详细内容（前10条）

1. ⭐ GSE274688 谱系主转录因子 p63 招募癌症特异性辅助因子 FOXK1 来介导鳞状细胞癌中的致癌 3D 染色质动态 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、carcinoma、regex:onco(logy|logist|gene|genic)、RNA-seq
• 📝 描述：Contributor : Namyoung JungSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensTranscriptional dysregulation by a lineage master transcription factor (TF) is a critical mechanism in cancer, involving alteration of three-dimensional (3D) chromatin architecture. However, the underlying mechanisms of altered master TF-dependent chromatin interactions in cancer cells remain unclear. Here, we employ multi-omic approaches to examine chromatin interactions dependent on p63, a master TF in epidermis, in squamous cell carcinomas (SCCs) compared to normal keratinocytes (KCs), integrating chromatin looping and accessibility, transcriptome, p63 binding and proteomics. p63 facilitates higher connectivity between the promoters of prognostic genes in SCCs, and distal enhancers. Many SCC-specific p63-dependent genes are connected to SCC-specific p63-dependent epigenetic signature via a cis-regulatory element (CRE) without the signature, referred to as ‘Secondary’ regulation mode. Notably, we identify FOXK1 as a cancer-specific cofactor, cooperating with p63 to shape the oncogenic chromatin landscape, inhibiting cell proliferation. Our findings suggest the p63-FOXK1 axis as a potential target for cancer therapy in SCCs.
• 🔗 查看原文

2. ⭐ GSE274413 谱系主转录因子 p63 招募癌症特异性辅助因子 FOXK1 来介导鳞状细胞癌中的致癌 3D 染色质动态变化 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、carcinoma、regex:onco(logy|logist|gene|genic)、ChIP-seq
• 📝 描述：Contributor : Namyoung JungSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensTranscriptional dysregulation by a lineage master transcription factor (TF) is a critical mechanism in cancer, involving alteration of three-dimensional (3D) chromatin architecture. However, the underlying mechanisms of altered master TF-dependent chromatin interactions in cancer cells remain unclear. Here, we employ multi-omic approaches to examine chromatin interactions dependent on p63, a master TF in epidermis, in squamous cell carcinomas (SCCs) compared to normal keratinocytes (KCs), integrating chromatin looping and accessibility, transcriptome, p63 binding and proteomics. p63 facilitates higher connectivity between the promoters of prognostic genes in SCCs, and distal enhancers. Many SCC-specific p63-dependent genes are connected to SCC-specific p63-dependent epigenetic signature via a cis-regulatory element (CRE) without the signature, referred to as ‘Secondary’ regulation mode. Notably, we identify FOXK1 as a cancer-specific cofactor, cooperating with p63 to shape the oncogenic chromatin landscape, inhibiting cell proliferation. Our findings suggest the p63-FOXK1 axis as a potential target for cancer therapy in SCCs.
• 🔗 查看原文

3. ⭐ GSE274411 谱系主转录因子 p63 招募癌症特异性辅助因子 FOXK1 来介导鳞状细胞癌中的致癌 3D 染色质动力学[ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、carcinoma、regex:onco(logy|logist|gene|genic)、ATAC-seq
• 📝 描述：Contributor : Namyoung JungSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensTranscriptional dysregulation by a lineage master transcription factor (TF) is a critical mechanism in cancer, involving alteration of three-dimensional (3D) chromatin architecture. However, the underlying mechanisms of altered master TF-dependent chromatin interactions in cancer cells remain unclear. Here, we employ multi-omic approaches to examine chromatin interactions dependent on p63, a master TF in epidermis, in squamous cell carcinomas (SCCs) compared to normal keratinocytes (KCs), integrating chromatin looping and accessibility, transcriptome, p63 binding and proteomics. p63 facilitates higher connectivity between the promoters of prognostic genes in SCCs, and distal enhancers. Many SCC-specific p63-dependent genes are connected to SCC-specific p63-dependent epigenetic signature via a cis-regulatory element (CRE) without the signature, referred to as ‘Secondary’ regulation mode. Notably, we identify FOXK1 as a cancer-specific cofactor, cooperating with p63 to shape the oncogenic chromatin landscape, inhibiting cell proliferation. Our findings suggest the p63-FOXK1 axis as a potential target for cancer therapy in SCCs.
• 🔗 查看原文

4. ⭐ GSE330869 髋部骨折患者术后谵妄与炎症和免疫通路中的表观遗传改变相关：一项全基因组DNA甲基化研究

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、genome、epigenetic、methylation
• 📝 描述：Contributors : Shota Nishitani ; Gen ShinozakiSeries Type : Methylation profiling by genome tiling arrayOrganism : Homo sapiensDelirium is a common yet underdiagnosed condition in elderly hospitalized patients. The lack of effective diagnostic and therapeutic methods can be attributed to the limited understanding of its pathophysiology. Delirium has recently been reported to be linked to neuroinflammation and epigenetic changes. The aim of this study was to validate the pathways in a larger cohort with a uniform type of surgery, while rigorously adjusting for potential covariates. This study primarily investigated DNA methylation (DNAm) changes before and after surgery in postoperative delirium (POD) among older adults having undergone femoral fracture surgery. After propensity analysis, 65 subjects were divided into 2 subgroups; one consisted of subjects who had blood samples collected preoperatively and on postoperative day 0, and the other consisted of those who had samples collected preoperatively and on postoperative day 3. We performed differential methylation analysis and enrichment analysis on each subgroup. Enrichment analysis using CpGs that exhibited substantial DNAm changes between pre- and postoperative day 0 samples in POD cases showed inflammation- and immunity-related pathways such as “leukocyte mediated immunity” and “NF-kappa B signaling pathway.” Inflammation- and immunity-related pathways became less noticeable between pre- and postoperative day 3 samples. Inflammation- and immunity-related pathways showed in this study align with previous studies across diverse populations, reinforcing the role of inflammation- and immunity-related epigenetic mechanisms in delirium including POD. Notably, these DNAm changes were potentially transient, corresponding to the typical onset of delirium, suggesting their potential as biomarkers for early diagnosis.
• 🔗 查看原文

5. ⭐ GSE290471 CBFA2T3-GLIS2 驱动的儿童急性巨核细胞白血病中增强子甲基化的转录重编程 [Hi-C]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、Hi-C、methylation
• 📝 描述：Contributor : Samrat Roy ChoudhurySeries Type : OtherOrganism : Homo sapiensChemotherapy resistance and relapse remain major challenges in pediatric acute myeloid leukemia (pAML), particularly in acute megakaryoblastic leukemia (AMKL) driven by the CBFA2T3-GLIS2 (C/G) fusion. To investigate the epigenetic mechanisms contributing to these challenges, we employed multi-epigenomic approaches to identify oncogenic enhancers at cis-regulatory elements (CREs) that drive aberrant gene expression.In this study, Promoter capture Hi-C (PCHi-C) was used to analyze long-range chromosomal interactions between promoters and distal regulatory regions in C/G+ M07e cells, compared to Hematopoietic Stem Cells (HSC)
• 🔗 查看原文

6. ⭐ GSE274416 谱系主转录因子 p63 招募癌症特异性辅助因子 FOXK1 来介导鳞状细胞癌中的致癌 3D 染色质动力学[HiChIP]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、carcinoma、regex:onco(logy|logist|gene|genic)
• 📝 描述：Contributor : Namyoung JungSeries Type : OtherOrganism : Homo sapiensTranscriptional dysregulation by a lineage master transcription factor (TF) is a critical mechanism in cancer, involving alteration of three-dimensional (3D) chromatin architecture. However, the underlying mechanisms of altered master TF-dependent chromatin interactions in cancer cells remain unclear. Here, we employ multi-omic approaches to examine chromatin interactions dependent on p63, a master TF in epidermis, in squamous cell carcinomas (SCCs) compared to normal keratinocytes (KCs), integrating chromatin looping and accessibility, transcriptome, p63 binding and proteomics. p63 facilitates higher connectivity between the promoters of prognostic genes in SCCs, and distal enhancers. Many SCC-specific p63-dependent genes are connected to SCC-specific p63-dependent epigenetic signature via a cis-regulatory element (CRE) without the signature, referred to as ‘Secondary’ regulation mode. Notably, we identify FOXK1 as a cancer-specific cofactor, cooperating with p63 to shape the oncogenic chromatin landscape, inhibiting cell proliferation. Our findings suggest the p63-FOXK1 axis as a potential target for cancer therapy in SCCs.
• 🔗 查看原文

7. ⭐ GSE274412 谱系主转录因子 p63 招募癌症特异性辅助因子 FOXK1 来介导鳞状细胞癌中的致癌 3D 染色质动力学 [CUT&RUN]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、carcinoma、regex:onco(logy|logist|gene|genic)
• 📝 描述：Contributor : Namyoung JungSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensTranscriptional dysregulation by a lineage master transcription factor (TF) is a critical mechanism in cancer, involving alteration of three-dimensional (3D) chromatin architecture. However, the underlying mechanisms of altered master TF-dependent chromatin interactions in cancer cells remain unclear. Here, we employ multi-omic approaches to examine chromatin interactions dependent on p63, a master TF in epidermis, in squamous cell carcinomas (SCCs) compared to normal keratinocytes (KCs), integrating chromatin looping and accessibility, transcriptome, p63 binding and proteomics. p63 facilitates higher connectivity between the promoters of prognostic genes in SCCs, and distal enhancers. Many SCC-specific p63-dependent genes are connected to SCC-specific p63-dependent epigenetic signature via a cis-regulatory element (CRE) without the signature, referred to as ‘Secondary’ regulation mode. Notably, we identify FOXK1 as a cancer-specific cofactor, cooperating with p63 to shape the oncogenic chromatin landscape, inhibiting cell proliferation. Our findings suggest the p63-FOXK1 axis as a potential target for cancer therapy in SCCs.
• 🔗 查看原文

8. ⭐ GSE338487 基于cDC1的有效癌症免疫疗法的抗原呈递要求

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、antigen、regex:immuno(logy|therapy|suppression)
• 📝 描述：Contributors : Josué E Pineda ; Tomoyuki Minowa ; Li Shen ; Stephanie S Watowich ; Matthew M GubinSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusType 1 conventional dendritic cells (cDC1s) are important for generating and sustaining antitumor immunity. Accordingly, the abundance of cDC1s in human tumors correlates with improved outcomes in cancer. Capitalizing on this role, we previously demonstrated that vaccination with murine cDC1s, generated in culture from bone marrow cells (termed here “in vitro–derived cDC1s”), elicits durable tumor control in multiple preclinical models; however, the immunological mechanisms underlying the efficacy of cDC1 vaccination remain unclear. Here, we examined whether in vitro–derived cDC1s resemble tumor-infiltrating DC populations and whether MHC-I and MHC-II antigen presentation contribute to cDC1-mediated tumor control following vaccination in melanoma. As expected, MHC-I or MHC-II deficiency had minimal impact on the transcriptional state of cDC1s in homeostasis or following stimulation with the adjuvant poly dI:dC. Moreover, in vitro–derived cDC1s cultured under steady-state conditions closely resembled tumor-infiltrating cDC1s, whereas their poly dI:dC–stimulated counterparts resembled CCR7+ tumor-infiltrating DC populations, also referred to as mregDCs or LAMP3+ DCs. Our data further show that both MHC-I and MHC-II contribute to tumor control upon cDC1 vaccination and that coexpression of MHC-I and MHC-II on the same cDC1 is necessary for a robust vaccine response. We also identified an important function for host cDC1s in supporting the efficacy of vaccination with in vitro–derived cDC1s, as judged by impaired tumor control in Irf8 + 32−/− mice, which lack endogenous cDC1s. Overall, these results indicate that effective antitumor responses depend on MHC-I and MHC-II antigen presentation by vaccine-delivered cDC1s, with additional contributions from host cDC1s.
• 🔗 查看原文

9. ⭐ GSE337706 探索血小板覆盖和裸露的循环肿瘤细胞：单细胞转录组学视角 [scRNA-seq Singleron]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、single-cell、scRNA
• 📝 描述：Contributors : Michal Sieczczynski ; Krzysztof Pastuszak ; Marcin Banacki ; Kamil Langowski ; Sylwia Lapinska-Szumczyk ; Anna Samelak-Czajka ; Paulina Jackowiak ; Iwona Inkielewicz-Stepniak ; Anna Supernat ; Anna Joanna ZaczekSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensCirculating tumor cells (CTCs) and platelets can be collected simultaneously during liquid biopsy; however, their interaction in the form of platelet-covered CTCs (pcCTCs) remains only partially understood. This submission contains single-cell RNA sequencing data generated from PBMC/buffy coat fractions from 29 donors: 12 patients with high-grade serous ovarian carcinoma, 4 non-malignant gynecological controls, 10 patients with breast cancer, and 3 healthy donor controls. The dataset was used to detect and characterize candidate naked CTCs and pcCTCs and to compare their transcriptomic profiles with platelet and cancer-related signatures.
• 🔗 查看原文

10. ⭐ GSE337705 探索血小板覆盖和裸露的循环肿瘤细胞：单细胞转录组学视角 [scRNA-seq 10x_Poznan]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、single-cell、scRNA
• 📝 描述：Contributors : Michal Sieczczynski ; Krzysztof Pastuszak ; Marcin Banacki ; Kamil Langowski ; Sylwia Lapinska-Szumczyk ; Anna Samelak-Czajka ; Paulina Jackowiak ; Iwona Inkielewicz-Stepniak ; Anna Supernat ; Anna Joanna ZaczekSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensCirculating tumor cells (CTCs) and platelets can be collected simultaneously during liquid biopsy; however, their interaction in the form of platelet-covered CTCs (pcCTCs) remains only partially understood. This submission contains single-cell RNA sequencing data generated from PBMC/buffy coat fractions from 29 donors: 12 patients with high-grade serous ovarian carcinoma, 4 non-malignant gynecological controls, 10 patients with breast cancer, and 3 healthy donor controls. The dataset was used to detect and characterize candidate naked CTCs and pcCTCs and to compare their transcriptomic profiles with platelet and cancer-related signatures.
• 🔗 查看原文

💡 该来源还有 54 条内容，详见 文末

详细内容（全部3条）

1. Amaranth – 通过对 UMI 读段和内部读段进行判别建模来增强单细胞转录组组装

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell
• 📝 描述：Amaranth improves transcript reconstruction from RNA sequencing data by modeling different read types, enabling more accurate isoform analysis at single-cell resolution…
• 🔗 查看原文

2. 研究人员揭示了早期基于RNA的生命体如何修复其基因组，从而为了解生命的起源提供了新的视角。

• ✍️ 作者：未知作者
• 🏷️ 关键词：genome
• 📝 描述：A newly engineered ribozyme repairs broken RNA, creating new opportunities for studying RNA evolution while improving the detection of damaged molecules through RNA sequencing…
• 🔗 查看原文

3. 为什么健康年轻的非吸烟者也会患肺癌？

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：An unexpected study found that young non-smokers with healthier diets had higher rates of lung cancer, raising questions about whether pesticide exposure from conventionally grown produce could play a role. Researchers stress that the findings are preliminary and require further studies before any conclusions can be drawn.
• 🔗 查看原文

• GSE337702 机械刚度促进肿瘤标记以引导放射性药物：单细胞RNA测序揭示MSC在肿瘤归巢后的命运
• GSE231690 DNA超螺旋的广泛传播和选择性拓扑异构酶的利用调节神经元基因组内的扭转应力[RNA-Seq]
• GSE338396 植物低投入全基因组亚硫酸氢盐测序方案
• GSE323965 转录特征表明 RB 功能可能预测子宫内膜癌对 CDK4/6 抑制剂的反应 [RNA-Seq]
• GSE314447 低生理 pH 值驱动 P300 介导的 PARP1 乙酰化并促进 PARP 抑制剂耐药性 [RNA-seq]
• GSE290551 CBFA2T3-GLIS2 驱动的儿童急性巨核细胞白血病中增强子甲基化的转录重编程 [RRBS]
• GSE290257 CBFA2T3-GLIS2驱动的儿童急性巨核细胞白血病中增强子甲基化介导的转录重编程
• GSE286961 深度学习发现 Pbx1 是造血干细胞衰老的网络枢纽 [Pbx1 RNA-seq]
• GSE286959 深度学习发现 Pbx1 是造血干细胞衰老的网络枢纽 [Pbx1 ATAC-seq]
• GSE286957 深度学习发现 Pbx1 是造血干细胞衰老的网络枢纽 [26 小时 RNA-seq]
• GSE245650 血红素调控的转录抑制因子 BACH1 保护巨噬细胞增强子的选择、激活和组织适应 [Capture Hi-C]
• GSE245647 血红素调控的转录抑制因子 BACH1 保护巨噬细胞增强子选择、激活和组织适应 [ChIP-seq]
• GSE338516 脂肪酸结合蛋白5缺乏症会损害肺泡巨噬细胞功能和代谢
• GSE313969 颅骨骨髓中的淋巴结构控制中枢神经系统的稳态和抗肿瘤免疫反应[硬脑膜/颅骨/胸骨]
• GSE309634 颅骨骨髓中的淋巴结构控制中枢神经系统的稳态和抗肿瘤免疫反应[颅骨/胸骨]
• GSE309632 颅骨骨髓中的淋巴结构控制中枢神经系统的稳态和抗肿瘤免疫反应 [颅骨/脑]
• GSE338478 从 Periconia caespitosa 中提取的新型麦角甾醇衍生物 Periconoid A 可诱导鼻咽癌细胞凋亡，并伴有炎症通路富集
• GSE338107 先天免疫激活谱与重组沙粒病毒载体的T细胞反应极化相关
• GSE231695 DNA超螺旋的广泛传递和选择性拓扑异构酶的利用调节神经元基因组内的扭转应力
• GSE231610 DNA超螺旋的广泛传播和选择性拓扑异构酶的利用调节神经元基因组内的扭转应力[TOP2Bcc-seq]
• GSE231609 DNA超螺旋的广泛传播和选择性拓扑异构酶的利用调节神经元基因组内的扭转应力[fastGRO-seq]
• GSE231608 DNA超螺旋的广泛传播和选择性拓扑异构酶的利用调节神经元基因组内的扭转应力[TMP-Seq]
• GSE338219 吡咯喹啉醌改善了自然衰老小鼠与增强线粒体生物能量相关的认知相关行为表现
• GSE327278 分析 HR+/HER2- 乳腺癌细胞系 MCF-7 获得性多西他赛耐药相关的转录变化
• GSE292334 肿瘤抑制因子SMAD4是基因组稳定性的守门人
• GSE337989 PARK2 对神经细胞状态的调节以及小分子 Parkin 激动剂的多巴胺能神经保护作用 [scRNA-seq]
• GSE337982 PARK2 对神经细胞状态的调节以及小分子 Parkin 激动剂的多巴胺能神经保护作用 [RNA-Seq]
• GSE323966 转录特征表明 RB 功能可能预测子宫内膜癌对 CDK4/6 抑制剂的反应 [WES]
• GSE314448 低生理 pH 值驱动 P300 介导的 PARP1 乙酰化并促进 PARP 抑制剂耐药性 [Cut & Run]
• GSE310972 单细胞染色体断裂定位鉴定出多种具有不同DNA复制时间特征的脆性位点类型
• GSE308816 综合转录组分析揭示多胺代谢受损是与年龄相关的肌肉衰退的因素之一。
• GSE303776 用于体外骨重塑和免疫细胞维持的 3D 人骨和骨髓芯片模型
• GSE303608 转录因子 Satb1 调节 TILs 的功能（RNA-seq）
• GSE303607 转录因子 Satb1 调节 TILs 的功能（scRNA-seq）
• GSE286960 深度学习发现 Pbx1 是造血干细胞衰老的网络枢纽 [Pbx1 Cut&Tag]
• GSE285235 R环维持H3K36me3的沉积，以防止SN卵母细胞发育过程中H3K4me3的入侵[RNA-Seq]
• GSE281921 单细胞染色体断裂定位鉴定出具有不同 DNA 复制时间特征的多个脆性位点类别 [BrdU-IP Repli-seq]
• GSE281920 单细胞染色体断裂定位识别出具有不同 DNA 复制时间特征的多个脆性位点类别 [scRepli-seq]
• GSE245649 血红素调控的转录抑制因子 BACH1 保护巨噬细胞增强子选择、激活和组织适应 [RNA-seq_muscle]
• GSE245648 血红素调控的转录抑制因子 BACH1 保护巨噬细胞增强子选择、激活和组织适应 [RNA-seq_BMDM]
• GSE245646 血红素调控的转录抑制因子 BACH1 保护巨噬细胞增强子的选择、激活和组织适应 [ATAC-seq_muscle]
• GSE245645 血红素调控的转录抑制因子 BACH1 保护巨噬细胞增强子选择、激活和组织适应 [ATAC-seq_BMDM]
• GSE338472 PGK1 通过稳定 SLC7A11 发挥铁死亡的非催化守门人作用 [RNA-Seq]
• GSE338462 探索 mTOR 通路作为 XLAS 小鼠模型中的治疗靶点。
• GSE338452 肾上腺素能受体阻滞剂诱导慢性原发性疼痛大鼠模型全血小RNA测序
• GSE334312 SpxA1 和 SpxA2 作为化学计量依赖性调节变阻器，调控 A 群链球菌毒力基因的表达——RNA-seq 数据集
• GSE313235 连接赖氨酸乙酰转移酶与癌基因介导的细胞死亡的二价分子胶 [CUT&RUN]
• GSE338160 斑马鱼幼体全器官横断后肠道的快速功能性再生受IL-22和IL-26的拮抗作用调控
• GSE338134 乳酸-Chac1轴调控铁死亡相关细胞死亡和肿瘤进展
• GSE338129 HP1α 耗竭和 TGFβ 激活对 3D 基因组组织产生拮抗作用。
• 对经硬粒链霉菌处理的玉米植株进行GSE338097 RNA-seq分析
• GSE337675 截短型 ASXL1 变体通过抑制线粒体丙酮酸载体重塑细胞代谢
• GSE271062 人类和果蝠细胞中尼帕病毒感染的比较转录组学研究
• GSE254260 不同时间点 H9 人类胚胎干细胞衍生皮质类器官切片培养物 (ALI-COs) 的单细胞 RNA 测序