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1. ⭐ GSE332618 利用空间组学鉴定和表征神经母细胞瘤中的肾上腺素能和间质癌细胞状态 [空间转录组学]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Patel Anand ; Oashenberg Orr ; Collins Natalie ; McEvoy Justina ; Allensworth Melody ; Turk Samantha ; Geiger Natalie ; Segerstolpe Asa ; Jiang Sizun ; Slyper Michal ; Huang Xin ; Caraccio Chiara ; Jin Hongjian ; Sheppard Heather ; Lu Meifen ; Xu Ke ; Chang Ti-Cheng ; Orr Brent ; Shirinifard Abbas ; Chapple Richard ; Shen Amber ; Clay Michael ; Tatevossian Ruth ; Reilly Colleen ; Patel Jaimin ; Lupo Marybeth ; Cline Cynthia ; Dionne Danielle ; Porter Caroline ; Waldman Julia ; Bai Yunhao ; Zhu Bojai ; Barrera Irving ; Murray Evan ; Vigneau Sebastien ; Napolitano Sara ; Wakiro Isaac ; Wu Jingyi ; Grimaldi Grace ; Dellostritto Laura ; Helvie Karla ; Rotem Asaf ; Lako Ana ; Cullen Nicole ; Pfaff Kathleen ; Karlstrom Asa ; Jane-Valbuena Judit ; Todres Ellen ; Thorner AaronSeries Type : OtherOrganism : Homo sapiensNeuroblastoma is a pediatric cancer arising from the developing sympathoadrenal lineage and cell lines derived from neuroblastoma patients have features of either adrenergic neurons (ADRN) or mesenchymal cells (MES). However, identification of MES neuroblastoma cells in patient tumors has been challenging and controversial. This may be due to inter- or intra-patient tumor heterogeneity or discrepancies between the established neuroblastoma cell lines and patient tumors. To characterize the intra- and inter-patient cellular heterogeneity, we analyzed 54 neuroblastoma tumors, spanning a broad range of clinical, genetic, and histologic features. We combined single-cell/nucleus RNA-seq (sc/scRNA-seq), bulk RNA-seq, spatial transcriptomics, and spatial proteomics. We discovered that the tumor cells are in distinct cellular neighborhoods from the non-malignant immune and stromal cells, but we could not identify MES neuroblastoma cells using the established gene expression signatures developed from cell lines. However, using ADRN/MES gene expression signatures developed from early passage orthotopic patient-derived xenografts, we were able to identify MES neuroblastoma tumor cells. We validated our results using RNA-seq, RNA in situ hybridization, immunostaining, chromatin profiling, spatial transcriptomics, functional studies in organoids, and electron microscopy. MES neuroblastoma tumor cells were more likely to be found in high-risk, MYCN amplified post-treatment samples. Taken together, our results demonstrate that MES neuroblastoma tumor cells are present in patient tumors and may correlate with response to therapy and outcome.
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2. ⭐ GSE332987 新辅助 Pepinemab 联合免疫检查点阻断疗法可重塑转移性黑色素瘤的肿瘤微环境

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune、tumor microenvironment
• 📝 描述：Contributors : Gregory B Lesinski ; Chrystal M Paulos ; Michael C Lowe ; Crystal L Mallow ; Ayana T RuffinSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensNeoadjuvant immune checkpoint inhibitors (ICIs) improve event-free survival in metastatic melanoma, yet resistance and recurrence remain common. We evaluated pepinemab, a Semaphorin 4D (SEMA4D)–blocking antibody, in combination with nivolumab and/or ipilimumab in a phase II neoadjuvant biomarker trial for patients with resectable metastatic melanoma. Patients received two neoadjuvant doses followed by curative-intent surgery and one year of adjuvant nivolumab. Pepinemab-containing regimens did not increase immune-related adverse events and did not delay or preclude curative-intent surgical resection. Mechanistically, pepinemab plus ICI was associated with immune remodeling features, including increased T and B cell infiltration and enrichment of type 1 conventional dendritic cells. These changes were associated with the formation of mature lymphoid aggregates resembling tertiary lymphoid structures that contained clonally expanded T cell receptor repertoires, consistent with localized cytotoxic activity. Together, these findings support further evaluation of SEMA4D blockade as a strategy to enhance neoadjuvant immunotherapy in melanoma.
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3. ⭐ GSE309805 单细胞图谱揭示血液恶性肿瘤中的致癌转录程序和免疫逃逸机制

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、regex:onco(logy|logist|gene|genic)、single-cell
• 📝 描述：Contributors : Chenguang Wang ; Ryan WilcoxSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensPrimary cutaneous T-cell lymphomas (CTCL) are a heterogeneous group of extranodal non-Hodgkin lymphomas. Outcomes for patients with advanced-stage disease are suboptimal, as few complete and durable responses are achieved with currently available therapeutic agents. However, improved understanding of oncogenic transcriptional programs in malignant T cells and their engagement with the tumor microenvironment (TME) may unveil therapeutic vulnerabilities. Therefore, we have compiled the largest available scRNA-seq CTCL atlas that includes >2 million skin and blood cells from 116 patients. We identified recurrent transcriptional programs in malignant T cells, a subset of which are associated with GATA-3 dependent transcriptional programs, especially in the setting of large cell transformation and advanced-stage disease. Many of the transcriptional programs identified are therapeutically targetable with clinically available agents, including HDAC, XPO1, JAK/CSF1R, and IKZF1/IKZF3 antagonists. The CTCL TME is dominated by infiltrating and exhausted effector and cytotoxic T cells that are restrained by a robust infiltrate of regulatory T cells (8%), transcriptionally polarized monocytes/macrophages (7%), and cancer-associated fibroblasts. Collectively, these findings have significant implications for the rationale design of combinatorial strategies targeting immune checkpoints, including PD-1. We have identified transcriptional programs, driven by oncogenic transcription factors, and constituents of the TME as therapeutic vulnerabilities in CTCL, and hope that the CTCL atlas constructed will provide a valuable resource for future studies exploiting these therapeutic vulnerabilities.
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4. GSE337477 利用单细胞RNA测序对DSS处理的Manf缺陷小鼠进行免疫谱分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、scRNA
• 📝 描述：Contributors : Dongyan Zhao ; Yufang Shi ; Rui LiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTo identify the immune cell populations associated with aggravated colitis in Manf-deficient mice after DSS treatment, we performed scRNA sequencing of CD45+ colonic immune cells
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5. GSE331531 利用空间组学鉴定和表征神经母细胞瘤中的肾上腺素能和间质癌细胞状态

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、spatial
• 📝 描述：Contributors : Patel Anand ; Oashenberg Orr ; Collins Natalie ; McEvoy Justina ; Allensworth Melody ; Turk Samantha ; Geiger Natalie ; Segerstolpe Asa ; Jiang Sizun ; Slyper Michal ; Huang Xin ; Caraccio Chiara ; Jin Hongjian ; Sheppard Heather ; Lu Meifen ; Xu Ke ; Chang Ti-Cheng ; Orr Brent ; Shirinifard Abbas ; Chapple Richard ; Shen Amber ; Clay Michael ; Tatevossian Ruth ; Reilly Colleen ; Patel Jaimin ; Lupo Marybeth ; Cline Cynthia ; Dionne Danielle ; Porter Caroline ; Waldman Julia ; Bai Yunhao ; Zhu Bojai ; Barrera Irving ; Murray Evan ; Vigneau Sebastien ; Napolitano Sara ; Wakiro Isaac ; Wu Jingyi ; Grimaldi Grace ; Dellostritto Laura ; Helvie Karla ; Rotem Asaf ; Lako Ana ; Cullen Nicole ; Pfaff Kathleen ; Karlstrom Asa ; Jane-Valbuena Judit ; Todres Ellen ; Thorner AaronSeries Type : OtherOrganism : Homo sapiensNeuroblastoma is a pediatric cancer arising from the developing sympathoadrenal lineage and cell lines derived from neuroblastoma patients have features of either adrenergic neurons (ADRN) or mesenchymal cells (MES). However, identification of MES neuroblastoma cells in patient tumors has been challenging and controversial. This may be due to inter- or intra-patient tumor heterogeneity or discrepancies between the established neuroblastoma cell lines and patient tumors. To characterize the intra- and inter-patient cellular heterogeneity, we analyzed 54 neuroblastoma tumors, spanning a broad range of clinical, genetic, and histologic features. We combined single-cell/nucleus RNA-seq (sc/scRNA-seq), bulk RNA-seq, spatial transcriptomics, and spatial proteomics. We discovered that the tumor cells are in distinct cellular neighborhoods from the non-malignant immune and stromal cells, but we could not identify MES neuroblastoma cells using the established gene expression signatures developed from cell lines. However, using ADRN/MES gene expression signatures developed from early passage orthotopic patient-derived xenografts, we were able to identify MES neuroblastoma tumor cells. We validated our results using RNA-seq, RNA in situ hybridization, immunostaining, chromatin profiling, spatial transcriptomics, functional studies in organoids, and electron microscopy. MES neuroblastoma tumor cells were more likely to be found in high-risk, MYCN amplified post-treatment samples. Taken together, our results demonstrate that MES neuroblastoma tumor cells are present in patient tumors and may correlate with response to therapy and outcome.
• 🔗 查看原文

6. GSE216650 人类肿瘤图谱试点项目 (HTAPP) 神经母细胞瘤甲基化芯片数据集

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、methylation
• 📝 描述：Contributors : Anand G Patel ; Michael A DyerSeries Type : Methylation profiling by genome tiling arrayOrganism : Homo sapiensGenome-wide methylation profiling of 35 neuroblastomas that are part of the HTAPP neuroblastoma cohort. Data was generated using the Illumina MethylationEPIC 850k bead array.
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7. GSE344393 PRCC-TFE3 形成脯氨酸依赖性凝聚体并重编程染色质以进行 tRCC 致癌转录 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：regex:onco(logy|logist|gene|genic)、RNA-seq
• 📝 描述：Contributors : Yiran Wang ; Ryan Blawski ; Wanlu Chen ; Ye Jin Lee ; Hongkai Ji ; Eneda Toska ; Danfeng CaiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensTranslocation renal cell carcinoma (tRCC) is an aggressive malignancy driven by MiT/TFE family transcription factor rearrangements, most notably TFE3 fusions. Among these, the PRCC::TFE3 fusion is a prominent oncogenic driver, yet the molecular mechanisms governing its transcriptional and tumorigenic activities remain poorly defined. Here, we demonstrate that PRCC::TFE3 forms dynamic, transcriptionally active nuclear condensates that are critical for its oncogenic function. We identify a proline-rich region within the PRCC fusion partner as the essential determinant of condensate formation. Disruption of this proline-rich region (PRW) abolishes condensate assembly, reverses fusion-driven chromatin accessibility and transcriptional reprogramming, and suppresses proliferative, migratory, and invasive phenotypes in patient-derived tRCC cell lines. Integrative RNA-seq, ATAC-seq, and CUT&RUN analyses reveal that PRCC::TFE3 condensates function as epigenetic regulatory hubs, coordinating extensive chromatin remodeling and recruitment of transcription factor networks—including TEAD-associated pathways—to amplify oncogenic programs. Furthermore, we identify HS3ST2 and ABCB5 as novel, condensate-dependent target genes and validate them as critical mediators of tRCC progression. Our findings establish PRCC::TFE3-mediated condensate formation as a fundamental mechanism of tRCC pathogenesis and highlight condensate-dependent transcriptional networks as potential therapeutic vulnerabilities in this clinically challenging disease.
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8. GSE344391 PRCC-TFE3 形成脯氨酸依赖性凝聚体并重编程染色质以进行 tRCC 致癌转录 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：regex:onco(logy|logist|gene|genic)、ATAC-seq
• 📝 描述：Contributors : Yiran Wang ; Ryan Blawski ; Wanlu Chen ; Ye Jin Lee ; Hongkai Ji ; Eneda Toska ; Danfeng CaiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensTranslocation renal cell carcinoma (tRCC) is an aggressive malignancy driven by MiT/TFE family transcription factor rearrangements, most notably TFE3 fusions. Among these, the PRCC::TFE3 fusion is a prominent oncogenic driver, yet the molecular mechanisms governing its transcriptional and tumorigenic activities remain poorly defined. Here, we demonstrate that PRCC::TFE3 forms dynamic, transcriptionally active nuclear condensates that are critical for its oncogenic function. We identify a proline-rich region within the PRCC fusion partner as the essential determinant of condensate formation. Disruption of this proline-rich region (PRW) abolishes condensate assembly, reverses fusion-driven chromatin accessibility and transcriptional reprogramming, and suppresses proliferative, migratory, and invasive phenotypes in patient-derived tRCC cell lines. Integrative RNA-seq, ATAC-seq, and CUT&RUN analyses reveal that PRCC::TFE3 condensates function as epigenetic regulatory hubs, coordinating extensive chromatin remodeling and recruitment of transcription factor networks—including TEAD-associated pathways—to amplify oncogenic programs. Furthermore, we identify HS3ST2 and ABCB5 as novel, condensate-dependent target genes and validate them as critical mediators of tRCC progression. Our findings establish PRCC::TFE3-mediated condensate formation as a fundamental mechanism of tRCC pathogenesis and highlight condensate-dependent transcriptional networks as potential therapeutic vulnerabilities in this clinically challenging disease.
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9. GSE331322 源自患者肿瘤的抗体可增强癌症免疫检查点阻断疗法的疗效

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune
• 📝 描述：Contributors : Jennifer A Wargo ; Manoj ChelvanambiSeries Type : OtherOrganism : Homo sapiensB-cells are associated with favorable response to immunotherapy, though the underlying mechanisms remain unclear. Here, we profiled tumor-infiltrating B-cells (TIL-Bs) and tertiary lymphoid structures (TLS) from α-PD-1 + α-CTLA-4 treated responders (R) and non-responders (NR) to identify immune signatures. TLS from responders exhibited upregulated inflammatory genes, and increased levels of cytotoxic immune cells.
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10. GSE330132 基于大规模多重测序的宿主细胞复活分析以单核苷酸和单细胞分辨率分析 DNA 修复 [scRNA]

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、scRNA
• 📝 描述：Contributors : Siyu Chen ; Yo Akiyama ; Sneh Toprani ; Gad Getz ; Nicholas Haradhvala ; Zachary NagelSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensDefects in DNA repair are clinical biomarkers for therapeutic vulnerabilities in multiple cancer types. However, the characterization of DNA repair in cancer remains bottlenecked by a lack of reliable genomic predictors and the low throughput of existing functional assays. Here, we present mmHCR-seq, a sequencing-based and massively multiplexed Host Cell Reactivation assay that enables parallel quantification of functional repair efficiency and accuracy across all major repair pathways via RNA-seq readout. We demonstrate that mmHCR-seq can detect deficiencies and measure kinetics of nine DNA repair pathways simultaneously. The single-nucleotide resolution revealed lesion-dependent kinetics for base excision repair intermediates. By integrating mmHCR-seq with single-cell RNA-seq, we mapped repair capacity in a 19-cell line pool at cellular resolution and coupled repair phenotypes to expression states. Therein, cell cycle effects were unraveled without the need for synchronization. Overall, mmHCR-seq provides a scalable, high-resolution platform for dissecting DNA repair mechanisms and identifying new repair-associated vulnerabilities in cancer.
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1. 利用单细胞RNA测序进行生物标志物发现的机器学习方法

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell
• 📝 描述：RNA sequencing combined with machine learning can identify complex gene-expression patterns and potential biomarkers hidden within diverse populations of individual cells…
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2. MiRQuery——一款用户友好的Web应用程序，用于对microRNA测序数据进行交互式分析和可视化。

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：MiRQuery makes RNA sequencing analysis more accessible by combining miRNA visualization, differential expression, target prediction, pathway analysis, and integration with mRNA…
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3. 超过1000个基因开关揭示了女性免疫力差异的原因

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity
• 📝 描述：More than 1,000 genetic switches behave differently in male and female immune cells, helping explain why women are much more vulnerable to autoimmune diseases such as lupus. Female immune systems appear genetically tuned for stronger inflammatory responses—a powerful defense against infection that may also make dangerous immune misfires more likely.
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• GSE329741 粒细胞中 EGFR 信号缺失可解除免疫抑制，使 CRC 转移灶对免疫检查点疗法敏感
• GSE326333 CREST 在成熟运动神经元中作为神经元特异性增强子和表观遗传调控因子之间的分子桥梁发挥作用 [ChIP-seq]
• GSE291385 肿瘤转移劫持肝脏造血功能促进免疫抑制
• GSE254341 靶向 Nat10 重编程调节性 T 细胞功能，增强肺癌抗 PD-1 免疫疗法的敏感性
• GSE344389 IDH1-R132H突变型与野生型小鼠神经胶质瘤神经球中新生转录的Bru-seq分析
• GSE337979 pth基因作为细菌抗生素耐药性的临床生物标志物
• GSE344555 双重免疫检查点阻断在复发性胶质母细胞瘤中诱导不同的全身性和肿瘤内免疫激活 [TCRb-seq]
• GSE344507 同源和异源mRNA及MVA疫苗接种后对SARS-CoV-2 XBB.1.5的长期免疫和保护作用
• GSE344392 PRCC-TFE3 形成脯氨酸依赖性凝聚体并重编程染色质以进行 tRCC 致癌转录 [CUT&RUN]
• GSE337136 PD-1阻断治疗的经典霍奇金淋巴瘤患者外周CD8+ T细胞的免疫表型分析[TCR-seq]
• GSE337135 PD-1阻断治疗的经典霍奇金淋巴瘤患者外周CD8+ T细胞的免疫表型分析
• GSE331041 融合转录因子 PAX3::FOXO1 的剂量控制横纹肌肉瘤细胞状态 [RNA-Seq]
• GSE330134 基于大规模多重测序的宿主细胞复活分析以单核苷酸和单细胞分辨率分析 DNA 修复 [扩增子]
• GSE326223 CREST 在成熟运动神经元中发挥着神经元特异性增强子和表观遗传调控因子之间的分子桥梁作用
• GSE300985 一个标准化的患者来源胶质母细胞瘤类器官平台，用于评估放射治疗疗效和克服耐药性
• GSE297127 融合转录因子 PAX3::FOXO1 的剂量控制横纹肌肉瘤细胞状态 [scRNA-Seq]
• GSE297125 融合转录因子 PAX3::FOXO1 的剂量控制横纹肌肉瘤细胞状态 [ChIP-Seq]
• GSE297122 融合转录因子 PAX3::FOXO1 的剂量控制横纹肌肉瘤细胞状态 [ATAC-Seq]
• GSE223442 真菌处理后，对 Ikka 或 Stat3 诱导型基因敲除小鼠的血细胞进行单细胞 RNA 测序
• GSE223080 RNA测序，分析了用真菌处理（伴或不伴尿酸或乳酸）的中性粒细胞。
• GSE215966 单细胞 RNA 测序数据来自经真菌处理的 Ikkα 或 Ikkα/Stat3 诱导型基因敲除小鼠的口腔和皮肤细胞。
• GSE192654 RNA测序数据来自经真菌或Calphostin C处理的A431细胞。
• GSE344020 产后奶牛酮症相关的骨骼肌转录组改变
• GSE343951 8月龄雄性和雌性hAβ-KI小鼠的骨骼肌抗疲劳能力受到不同的影响。
• GSE343826 CircATP5C1 通过泛素依赖的方式促进 HNRNPR 核输出和 BCL2L1 上调，从而驱动乳头状甲状腺癌的进展。
• GSE343774 脊椎动物胰腺肿瘤发生过程中转录细胞状态的进化保守表观遗传调控
• GSE343497 干细胞分化过程中染色体构象和核组织的逐步重组 [ATAC-seq]
• GSE343496 干细胞分化过程中染色体构象和核组织的逐步重组 [RNA-Seq]
• GSE343495 干细胞分化过程中染色体构象和核组织的逐步重组 [Hi-C]
• GSE343493 干细胞分化过程中染色体构象和核组织的逐步重组 [ChIP-Seq]
• GSE335046 TNF阻断可减弱单核细胞衍生巨噬细胞的促炎性CRS特征。
• GSE306643 ZC3H14 介导小鼠早期胚胎发育中核斑点组装的调控机制 [scRNA-Seq]
• GSE306183 M2 小胶质细胞来源的外泌体抑制神经病理性疼痛中的 p38 MAPK 信号通路和 GPX4 介导的神经元铁死亡 [EXO_miRNAseq]
• GSE306182 M2 小胶质细胞衍生的外泌体抑制神经病理性疼痛中的 p38 MAPK 信号通路和 GPX4 介导的神经元铁死亡 [N2A_miRNA-seq]
• GSE306181 M2 小胶质细胞衍生的外泌体抑制神经病理性疼痛中的 p38 MAPK 信号通路和 GPX4 介导的神经元铁死亡 [BV2_mRNAseq]
• GSE306086 M2型小胶质细胞来源的外泌体抑制神经病理性疼痛中的p38 MAPK信号通路和GPX4介导的神经元铁死亡
• GSE305982 细胞因子刺激培养的角质形成细胞和成纤维细胞
• GSE343664 香椿‘舒亚红’休眠芽和活跃生长芽的比较转录组动态
• GSE327958 MDA-MB-231乳腺癌细胞对PDE4DIP靶向siRNA的转录组反应
• GSE326497 DNA N6甲基化调控毛霉目真菌的致病性