in genome organization has been widely studied, the role of the nucleolus has only recently come under investigation. Here, we present a new method called nucleolus architecture mapping (NAM) for identifying nucleolus-associated genomic domains (NADs) at a single nucleolus resolution. NAM combines laser capture microdissection and DNA sequencing. We applied NAM to embryonic stem cells (ESCs) and neural progenitor cells and observed a distinct pattern of nucleolus-to-nucleolus heterogeneity for NADs. NAM not only identified characteristic features of NADs, such as high levels of H3K9me2, depletion of H3K27me3, low active histone marks, and repressed gene expression but also revealed that the genomic domains seen in cell population studies to contact both nucleoli and nuclear lamina (NAD/LAD regions) can contact the nucleolus in one cell and the NL in another cell, but rarely both nucleolus and NL in the same cell. Additionally, we found that ribosomal protein (RP) genes are frequently associated with the nucleolus, suggesting a potential direct crosstalk between the nucleolus and the regulation of RP genes, and hence ribosome biogenesis. We also performed NAM upon perturbation of the nucleolus structure by inhibiting PolI transcription with Actinomycin D. This showed a loss of mostly NADs from the nucleolus other than the chromosomes containing rRNA genes, demonstrating that nucleolar integrity is required for genomic contacts with the nucleoli. Additionally, NAM applied to hybrid ESCs demonstrates a predominantly monoallelic distribution of NADs in single cells. We identify parental-specific NADs exhibiting a non-uniform distribution across different chromosomes. Our findings underscore NAM as an invaluable tool for investigating nucleolar organization in individual cells and, potentially, genome organization in other large phase-separated organelles in the future.
• 🔗 查看原文

8. ⭐ GSE269198 利用激光捕获核仁显微切割测序 (RNA-Seq) 分析单个核仁中的基因组结构

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、RNA-seq、genome
• 📝 描述：Contributors : Kaivalya Walavalkar ; Raffaella SantoroSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe three-dimensional architecture of the eukaryotic genome is a critical determinant in the regulation of gene expression programs. Repressive chromatin regions are localized either at the nuclear lamina or the nucleolus. While the role of the nuclear lamina in genome organization has been widely studied, the role of the nucleolus has only recently come under investigation. Here, we present a new method called nucleolus architecture mapping (NAM) for identifying nucleolus-associated genomic domains (NADs) at a single nucleolus resolution. NAM combines laser capture microdissection and DNA sequencing. We applied NAM to embryonic stem cells (ESCs) and neural progenitor cells and observed a distinct pattern of nucleolus-to-nucleolus heterogeneity for NADs. NAM not only identified characteristic features of NADs, such as high levels of H3K9me2, depletion of H3K27me3, low active histone marks, and repressed gene expression but also revealed that the genomic domains seen in cell population studies to contact both nucleoli and nuclear lamina (NAD/LAD regions) can contact the nucleolus in one cell and the NL in another cell, but rarely both nucleolus and NL in the same cell. Additionally, we found that ribosomal protein (RP) genes are frequently associated with the nucleolus, suggesting a potential direct crosstalk between the nucleolus and the regulation of RP genes, and hence ribosome biogenesis. We also performed NAM upon perturbation of the nucleolus structure by inhibiting PolI transcription with Actinomycin D. This showed a loss of mostly NADs from the nucleolus other than the chromosomes containing rRNA genes, demonstrating that nucleolar integrity is required for genomic contacts with the nucleoli. Additionally, NAM applied to hybrid ESCs demonstrates a predominantly monoallelic distribution of NADs in single cells. We identify parental-specific NADs exhibiting a non-uniform distribution across different chromosomes. Our findings underscore NAM as an invaluable tool for investigating nucleolar organization in individual cells and, potentially, genome organization in other large phase-separated organelles in the future.
• 🔗 查看原文

9. ⭐ GSE308007 人类内嗅皮层在不同阿尔茨海默病风险人群中的空间和单细胞转录组学研究

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer、spatial、transcriptomics
• 📝 描述：Contributors : Louise A Huuki-Myers ; Heena R Divecha ; Svitlana V Bach ; Madeline R Valentine ; Nicholas J Eagles ; Bernard Mulvey ; Rahul A Bharadwaj ; Ruth Zhang ; James R Evans ; Melissa Grant-Peters ; Ryan A Miller ; Joel E Kleinman ; Shizhong Han ; Thomas M Hyde ; Stephanie C Page ; Danie R Weinberger ; Keri Martinowich ; Mina Ryten ; Kristen R Maynard ; Leonardo Collado-TorresSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensWe present the first spatially-resolved transcriptomics and single-nucleus RNA-sequencing integrated dataset from the entorhinal cortex (ERC) of postmortem human brain donors. ERC is implicated in early progression of Alzheimer’s Disease (AD) and we chose this brain region to study gene expression changes associated with AD risk by comparing APOE E2 and E4 allele carriers. Donors with no AD diagnosis or widespread neurodegeneration were exclusively selected. As AD risk is increased in African Ancestry in contrast to European Ancestry backgrounds, and AD risk is also increased in women compared to men, our dataset included donors from these different backgrounds. We identified a pre-myleinating oligodendrocyte sub-cluster with transcriptomic changes strongly associated with APOE E4 carriers. These changes were present in both ancestry backgrounds, although they were more pronounced in African Ancestry donors. To facilitate future studies based on this dataset, we provided the raw and processed data, and created interactive web applications.
• 🔗 查看原文

10. ⭐ GSE218024 STING激动剂可克服卵巢癌中STAT3介导的免疫抑制和对PARP抑制剂的适应性耐药性

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、regex:immuno(logy|therapy|suppression)、resistance
• 📝 描述：Contributors : Liya Ding ; Qiwei Wang ; Shaozhen Xie ; Ziying Lin ; Jean J ZhaoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusBackground: PARP inhibition (PARPi) has demonstrated potent therapeutic efficacy in patients with BRCA-mutant ovarian cancer. However, acquired resistance to PARPi remains a major challenge in the clinic. Methods: PARPi-resistant ovarian cancer mouse models were generated by long-term treatment of olaparib in syngeneic Brca1-deficient ovarian tumors. STAT3-mediated immunosuppression was investigated in vitro by co-culture experiments and in vivo by analysis of immune cells in the TME of human and mouse PARPi-resistant tumors. Whole genome transcriptome analysis was performed to assess the anti-tumor immunomodulatory effect of STING (stimulator of interferon genes) agonists on myeloid cells in the TME of PARPi-resistant ovarian tumors. A STING agonist was used to overcome STAT3-mediated immunosuppression and acquired PARPi resistance in syngeneic and PDX models of ovarian cancer. Results: In this study, we uncover an adaptive resistance mechanism to PARP inhibition mediated by tumor associated macrophages (TAMs) in the tumor microenvironment (TME). Markedly increased populations of pro-tumor macrophages are found in BRCA-deficient ovarian tumors that rendered resistance to PARPi in both murine models and patients. Mechanistically, PARP inhibition elevates the STAT3 signaling pathway in tumor cells, which in turn promotes pro-tumor polarization of TAMs. STAT3 ablation in tumor cells mitigates polarization of pro-tumor macrophages and increases tumor-infiltrating T-cells upon PARP inhibition. These findings are corroborated in patient-derived, PARPi-resistant BRCA1-mutant ovarian tumors. Importantly, STING agonists reshape the immunosuppressive TME by reprogramming myeloid cells and overcome the TME-dependent adaptive resistance to PARPi in ovarian cancer. This effect is further enhanced by addition of PD-1 blockade. Conclusions: We elucidate an adaptive immunosuppression mechanism rendering resistance to PARPi in BRCA1-mutant ovarian tumors. This is mediated by enrichment of pro-tumor TAMs propelled by PARPi-induced STAT3 activation in tumor cells. We also provide a new strategy to reshape the immunosuppressive TME with STING agonist and overcome PARPi resistance in ovarian cancer.
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1. CanSig 基准从单细胞转录组数据中发现可重复癌细胞状态的方法

• ✍️ 作者：未知作者
• 🏷️ 关键词：单细胞、转录组
• 📝 描述：Secret hovertext: 单细胞 RNA 测序（scRNA-seq）有助于发现定义患者细胞状态的基因表达特征，可用于患者分层和精准肿瘤学。然而，用于分析这些数据的计算方法缺乏标准化，阻碍了特征检测的可重复性。为了解决这个问题，我们开发了 CanSig，这是一种综合基准测试工具，用于评估识别癌症转录特征的方法。CanSig 将批量校正和生物信号保存的指标与转录特征相关指标集成在一起，根据特征重新发现、跨数据集可重复性和临床相关性对方法进行评分。CanSig 被应用于来自五种人类癌症类型（胶质母细胞瘤、乳腺癌、肺腺癌、横纹肌肉瘤和皮肤鳞状细胞癌）的 12 个 scRNA-seq 数据集的 13 种方法，代表 185 名患者和 174,000 个恶性细胞。这些方法识别的特征与临床相关结果相关，包括患者生存和淋巴结转移。这些结果确定 Harmony、BBKNN 和 fastMNN 是发现癌症共享转录状态得分最高的整合方法。总体而言，CanSig
• 🔗 查看原文

2. 通过双向阻断 CXCL12/CXCR4 轴抑制三阴性乳腺癌复发转移的增强型癌症纳米疫苗

• ✍️ 作者：未知作者
• 🏷️ 关键词：癌症、疫苗
• 📝 描述：Secret hovertext: 原位癌症疫苗是一种新的癌症免疫治疗方法，但癌组织局部免疫抑制微环境限制了其免疫反应和治疗效果。CXCL12/CXCR4 轴在形成免疫抑制微环境中起关键作用。本研究以 siCXCR4（S）为“免疫佐剂”，与羟喜树碱（HCPT）共同加载，开发原位癌纳米疫苗（HCPT/S@CaP/HA），协同抑制三阴性乳腺癌（TNBC）的生长、复发和转移。HCPT/S@CaP/HA 主动靶向原位 TNBC 细胞和癌相关成纤维细胞（CAFs），诱导原位 TNBC 细胞免疫原性死亡，促进树突状细胞（DC）的成熟。同时，HCPT/S@CaP/HA 还减少了 CAFs 对 CXCL12 的分泌，并沉默了 TNBC 组织中 CXCR4 的表达，双向阻断 CXCL12/CXCR4 轴，从而协同逆转免疫抑制微环境，增强原位 TNBC 组织中细胞毒性 T 淋巴细胞的浸润和活性，进而抑制原位 TNBC 的生长。此外，HCPT/S@CaP/HA
• 🔗 查看原文

3. 免疫检查点抑制剂相关的心血管毒性作用

• ✍️ 作者：未知作者
• 🏷️ 关键词：免疫、心血管
• 📝 描述：Secret hovertext: 重要性 免疫检查点抑制剂 （ICI） 疗法的引入改善了癌症预后，但代价是不良事件，主要与免疫系统有关。心血管 （CV） 毒性作用，尤其是心肌炎，是国际心脏肿瘤学会由肿瘤学、血液学和心脏病学专家代表发表的本立场声明的主题。观察 ICI 疗法的 CV 毒性作用包括炎症相关疾病，如心肌炎、心包炎和血管炎，以及慢性炎症的加重，如伴有急性缺血并发症（心肌梗塞和中风）的动脉粥样硬化。接受 ICI 治疗的患者还可能出现心功能障碍、应激性心肌病（章鱼壶或心尖气球综合征）和心力衰竭，而心肌没有炎症细胞浸润。房性和室性心律失常可在全身炎症环境、心肌炎或缺血的情况下出现。在所有潜在的 CV 不良反应中，心肌炎仍然是最令人担忧的，尽管死亡率随着时间的推移而下降，表现范围不断扩大，从意义不确定的肌钙蛋白升高到冒烟、非严重、重度或暴发性心肌炎。结论和相关性心肌炎的担忧继续在接受 ICI 治疗的患者中主导 CV 毒性作
• 🔗 查看原文

4. 基于 PLGA 的聚合物纳米载体在结直肠癌治疗中的进展：通过受控递送策略克服化疗耐药性

• ✍️ 作者：未知作者
• 🏷️ 关键词：耐药
• 📝 描述：Secret hovertext: 结直肠癌 （CRC） 是全球最常见的恶性肿瘤之一，男性的发病率明显更高。尽管有多种化疗选择，但由于药物溶解度差、肠道吸收受限、全身清除快和多重耐药性，临床疗效仍然有限。聚乳酸-乙醇酸共聚物（PLGA）是一种成熟的可生物降解和生物相容性共聚物，因其在开发先进药物递送系统的潜力而受到广泛关注。其可调节的降解动力学由乳酸与乙醇酸的比例控制，能够精确调节药物释放曲线。基于 PLGA 的纳米载体具有多种治疗优势，包括提高溶解度、延长结肠保留时间和靶向递送抗癌药物。此外，共聚物、配体或刺激反应部分的表面功能化已证明细胞摄取、肿瘤特异性和对 CRC 细胞的细胞毒性增强。本文重点介绍了 PLGA 纳米载体在结直肠癌治疗中的合成、功能设计和生物医学应用的最新进展，强调了它们在克服化疗耐药性和脱靶毒性等关键挑战方面的作用。这些进步凸显了基于 PLGA 的聚合物系统在提高抗癌疗法的治疗指数和转化可行性方面的潜力。
• 🔗 查看原文

5. Paneth 样转变驱动结直肠癌中 KRAS 和 EGFR 双重靶向的耐药性

• ✍️ 作者：未知作者
• 🏷️ 关键词：耐药
• 📝 描述：Secret hovertext: 虽然双重 KRAS 和表皮生长因子受体 （EGFR） 抑制在治疗 KRAS 突变结直肠癌 （CRC） 方面显示出希望，但耐药性仍然是一个主要挑战。使用基因工程小鼠模型、患者来源的类器官和异种移植物以及临床标本，我们发现在联合 KRAS 和 EGFR 抑制下存活的结直肠肿瘤获得了潘氏样细胞状态——一种通常局限于肠隐窝的分泌谱系。谱系追踪表明，CRC 细胞通过转变为潘氏样状态来逃避双重治疗。通过综合转录组分析和 CRISPR 基因筛选，我们确定 SMAD1 是该谱系可塑性的关键调节因子，通过直接激活 FGFR3 来促进耐药性。FGFR3 的遗传或药理学抑制可防止潘氏样转化，恢复药物敏感性，并在多个临床前模型中与 KRAS-EGFR 抑制协同作用。这些发现表明，SMAD1-FGFR3 轴触发潘氏样可塑性，以驱动 CRC 中的 KRAS-EGFR 双重治疗耐药性，并强调 FGFR3 阻断是克服可塑性驱动的药物耐受性的一种有前途的策略。
• 🔗 查看原文

6. 癌症锻炼：体育锻炼作为癌症治疗的药物

• ✍️ 作者：未知作者
• 🏷️ 关键词：癌症
• 📝 描述：Secret hovertext: 运动作为癌症的辅助疗法具有巨大的潜力，不仅可以改善生活质量，还可以影响肿瘤进展、治疗反应和生存。其临床整合仍然受到模型变异性、异质性干预措施和缺乏预测性生物标志物的限制。随着该领域的进步，除了强调实际的临床转化外，识别运动的分子效应器也至关重要。本评论强调了运动的抗肿瘤作用，并评估了运动如何从支持性治疗发展为癌症治疗的有针对性的循证组成部分。
• 🔗 查看原文

7. MED1 驱动的 ecDNA 超级增强子在癌症中的应用

• ✍️ 作者：未知作者
• 🏷️ 关键词：癌症
• 📝 描述：Secret hovertext: 富含增强子的染色体外环状 DNA （ecDNA） 驱动致癌转录和肿瘤进展，但其机制仍然难以捉摸。在本期《 癌细胞》 杂志上，魏等人发现了 MED1 驱动的 ecDNA 超级增强子作为调控中心，并表明破坏含有 ecDNA 的缩合物会选择性地损害转录并以癌症类型特异性的方式诱导细胞死亡。
• 🔗 查看原文

详细内容（全部5条）

1. GREGoR——加速罕见病基因组学研究

• ✍️ 作者：未知作者
• 🏷️ 关键词：genomics
• 📝 描述：Researchers use RNA sequencing and global data sharing through the GREGoR Consortium to improve rare disease diagnosis and advance genomic understanding across thousands of unsolved cases…
• 🔗 查看原文

2. 长读长测序能够解析等位基因特异性位点的异构体复杂性

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：Using long-read RNA sequencing, researchers uncover how allele-specific differences shape gene expression, revealing complex isoforms and confirming imprinting patterns at key…
• 🔗 查看原文

3. 领先的基因组学研究推动创新并直接影响人类。

• ✍️ 作者：未知作者
• 🏷️ 关键词：genomics
• 📝 描述：Researchers at UC Santa Cruz highlight how RNA sequencing and genomics innovations are transforming cancer diagnostics, personalized medicine, and ecological research through collaboration and technological advancement…
• 🔗 查看原文

4. 你的焦虑可能由大脑中隐藏的免疫细胞控制。

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune
• 📝 描述：Researchers have uncovered surprising evidence that anxiety may be controlled not by neurons but by two dueling groups of immune cells inside the brain. These microglia act like biological pedals—one pushing anxiety forward and the other holding it back.
• 🔗 查看原文

5. 科学家发现一种能模拟运动并延缓衰老的分子

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging
• 📝 描述：Exercise appears to spark a whole-body anti-aging cascade, and scientists have now mapped out how it happens—and how a simple oral compound can mimic it. By following volunteers through rest, intense workouts, and endurance training, researchers found that the kidneys act as the hidden command center, flooding the body with a metabolite called betaine that restores balance, rejuvenates immune cells, and cools inflammation. Even more striking, giving betaine on its own reproduced many benefits of long-term training, from sharper cognition to calmer inflammation.
• 🔗 查看原文

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• GSE303125 抑制血红素生物合成可触发急性髓系白血病中的铜凋亡 [RNA-Seq OCIAML3_ALAS1_KO_and_SA]
• GSE303124 抑制血红素生物合成可触发急性髓系白血病中的铜凋亡 [RNA-Seq Hoxb8_R882H_v_EV]
• GSE303121 抑制血红素生物合成可引发急性髓系白血病细胞凋亡 [RNA-Seq DIN]
• GSE303120 抑制血红素生物合成可引发急性髓系白血病细胞的铜凋亡 [ChIP-Seq]
• GSE293334 转录因子等位基因拓扑中心化驱动致癌多增强子转录调控 [ChIP-seq]
• GSE293332 转录因子等位基因拓扑中心化驱动致癌多增强子转录调控 [Hi-C]
• GSE293331 转录因子驱动等位基因拓扑中心化，进而调控致癌多增强子转录 [RNA-seq]
• GSE293330 转录因子驱动等位基因拓扑中心化，进而调控致癌多增强子转录 [ATAC-seq]
• GSE293131 增强子重连在肌肉干细胞衰老过程中协调炎症和细胞身份丧失 [Hi-C]
• GSE293130 增强子重连调控肌肉干细胞衰老过程中的炎症和细胞身份丧失 [RNA-seq]
• GSE293128 增强子重连协调肌肉干细胞衰老过程中的炎症和细胞身份丧失 [ATAC-seq]
• GSE292362 p53 驱动与乳腺癌管腔细胞特性相关的表观遗传程序 [CUT&RUN]
• GSE286985 基因表达和染色质可及性的整合单细胞分析揭示 CTCF 是干细胞分化和肺形态发生的关键调节因子 [scRNA-seq]
• GSE282468 组蛋白变体 H2BE 在大脑中具有年龄和细胞类型特异性效应 [RNASeq]
• GSE279146 通过激光捕获核仁显微切割测序 (ActD_RNAseq) 分析单个核仁中的基因组结构
• GSE275693 通过单核多组学 [ChIP-Seq] 揭示花粉中调控基因表达的拮抗表观遗传机制
• GSE270063 原始多能性的退出包含一个代谢诱导的端粒稳态检查点 [RNA-seq]
• GSE269200 利用激光捕获核仁显微切割测序 (NoLMseq) 分析单个核仁中的基因组结构
• GSE253432 原始多能性的退出包含代谢诱导的端粒稳态检查点 [scRNA-seq]
• GSE235711 炎症性呼吸道鼻腔的免疫上皮相互作用和组织重塑 [scRNA-seq]
• GSE296487 利用DNA甲基化谱作为分子分型工具：一项基于儿科人群的中枢神经系统肿瘤研究
• GSE279978 体外神经元RNA测序、体内皮层单核RNA测序、DOT1L缺失模型中H3K79me2的体内皮层ChIP测序
• GSE309781 甲基化组数据集，采用犬全血全基因组亚硫酸氢盐测序 (WGBS) 获得。
• GSE309117 肝细胞特异性表皮生长因子受体 (EGFR) 缺失可减轻对乙酰氨基酚诱导的小鼠肝损伤 [RNA-seq Illumina]
• GSE309115 肝细胞特异性表皮生长因子受体 (EGFR) 缺失可减轻对乙酰氨基酚诱导的小鼠肝损伤 [RNA-seq AVITI]
• GSE307968 HTGTS-TCR-seq 用于分析小鼠和人类 T 细胞受体 α 和 β 基因重排和多样性 [RNA-seq]
• GSE307734 微生物群衍生的胆汁酸通过肺泡巨噬细胞的代谢重编程来改善肺部炎症
• GSE307663 转录因子 ZNF263 启动人类胚胎干细胞的多能性丧失和早期分化 [RNA-Seq 2]
• GSE307615 围绝经期雌二醇与孕酮失衡通过 ERRα 失调和能量稳态失衡驱动阿尔茨海默病风险 [EnrichedNeuron_RNASeq]
• GSE306104 广泛存在的低亲和力基序增强了小鼠胚胎干细胞的染色质可及性和调控潜力 [ATAC-seq]
• GSE302422 黑色素瘤RNA测序
• GSE300097 组蛋白变体 H2BE 在大脑中年龄和细胞类型特异性效应 [E2F_CUT&Tag]
• GSE300096 组蛋白变体 H2BE 在大脑中年龄和细胞类型特异性效应 [Cortex_CUT&Tag]
• GSE298115 小鼠甲状旁腺细胞表达Gcm2激活变体的空间转录组分析
• GSE295606 真皮脂肪细胞通过代谢通讯激活毛囊干细胞 [SP]
• GSE295605 真皮脂肪细胞通过代谢通讯激活毛囊干细胞 [SDS II]
• GSE293757 ZEB2 和 SP1 的协同作用上调 PD-L1 和 CCL2，从而促进肿瘤细胞的免疫抑制活性。
• GSE293335 转录因子等位基因拓扑中心化驱动致癌多增强子转录调控 [Micro-C]
• GSE293333 转录因子等位基因拓扑中心化驱动致癌多增强子转录调控 [HiChIP]
• GSE293129 增强子重连在肌肉干细胞衰老过程中协调炎症和细胞身份丧失 [CUT&RUN]
• GSE286981 基因表达和染色质可及性的整合单细胞分析揭示 CTCF 是干细胞分化和肺形态发生的关键调节因子 [多组学]
• GSE282595 FoxO1 和 Pparα 在肝脏基因表达和代谢适应中的协同作用
• GSE282520 组蛋白变体 H2BE 在大脑中年龄和细胞类型特异性效应 [snRNA-seq]
• GSE282519 组蛋白变体 H2BE 在大脑中具有年龄和细胞类型特异性效应 [Cut&Tag]
• GSE282469 组蛋白变体 H2BE 在大脑中年龄和细胞类型特异性效应 [ATACSeq]
• GSE282467 组蛋白变体 H2BE 在大脑中的年龄和细胞类型特异性效应 [完整 RNA 测序]
• GSE281455 衰老突触体中与核糖体相关的RNA
• GSE281453 衰老过程中突触体的转录组分析
• GSE279884 围绝经期雌二醇与孕酮失衡通过 ERRα 失调和能量失衡驱动阿尔茨海默病风险 [VCD_Cycle14]
• GSE279883 围绝经期雌二醇与孕酮失衡通过 ERRα 失调和能量失衡驱动阿尔茨海默病风险 [VCD_Cycle7]
• GSE279882 围绝经期雌二醇与孕酮失衡通过 ERRα 失调和能量失衡驱动阿尔茨海默病风险 [VCD+P4_Cycle14]
• GSE275831 通过单核多组学 [snmCT-seq] 揭示花粉中调控基因表达的拮抗表观遗传机制
• GSE275821 TOP2B 与 ATRX 协同作用，解析 G-四链体并维持胶质瘤中复制叉的稳定性
• GSE275267 通过单核多组学揭示花粉中调控基因表达的拮抗性表观遗传机制
• GSE273001 整合 RNA-seq 和 CLIP-seq 分析揭示了 hnRNP-F 在高糖条件下对 TNFα/NFκB 信号通路的调控作用
• GSE270658 单细胞分析鉴定出正在经历衰老的特定 RPE 亚群
• GSE269897 先锋转录因子之间的分子和上位性相互作用塑造核小体动力学和细胞分化 [ChIP-Seq]
• GSE268713 先锋转录因子之间的分子和上位性相互作用塑造核小体动力学和细胞分化 [ATAC-seq]
• GSE268573 围绝经期雌二醇与孕酮失衡通过 ERRα 失调和能量失衡驱动阿尔茨海默病风险 [VCD_Treatment]
• GSE268572 围绝经期雌二醇与孕酮失衡通过 ERRα 失调和能量失衡驱动阿尔茨海默病风险 [Esrra_shRNA]
• GSE267441 先锋转录因子之间的分子和上位性相互作用塑造核小体动力学和细胞分化 [RNA-seq]
• GSE264047 线粒体-溶酶体串扰决定 Treg 细胞的逐步分化，从而限制炎症相关的免疫病理 [bulk RNA-seq]
• GSE263803 线粒体-溶酶体串扰决定 Treg 细胞的逐步分化，从而限制炎症相关的免疫病理 [scRNA-seq3]
• GSE262495 线粒体-溶酶体串扰决定 Treg 细胞的逐步分化，从而限制炎症相关的免疫病理 [scRNA-seq2]
• GSE262494 线粒体-溶酶体串扰决定 Treg 细胞的逐步分化，从而限制炎症相关的免疫病理 [scRNA-seq1]
• GSE254457 中药数字化转型：利用消化中药诱导转录组测序将其转化为生物实体数据_second_SW1783_batchE
• GSE254455 中药数字化转型：利用消化中药诱导转录组测序将其转化为生物实体数据_second_SW1783_batchD
• GSE254453 中药数字化转型：利用消化中药诱导转录组测序将其转化为生物实体数据_second_SW1783_batchC
• GSE254452 中药数字化转型：利用消化中药诱导转录组测序将其转化为生物实体数据_second_SW1783_batchB
• GSE254450 中药数字化转型：利用消化中药诱导转录组测序将其转化为生物实体数据_second_SW1783_batchA
• GSE252818 中药数字化转型：利用消化中药诱导转录组测序将其转化为生物实体数据_second_A549_batchE
• GSE252817 中药数字化转型：利用消化中药诱导转录组测序将其转化为生物实体数据_second_A549_batchD
• GSE252816 中药数字化转型：利用消化中药诱导转录组测序将其转化为生物实体数据_second_A549_batchC
• GSE252815 中药数字化转型：利用消化中药诱导转录组测序将其转化为生物实体数据_second_A549_batchB
• GSE252814 中药数字化转型：利用消化中药诱导转录组测序将其转化为生物实体数据_second_A549_batchA
• GSE250626 中药数字化转型：利用消化中药诱导转录组测序将其转化为生物实体数据_second_HT29_batchE
• GSE250625 中药数字化转型：利用消化中药诱导转录组测序将其转化为生物实体数据_second_HT29_batchD
• GSE250624 中药数字化转型：利用消化中药诱导转录组测序将其转化为生物实体数据_second_HT29_batchC
• GSE250623 中药数字化转型：利用消化中药诱导转录组测序将其转化为生物实体数据_second_HT29_batchB
• GSE250621 中药数字化转型：利用消化中药诱导转录组测序将其转化为生物实体数据_second_HT29_batchA
• GSE248974 中药数字化转型：利用消化中药诱导的转录组测序将其转化为生物实体数据_second_HepG2_batchE
• GSE248973 中药数字化转型：利用消化中药诱导的转录组测序将其转化为生物实体数据_second_HepG2_batchD
• GSE248972 中药数字化转型：利用消化中药诱导的转录组测序将其转化为生物实体数据_second_HepG2_batchC
• GSE248970 中药数字化转型：利用消化中药诱导的转录组测序将其转化为生物实体数据_second_HepG2_batchB
• GSE248969 中药数字化转型：利用消化中药诱导的转录组测序将其转化为生物实体数据_second_HepG2_batchA
• GSE248492 转录因子 ZNF263 启动人类胚胎干细胞的多能性丧失和早期分化 [MEKi RNA-Seq]
• GSE242905 转录因子 ZNF263 启动人类胚胎干细胞的多能性丧失和早期分化 [scRNA-seq]
• GSE242904 转录因子 ZNF263 启动人类胚胎干细胞的多能性丧失和早期分化 [RNA-seq]
• GSE242827 转录因子 ZNF263 启动人类胚胎干细胞的多能性丧失和早期分化 [ChIP-seq]
• GSE241407 FXR-Casp6 轴介导的胆汁酸/肠道菌群感知调节新生儿 β 细胞数量扩张 [scRNA-Seq]
• GSE241406 FXR-Casp6 轴介导的胆汁酸/肠道菌群感知调节新生儿 β 细胞数量扩张 [scATAC-Seq]
• GSE240175 牛胚胎干细胞在胚胎和胚外分化中的可塑性 [ 批量 RNA 测序]
• GSE240174 牛胚胎干细胞在胚胎和胚外分化中的可塑性 [scRNA-seq]
• GSE239988 真皮脂肪细胞通过代谢通讯激活毛囊干细胞 [SDS]
• GSE239986 真皮脂肪细胞通过代谢通讯激活毛囊干细胞 [HFSC]
• GSE227950 四聚体 MADS-box 转录因子在花命运决定中的作用 [RNA-seq]
• GSE227949 四聚体 MADS-box 转录因子在花命运决定中的作用 [ATAC-seq]
• GSE227948 四聚体 MADS-box 转录因子在花命运决定中的作用 [ChIP-seq]
• GSE307259 c-JUN 增强 CRISPR 敲入抗 B7-H3 CAR T 细胞功能，用于治疗小细胞肺癌和胸腔 SMARCA4 缺陷型未分化肿瘤
• GSE305571 小鼠胚胎干细胞 (mESC) 中 Mpp8 和 Tasor-DNA 结合的全基因组分析 [CUT&Tag]
• GSE293459 持续性肿瘤细胞中开放染色质特征的单细胞分辨率
• GSE293036 全基因组发现多发性硬化症遗传风险变异等位基因调控活性
• GSE292609 对照组和 DOT1L HET 皮质核的 ChIP-seq 分析。
• GSE290944 DOT1L活性限制转录延伸速度，并促进RNAPII暂停，从而促进AID介导的诱变。[ChIP-seq]
• GSE289150 染色质重塑因子 OsCLSY4 功能丧失导致 RdDM 介导的胚乳特异性基因错误表达，从而影响籽粒品质 [RNA-Seq]
• GSE284085 细胞外基质驱动鸟苷酸生成，并保护胰腺癌细胞免受奥沙利铂诱导的 DNA 损伤。
• 利用 GS​​E284082 RNA-seq 分析 ADAR1i-124 或 5-AZA-CdR 处理的 YUMM1.7 小鼠黑色素瘤细胞，以研究其对 RNA 编辑的影响
• GSE277854 双宿主-病原体 RNA-Seq Aphanius dispar 和耳念珠菌卵黄囊显微注射
• GSE272883 RNA-seq 分析 Luciferase 对照感染和 DOT1L shRNA 感染的原代皮层神经元。
• GSE265944 MASTR-seq：利用测序技术对短串联重复序列进行多重分析
• GSE233974 DOT1L活性限制转录延伸速度，并促进RNAPII暂停，从而促进AID介导的诱变。[RNA-Seq]
• GSE297577 用靶向 AR 和 AR-V7 的 ITRI-148 PROTAC 处理的去势抵抗性前列腺癌细胞的转录谱
• GSE293829 CDK12失活诱导的IPA增强BRD4S的相分离驱动癌症转移
• GSE267065 工程化 3 号染色体和 8 号染色体同源非整倍体细胞模型中的转录组分析和核糖体足迹。
• GSE309765 siDhx37 敲低后小鼠 Sertoli 细胞系的 RNA-seq 分析
• GSE301824 多发性硬化症病变的分子和空间分析表明，脂质外排功能障碍是慢性活动性炎症的驱动因素
• GSE282012 RNA-seq 在电离辐射条件下敲低 SIRT7 的角质形成细胞中
• GSE281873 TRIM21 通过促进心脏成纤维细胞中 TRAF3 溶酶体降解来增强 IL-17A 信号传导并驱动自身免疫性心肌炎