详细内容（前10条）

1. ⭐ GSE319609 DNA甲基转移酶抑制可阻止铂类药物诱导的卵巢癌干细胞富集[RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq、enrichment
• 📝 描述：Contributors : Heather M O’Hagan ; Truc T VuongSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensPlatinum-based therapy is the standard first-line treatment for high-grade serous ovarian cancer (HGSC). However, most patients develop resistance and recurrence despite an initial response to therapy. Ovarian cancer stem cells (OCSCs) are enriched in recurrent tumors and contribute to platinum resistance. These tumors also show promoter DNA hypermethylation, and DNA methyltransferase inhibitors (DNMTis) have been shown to restore sensitivity in platinum-resistant ovarian cancer cells. Here, we demonstrated that combining DNMTi with platinum prevented the platinum-induced enrichment of OCSCs and identified NF-κB and STAT3 signaling pathways as potential regulators of platinum-induced OCSC enrichment. STAT3 was active at baseline in OC cells and platinum treatment alone activated NF-κB while maintaining STAT3 activity. Platinum combined with DNMTi decreased STAT3 activation, while still inducing NF-κB activation. Knockdown experiments demonstrated that the presence of both NF-κB and STAT3 was necessary for platinum-induced OCSC enrichment. Analysis of STAT3 and NF-κB subunit p65 CUT&RUN data showed increased binding in introns and intergenic regions in response to platinum. Additionally, DNMTi enriched NF-κB binding at endogenous retroviruses (ERVs), which correlated with changes in expression of nearby genes when DNMTi was combined with platinum. We conclude that combining DNMTi with platinum modulates STAT3 and NF-κB activation and genomic binding, potentially influencing target gene expression and preventing platinum-induced enrichment of OCSCs.
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2. ⭐ GSE299940 皮质中 H3K27ac 调控基因表达的改变与小鼠衰老过程中的认知衰退和情感行为相关：全基因组表观遗传学分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、genome、epigenetic
• 📝 描述：Contributors : Sarah B Scheinman ; Gemma L Carvill ; Hongxin DongSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusHistone acetylation plays a critical role in the regulation of gene expression in humans and animals, influencing various biological processes, including brain function during aging. Understanding the alterations in histone acetylation during aging could provide insights into the molecular mechanisms underlying age-related cognitive decline. In this study, we investigated the dynamics of histone acetylation and its functional effects in the brain during aging by characterizing and comparing differences in memory and affective behavior, histone H3 levels, expression of histone-modifying enzymes HDACs and HAT, genome-wide H3K27ac abundancy, an active enhancer, and gene expression between young (2-3 months old) and aged (18-20 months old) genetically identical mice. Our results demonstrate that aging induces a variety behavioral phenotypes including a decline in activity/locomotion, increase in anxiety, and memory impairment, that occurs in conjunction with dysregulation of HDAC 1, 2, and 3, HAT p300 and genome-wide differential abundancy of H3K27ac at a variety of gene promoters. Importantly, we also demonstrated that age-related reductions in H3K27ac at gene promoters were associated with decreased expression levels of genes related to DNA damage and aging including Map3K1, Rev1, and Cdk2ap1. Overall, our study suggests the role of histone acetylation as a regulator of gene expression during brain aging and that changes in histone acetylation are associated with age-related alterations in memory and cognitive decline.
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3. ⭐ GSE303100 通过全基因组 CRISPR-Cas9 筛选解析实验性胶质瘤中 CDK4/6 抑制的耐药性

• ✍️ 作者：未知作者
• 🏷️ 关键词：glioma、resistance、genome
• 📝 描述：Contributors : Daniel J Merk ; Ghazaleh TabatabaiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensCDK4/6 inhibitors exhibit therapeutic potential in several tumor entities. Their clinical efficacy in glioblastoma might be limited by intrinsic and acquired resistance mechanisms. Understanding underlying genetic and molecular factors of this resistance might inform the design of effective therapeutic strategies. Genome-wide CRISPR-Cas9 screens offer a powerful approach to systematically identify resistance drivers and synthetic lethal interactions, paving the way for rational combination therapies.We conducted genome-wide CRISPR-Cas9 knockout and activation screens in human glioma cell lines LN229 and GS9 under CDK4/6 inhibition using Brunello and Calabrese libraries. Top hits were validated using functional assays. Furthermore, we conducted bulk RNA sequencing of treated and untreated cells for transcriptomic insights into drug response modifiers and molecular pathways involved.Functional genomics identified Ambra1 and CCNE1 as key drivers of resistance. Both Ambra1 knockout and CCNE1 overexpression, conferred resistance across both long-term and stem-like glioma models. Additionally, knockout of CHEK1 and FAM122A uncovered synthetic lethal interactions with CDK4/6 inhibition. Functional validation confirmed that glioma cells rely on CHEK1 or FAM122A for cell cycle progression, with cell line specific sensitivity. Transcriptomic analyses consistently highlighted alterations in pathways associated with cell cycle regulation, DNA replication, and the Fanconi anemia pathway. Of note, several differentially expressed genes overlapped with screen hits, supporting the robustness of our findings. Notably, pharmacological inhibition of CHEK1, both in vitro and ex vivo, enhanced sensitivity to CDK4/6 inhibition in a sequence-dependent manner, indicating a critical role of the sequence of drug administration.
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4. GSE279017 头颈部鳞状细胞癌的空间转录组分析揭示了混合型上皮-间质转化的新型调控因子

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、spatial
• 📝 描述：Contributors : Dor Simkin ; Thomas F Barrett ; Michael J Moore ; Alissa Greenwald ; Michael Mints ; Ryan S Jackson ; Patrik Pipkorn ; Jason T Rich ; Paul A Zolkind ; Richard A Harbison ; Randall C Paniello ; Jose P Zevallos ; Anuraag S parikh ; Douglas Adkins ; Wade L Thorstad ; Rebecca Chernock ; Itay Tirosh ; Sidharth V PuramSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensHead and neck squamous cell carcinoma (HNSCC) is characterized by a high degree of intra- and inter-tumoral heterogeneity. Here we use spatial transcriptomics (ST) to profile both HPV-positive and HPV-negative HNSCC, uncovering distinct patterns of spatial organization of malignant cells and the surrounding tumor microenvironment across groups of tumors. First, we find that HPV-positive HNSCC is characterized by high cellular density in all cellular compartments with distinct expression of hypoxia, senescence, and cell cycle-associated genes in the malignant compartment. In HPV-negative HNSCC, we find two distinct spatial patterns of a partial epithelial-to-mesenchymal transition (p-EMT) program. One pattern is spatially associated with fibroblasts, characterized by p-EMT at the leading edge of tumor nests (“p-EMT edge”), and mediated by TGFB-signaling. The other pattern features high p-EMT expression in the core of tumor nests (“p-EMT core”). In p-EMT core tumors, we observe high co-localization of p-EMT cells with an inflammatory response program including neutrophils and macrophages, as well as differential expression of distinct ligands, including OSM. In vitro experiments demonstrate that OSM can induce the p-EMT state in multiple HNSCC models. Together these findings suggest that multiple p-EMT phenotypes exist across HPV-unrelated HNSCC and are mediated by distinct cell-to-cell signaling mechanisms, highlighting potential novel therapeutic vulnerabilities.
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5. GSE332978 DNA甲基转移酶抑制剂可预防铂类药物诱导的卵巢癌干细胞富集

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、enrichment
• 📝 描述：Contributors : Heather M O’Hagan ; Truc T VuongSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensPlatinum-based therapy is the standard first-line treatment for high-grade serous ovarian cancer (HGSC). However, most patients develop resistance and recurrence despite an initial response to therapy. Ovarian cancer stem cells (OCSCs) are enriched in recurrent tumors and contribute to platinum resistance. These tumors also show promoter DNA hypermethylation, and DNA methyltransferase inhibitors (DNMTis) have been shown to restore sensitivity in platinum-resistant ovarian cancer cells. Here, we demonstrated that combining DNMTi with platinum prevented the platinum-induced enrichment of OCSCs and identified NF-κB and STAT3 signaling pathways as potential regulators of platinum-induced OCSC enrichment. STAT3 was active at baseline in OC cells and platinum treatment alone activated NF-κB while maintaining STAT3 activity. Platinum combined with DNMTi decreased STAT3 activation, while still inducing NF-κB activation. Knockdown experiments demonstrated that the presence of both NF-κB and STAT3 was necessary for platinum-induced OCSC enrichment. Analysis of STAT3 and NF-κB subunit p65 CUT&RUN data showed increased binding in introns and intergenic regions in response to platinum. Additionally, DNMTi enriched NF-κB binding at endogenous retroviruses (ERVs), which correlated with changes in expression of nearby genes when DNMTi was combined with platinum. We conclude that combining DNMTi with platinum modulates STAT3 and NF-κB activation and genomic binding, potentially influencing target gene expression and preventing platinum-induced enrichment of OCSCs.
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6. GSE319610 DNA甲基转移酶抑制可阻止铂类药物诱导的卵巢癌干细胞富集 [Cut & Run]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、enrichment
• 📝 描述：Contributors : Heather M O’Hagan ; Truc T VuongSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensPlatinum-based therapy is the standard first-line treatment for high-grade serous ovarian cancer (HGSC). However, most patients develop resistance and recurrence despite an initial response to therapy. Ovarian cancer stem cells (OCSCs) are enriched in recurrent tumors and contribute to platinum resistance. These tumors also show promoter DNA hypermethylation, and DNA methyltransferase inhibitors (DNMTis) have been shown to restore sensitivity in platinum-resistant ovarian cancer cells. Here, we demonstrated that combining DNMTi with platinum prevented the platinum-induced enrichment of OCSCs and identified NF-κB and STAT3 signaling pathways as potential regulators of platinum-induced OCSC enrichment. STAT3 was active at baseline in OC cells and platinum treatment alone activated NF-κB while maintaining STAT3 activity. Platinum combined with DNMTi decreased STAT3 activation, while still inducing NF-κB activation. Knockdown experiments demonstrated that the presence of both NF-κB and STAT3 was necessary for platinum-induced OCSC enrichment. Analysis of STAT3 and NF-κB subunit p65 CUT&RUN data showed increased binding in introns and intergenic regions in response to platinum. Additionally, DNMTi enriched NF-κB binding at endogenous retroviruses (ERVs), which correlated with changes in expression of nearby genes when DNMTi was combined with platinum. We conclude that combining DNMTi with platinum modulates STAT3 and NF-κB activation and genomic binding, potentially influencing target gene expression and preventing platinum-induced enrichment of OCSCs.
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7. GSE314181 母体反式十八碳烯酸重塑新生儿 T 细胞发育和免疫印记（LIME-seq）

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、T cell
• 📝 描述：Contributors : Cheng-Wei Ju ; Yiqian Pan ; Hao Fan ; Chuan HeSeries Type : OtherOrganism : Mus musculusHow maternal nutrition influences neonatal immune development and imprinting through breastfeeding remains largely unclear. Here, we report that maternal supplementation with 25 trans-vaccenic acid (TVA) – the predominant naturally occurring trans-fatty acid in human breast milk (HBM) – promotes neonatal T cell development in mice, particularly expanding the naïve CD4+ T cell population with enhanced readiness. This implements a shift from T helper (Th)2- biased neonatal immune responses to Th1-skewing, resulting in improved adaptive immunity against viral infection and lung inflammation. Mechanistically, TVA via breastfeeding reprograms neonatal naïve CD4+ 30 T cells through a G protein coupled receptor (GPR43)-CCCTC-binding factor axis for enhanced cooperation with transcription factor TBX21, which also exhibits a longlasting immune imprinting effect. Furthermore, TVA levels in HBM from mothers of preterm infants inversely correlate with the incidence of inflammation-associated bronchopulmonary dysplasia in their preterm infants. Our findings establish the multifaceted benefits of maternal 35 nutrition and breastfeeding via TVA in promoting infant immune homeostasis and protective immunity.
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8. GSE311404 联合 BET 溴结构域和 DNMT 抑制靶向前列腺癌的谱系可塑性 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、ChIP-seq
• 📝 描述：Contributors : William K Storck ; Karan Bedi ; Raymond Cavalcante ; Eva Rodansky ; Joel Yates ; Joshi J AlumkalSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusLineage plasticity is increasingly recognized as a resistance mechanism to androgen receptor (AR) inhibition in prostate cancer. Loss of the tumor suppressors TP53 and RB1 is common in tumors exhibiting lineage plasticity; however, mechanisms by which TP53/RB1 loss promotes this phenotype remain poorly understood, and effective treatments are limited. To identify the histone acetylation alterations that occur with TP53/RB1 loss chromatin reprogramming, we performed H3K27Ac ChIP-seq on TP53/RB1-deficient vs. TP53/RB1-intact cell lines.
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9. GSE311400 BET溴结构域和DNMT抑制剂联合靶向前列腺癌的谱系可塑性[ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、ATAC-seq
• 📝 描述：Contributors : William K Storck ; Karan Bedi ; Raymond Cavalcante ; Eva Rodansky ; Joel Yates ; Joshi J AlumkalSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusLineage plasticity is increasingly recognized as a resistance mechanism to androgen receptor (AR) inhibition in prostate cancer. Loss of the tumor suppressors TP53 and RB1 is common in tumors exhibiting lineage plasticity; however, mechanisms by which TP53/RB1 loss promote this phenotype remain poorly understood, and effective treatments are limited. Thus we used multi-omic profiling of TP53/RB1 loss prostate cancer models to identify alterations in chromatin accessibility, DNA methylation, and gene expression associated with lineage plasticity.
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10. GSE289161 母乳中的反式十八碳烯酸可启动新生儿T细胞免疫

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、T cell
• 📝 描述：Contributor : Hao FanSeries Type : Expression profiling by high throughput sequencing ; Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusNutrients in breastmilk can play a critical role in neonatal immune development, we employing a combination of single cell transcriptomics and epigenomic analysis to test how the milk nutrient Trans-vaccenic acid affect neonatal spleen immune cell development.
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1. 长寿家族揭示了健康老龄化的罕见遗传线索

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging
• 📝 描述：A study of long-lived families has identified rare genetic variants that may help people stay healthier for much longer as they age. One standout mutation appears to temper inflammation, potentially delaying disease and extending years of healthy living.
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2. 微管蛋白可防止与阿尔茨海默病和帕金森病相关的有毒脑蛋白聚集。

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：Scientists at Baylor College of Medicine may have uncovered a promising new way to combat Alzheimer’s and Parkinson’s disease. Instead of trying to stop Tau and alpha-synuclein proteins from gathering into tiny droplets inside brain cells, the researchers found that tubulin—the protein that builds the cell’s internal transport network—can redirect these proteins away from forming toxic clumps and toward healthy, productive work.
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3. 一项重要研究发现，电子烟可能导致肺癌和口腔癌。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Researchers have concluded that nicotine vapes are likely to cause lung and oral cancers, based on evidence ranging from human biomarkers to animal and laboratory studies. The findings challenge the idea that vaping is a harmless alternative to smoking and suggest health risks may be emerging much sooner than many expected.
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• GSE320594 通过全基因组 CRISPR-Cas9 筛选鉴定实验性胶质瘤中 CDK4/6 抑制剂反应的分子调节因子
• GSE307896 评估头颈部鳞状细胞癌获得性抗EGFR靶向治疗耐药后基因表达的变化
• GSE304657 树突状细胞功能障碍独立预测急性淋巴细胞白血病预后不良
• GSE303690 对头颈部鳞状细胞癌患者匹配的癌相关成纤维细胞和非肿瘤成纤维细胞的基因表达谱进行分析
• GSE301253 基因转录组学揭示 HOXC9 调控食管鳞状细胞癌的进展
• GSE300992 沙门氏菌SopB通过磷酸酶非依赖性途径抑制黏膜炎症和疾病进展
• GSE335884：急性弓形虫感染期间C57BL/6J小鼠腹膜渗出细胞的单细胞CITE-seq测序
• GSE335757 FBX-DMEP 通过微管蛋白相关的有丝分裂失调抑制肝细胞癌
• GSE335393 人类iPSC衍生Sertoli样细胞中MNDA的ChIP-seq分析
• GSE326232 GATA6 缺失驱动的谱系可塑性促进结直肠癌转移 [H3K27ac_CUT&RUN]
• GSE326231 GATA6 缺失驱动的谱系可塑性促进结直肠癌转移 [GATA6_CUT&RUN]
• GSE324171 平滑肌肉瘤空间分辨多组学图谱鉴定出两种具有临床意义的表观遗传驱动细胞状态 [CUT&RUN]
• GSE324064 平滑肌肉瘤空间分辨多组学图谱鉴定出两种具有临床意义的表观遗传驱动细胞状态
• GSE314571 独特的 CAR-T 细胞表型在有限剂量下介导治疗反应
• GSE311403 BET溴结构域和DNMT抑制剂联合靶向前列腺癌的谱系可塑性[ERRBS]
• GSE311321 联合 BET 溴结构域和 DNMT 抑制剂靶向前列腺癌谱系可塑性
• GSE309034 BET溴结构域和DNMT抑制剂联合靶向前列腺癌的谱系可塑性[BETi_DNMTi_human_RNAseq]
• GSE309033 BET溴结构域和DNMT抑制剂联合靶向前列腺癌的谱系可塑性[BETi_DNMTi_mouse_RNAseq]
• GSE290756 GATA6缺失驱动的谱系可塑性促进结直肠癌转移
• GSE290753 GATA6 缺失驱动的谱系可塑性促进结直肠癌转移 [RNA-seq_GATA6KO]
• GSE290752 GATA6 缺失驱动的谱系可塑性促进结直肠癌转移 [RNA-seq_met]
• GSE290751 GATA6 缺失驱动的谱系可塑性促进结直肠癌转移 [ATAC-seq_met]
• GSE289160 母乳中的反式十八碳烯酸可激活新生儿T细胞抵抗病毒感染
• 金黄色葡萄球菌感染的nmr-2(ok3324)和野生型(WT)N2秀丽隐杆线虫的GSE261802 RNA测序
• GSE261728 秀丽隐杆线虫 nmr-2(ok3324) 和野生型 (WT) N2 的 RNA 测序
• GSE319079 对在完全培养基中培养 24 小时的 p27+/+ 和 p27-/- 小鼠胚胎成纤维细胞进行 RNA-Seq 分析
• GSE306480 西妥昔单抗诱导的头颈部鳞状细胞癌细胞系基因表达变化分析
• GSE303798 评估西妥昔单抗诱导的头颈部鳞状细胞癌残留PDX肿瘤中的基因表达变化
• GSE295235 早期阿米巴结肠炎小鼠结肠的单细胞转录组分析