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1. ⭐ GSE307931 循环转录组分析检测基因特征、免疫细胞活化和丰度，以预测膀胱癌免疫治疗反应

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、regex:immuno(logy|therapy|suppression)、transcriptome
• 📝 描述：Contributors : Sandy Chevrier ; Corentin Richard ; Romain BoidotSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBackground. Immune Checkpoint Blockers (ICB) have revolutionized oncology by achieving durable tumor responses in advanced cancers. Nevertheless, currently approved biomarkers (PD-L1, MSI, TMB) have suboptimal positive and negative predictive values for tumor response and survival. Patients and Methods. We aimed to assess the value of RNA sequencing from circulating blood, a new type of liquid biopsy, to predict responses to ICB. We performed total paired-end RNA sequencing at 20 million reads and analyzed differential gene expression, signaling pathway activation, and immune cell abundances according to cancer outcomes. The analysis was conducted on baseline frozen whole blood samples from 164 patients prospectively enrolled in the IOPREDI study. Results. We found that some immune-related genes and signaling pathways were highly expressed in patients who achieved a durable clinical benefit. Furthermore, analyses of both progression-free survival (PFS) and overall survival (OS) confirmed significantly higher expression levels of immune-related signaling pathways in long-term survivors. Gene expression signatures capable of classifying patients based on clinical response or PFS were also identified. Interestingly, deconvolution analysis revealed a significant higher abundance of resting NK cells in patients with prolonged PFS or OS, in contrast to other cytotoxic cell types. Finally, high expression of the CST7 gene and increased abundance of naïve B lymphocytes were associated with immune-related adverse events (irAEs). Conclusion. Total RNA sequencing from whole blood provides high-quality data to predict clinical response, survival, and occurrence of irAEs. The use of this liquid biopsy prior to immune checkpoint blockage could improve treatment efficacy and irAEs management.
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2. GSE313350 天冬酰胺合成酶和G蛋白偶联雌激素受体是KRAS突变型结直肠癌中营养供应的关键反应因子

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、KRAS
• 📝 描述：Contributors : Lingeng Lu ; Caroline Johnson ; Sajid KhanSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensSurvival differences exist in colorectal cancer (CRC) patients by sex and disease stage. However, the potential molecular mechanism(s) are not well understood. Here we show that asparagine synthetase (ASNS) and G protein-coupled estrogen receptor-1 (GPER1) are critical sensors of nutrient depletion and linked to poorer outcomes for females with CRC. In a 3D spheroid model of isogenic SW48 KRAS wild-type (WT) and G12A mutant (MT) cells grown under a restricted nutrient supply, we found that glutamine depletion inhibited cell growth in both cell types, whereas ASNS and GPER1 expression were upregulated in KRAS MT versus WT. Estradiol decreased growth in KRAS WT but had no effect on MT cells. In a clinical colon cancer cohort of The Cancer Genome Atlas, both high GPER1 and ASNS expression were associated with poorer overall survival for females only in advanced stage tumors. These results suggest KRAS MT cells have mechanisms in place that respond to decreased nutrient supply, typically observed in advanced tumors, by increasing the expression of ASNS and GPER1 to drive cell growth. Furthermore, KRAS MT cells are resistant to the protective effects of estradiol under nutrient deplete conditions. The findings indicate that GPER1 and ASNS expression in the link of nutrient supply and KRAS mutations shed additional light on the mechanisms behind sex differences in metabolism and growth in CRC and have clinical implications in the precision management of KRAS MT CRC.
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3. GSE311963 CD38 赋予局部抗原特异性 Foxp3+ Treg 细胞应激耐受性，从而实现对中枢神经系统炎症的区室化控制

• ✍️ 作者：未知作者
• 🏷️ 关键词：antigen、inflammation
• 📝 描述：Contributors : Andreas Muschaweckh ; Hsin-Hsiang Chen ; Rupert Öllinger ; Christopher Sie ; Thomas KornSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusFoxp3-expressing regulatory T (Treg) cells protect from systemic autoimmunity. However, little is known about the significance of Treg cells in inflammation-experienced tissues. Using experimental autoimmune encephalomyelitis (EAE), we show that Treg cells accumulate and persist in the central nervous system (CNS) until long after the resolution of the bulk of the inflammatory infiltrate. CNS-specific local depletion of post-inflammatory Treg cells, but not systemic depletion of Treg cells, immediately rekindles autoimmune inflammatory flares in the CNS by residual local effector T cells. Expression of the NAD-consuming ecto-enzyme CD38 is crucial for the functional adaptation of post-inflammatory CNS Treg cells to a stressful microenvironment, in which access to IL-2 is limited. CD38 counteracts ADP-ribosylation of the IL-2R and, thus, maintains its high sensitivity to IL-2. Their fully functional high-affinity IL-2 receptor prevents the loss of tissue-resident antigen-specific Treg cells. These “stress-tolerant” CNS Treg cells impede the collapse of immune homeostasis in the CNS once acute inflammation is controlled.
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4. GSE311075 TRMT112 在三阴性乳腺癌中驱动肿瘤生长和转移促进程序

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer
• 📝 描述：Contributors : Dongquan Chen ; Lalita Samant ; Rajeev Samant ; Amr ElhamamsySeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensRibosomal RNA Modifying Proteins (RRMPs) are integral to ribosome biogenesis, executing post-transcriptional modifications that influence translation fidelity and efficiency. Dysregulation of RRMPs has been increasingly implicated in cancer progression, yet their collective role across malignancies remains largely unexplored. Here, we performed a multi-omics analysis of 22 RRMPs across diverse cancer types using The Cancer Genome Atlas, the Molecular Taxonomy of Breast Cancer International Consortium, and additional high-throughput datasets. Our analysis revealed widespread genomic alterations and transcriptional dysregulation of RRMPs across malignancies, with distinct expression patterns in breast cancer subtypes. Notably, Triple-Negative Breast Cancer (TNBC) exhibited the highest RRMPs enrichment, which correlated with increased genomic instability including elevated tumor mutational burden and aneuploidy scores, and poor survival outcomes. Among the RRMPs, tRNA methyltransferase activator subunit 11-2 (TRMT112) emerged as a key regulator of tumor progression. Functional assays demonstrated that TRMT112 knockdown in TNBC cells significantly reduced proliferation, migration, invasion, and metastatic potential, whereas its overexpression enhanced these tumorigenic properties. Polysome profiling and RNA sequencing of actively translated transcripts revealed that TRMT112 reprograms the translational landscape by promoting pro-metastatic and stromal remodeling pathways while suppressing immune-related processes. In vivo studies using an orthotopic breast cancer model further confirmed that TRMT112 depletion impairs tumor growth and reduces metastatic burden. Collectively, our findings establish RRMPs as critical modulators of cancer progression and identify TRMT112 as a key driver of aggressive phenotypes in TNBC. The dysregulation of TRMT112 across breast cancer subtypes highlights its potential as both a prognostic biomarker and a therapeutic target. These insights provide a mechanistic foundation for future interventions aimed at targeting TRMT112-driven translational programs in aggressive breast cancer.
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5. GSE304030 oHSV介导的JAG1阻断诱导胶质瘤衰老相关分泌表型，从而增强巨噬细胞活化并提高其对西妥昔单抗介导的衰老细胞清除的敏感性

• ✍️ 作者：未知作者
• 🏷️ 关键词：macrophage、glioma
• 📝 描述：Contributors : Kimberly A Rivera-Caraballo ; Tae Jin Lee ; Arnoneel Sinha ; Marco Orecchioni ; Karina Vazquez-Arreguin ; Shilpa Sharma ; Kimya Jones ; Upasana Sahu ; Sara A Murphy ; Bangxing Hong ; Ravindra Kolhe ; Ashok Sharma ; Balveen KaurSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiens ; Mus musculusOncolytic HSV-1 (oHSV) treatment induces Notch signaling and myelosuppression in the tumor microenvironment (TME) of preclinical models. In the clinic, upregulation of JAG1 gene expression was observed in recurrent high-grade glioma patients treated with CAN-3110. Since JAG1 is expressed on both glioma cells and tumor-associated macrophages (TAMs), and its expression correlated with a worse prognosis, we engineered a JAG1-antagonizing oHSV (OncoD-0J1) and interrogated its impact on the tumor and myeloid TME. OncoD-0J1 antagonized JAG1-mediated Notch signaling and had a significant therapeutic advantage in vivo, which relied on Notch signature in tumor cells. Kinome profiling revealed that OncoD-0J1 treatment suppressed CDK1, resulting in a G2/M cell cycle checkpoint as seen by cell cycle analysis. Cell cycle arrest led to senescence and correlated with increased reactive oxygen species, p62 accumulation, autophagosome accumulation, and senescence-associated beta-galactosidase activity. This resulted in increased production of inflammatory chemokines and DAMPs such as IL-1β and extracellular ATP. RNA sequencing of murine macrophages co-cultured with infected human tumor cells showed enrichment of chemotactic and pro-inflammatory pathways as well as increased Fc receptor activation following OncoD-0J1 infection. Single-cell RNA sequencing and flow cytometric analysis of F4/80+ cells isolated from infected tumors showed a shift from tumor-supporting TAMs to inflammatory macrophages upon OncoD-0J1 treatment. Senescent cells showed heightened EGFR activation as a mechanism to escape death, which created a unique vulnerability for cetuximab as a senolytic agent. Combination therapy reduced EGFR signaling and induced macrophage-mediated antibody-dependent cellular cytotoxicity, thereby increasing the anti-tumor therapeutic response of OncoD-0J1 as a monotherapy.
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6. GSE303833 oHSV介导的JAG1阻断诱导胶质瘤衰老相关分泌表型，从而增强巨噬细胞活化并提高对西妥昔单抗介导的衰老细胞清除的敏感性 III

• ✍️ 作者：未知作者
• 🏷️ 关键词：macrophage、glioma
• 📝 描述：Contributors : Kimberly A Rivera-Caraballo ; Tae Jin Lee ; Arnoneel Sinha ; Marco Orecchioni ; Karina Vazquez-Arreguin ; Shilpa Sharma ; Kimya Jones ; Upasana Sahu ; Sara A Murphy ; Bangxing Hong ; Ravindra Kolhe ; Ashok Sharma ; Balveen KaurSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusOncolytic HSV-1 (oHSV) treatment induces Notch signaling and myelosuppression in the tumor microenvironment (TME) of preclinical models. In the clinic, upregulation of JAG1 gene expression was observed in recurrent high-grade glioma patients treated with CAN-3110. Since JAG1 is expressed on both glioma cells and tumor-associated macrophages (TAMs), and its expression correlated with a worse prognosis, we engineered a JAG1-antagonizing oHSV (OncoD-0J1) and interrogated its impact on the tumor and myeloid TME. OncoD-0J1 antagonized JAG1-mediated Notch signaling and had a significant therapeutic advantage in vivo, which relied on Notch signature in tumor cells. Kinome profiling revealed that OncoD-0J1 treatment suppressed CDK1, resulting in a G2/M cell cycle checkpoint as seen by cell cycle analysis. Cell cycle arrest led to senescence and correlated with increased reactive oxygen species, p62 accumulation, autophagosome accumulation, and senescence-associated beta-galactosidase activity. This resulted in increased production of inflammatory chemokines and DAMPs such as IL-1β and extracellular ATP. RNA sequencing of murine macrophages co-cultured with infected human tumor cells showed enrichment of chemotactic and pro-inflammatory pathways as well as increased Fc receptor activation following OncoD-0J1 infection. Single-cell RNA sequencing and flow cytometric analysis of F4/80+ cells isolated from infected tumors showed a shift from tumor-supporting TAMs to inflammatory macrophages upon OncoD-0J1 treatment. Senescent cells showed heightened EGFR activation as a mechanism to escape death, which created a unique vulnerability for cetuximab as a senolytic agent. Combination therapy reduced EGFR signaling and induced macrophage-mediated antibody-dependent cellular cytotoxicity, thereby increasing the anti-tumor therapeutic response of OncoD-0J1 as a monotherapy.
• 🔗 查看原文

7. GSE303830 oHSV介导的JAG1阻断诱导胶质瘤衰老相关分泌表型，从而增加巨噬细胞活化并增强对西妥昔单抗介导的衰老细胞清除的敏感性 I

• ✍️ 作者：未知作者
• 🏷️ 关键词：macrophage、glioma
• 📝 描述：Contributors : Kimberly A Rivera-Caraballo ; Tae Jin Lee ; Arnoneel Sinha ; Marco Orecchioni ; Karina Vazquez-Arreguin ; Shilpa Sharma ; Kimya Jones ; Upasana Sahu ; Sara A Murphy ; Bangxing Hong ; Ravindra Kolhe ; Ashok Sharma ; Balveen KaurSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensOncolytic HSV-1 (oHSV) treatment induces Notch signaling and myelosuppression in the tumor microenvironment (TME) of preclinical models. In the clinic, upregulation of JAG1 gene expression was observed in recurrent high-grade glioma patients treated with CAN-3110. Since JAG1 is expressed on both glioma cells and tumor-associated macrophages (TAMs), and its expression correlated with a worse prognosis, we engineered a JAG1-antagonizing oHSV (OncoD-0J1) and interrogated its impact on the tumor and myeloid TME. OncoD-0J1 antagonized JAG1-mediated Notch signaling and had a significant therapeutic advantage in vivo, which relied on Notch signature in tumor cells. Kinome profiling revealed that OncoD-0J1 treatment suppressed CDK1, resulting in a G2/M cell cycle checkpoint as seen by cell cycle analysis. Cell cycle arrest led to senescence and correlated with increased reactive oxygen species, p62 accumulation, autophagosome accumulation, and senescence-associated beta-galactosidase activity. This resulted in increased production of inflammatory chemokines and DAMPs such as IL-1β and extracellular ATP. RNA sequencing of murine macrophages co-cultured with infected human tumor cells showed enrichment of chemotactic and pro-inflammatory pathways as well as increased Fc receptor activation following OncoD-0J1 infection. Single-cell RNA sequencing and flow cytometric analysis of F4/80+ cells isolated from infected tumors showed a shift from tumor-supporting TAMs to inflammatory macrophages upon OncoD-0J1 treatment. Senescent cells showed heightened EGFR activation as a mechanism to escape death, which created a unique vulnerability for cetuximab as a senolytic agent. Combination therapy reduced EGFR signaling and induced macrophage-mediated antibody-dependent cellular cytotoxicity, thereby increasing the anti-tumor therapeutic response of OncoD-0J1 as a monotherapy.
• 🔗 查看原文

8. GSE263812 小鼠慢性 GVHD 期间肝脏和肺中 CD4⁺ Tm 亚群的整合转录组学、表观遗传学和 TCR 克隆性分析 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：scRNA、epigenetic
• 📝 描述：Contributors : Defu Zeng ; Xiwei Wu ; Xiaohui Kong ; Hyejin ChoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusPathogenic CD4+ T cells perpetuate chronic tissue inflammation, but mechanisms remain largely undefined. Here, with transcriptome, epigenome, and clonal analysis, we compared CD4+Tm subsets among the liver and lung in the No GVHD and cGVHD recipients. Four CD4+Tm subsets identified with Ly108 versus CD69 expression were compared.
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9. GSE263811 小鼠慢性 GVHD 期间肝脏和肺中 CD4⁺ Tm 亚群的转录组学、表观遗传学和 TCR 克隆性综合分析 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、epigenetic
• 📝 描述：Contributors : Defu Zeng ; Xiwei Wu ; Xiaohui Kong ; Hyejin ChoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusPathogenic CD4+ T cells perpetuate chronic tissue inflammation, but mechanisms remain largely undefined. Here, with transcriptome, epigenome, and clonal analysis, we compared CD4+Tm subsets among the liver and lung in the No GVHD and cGVHD recipients. Four CD4+Tm subsets identified with Ly108 versus CD69 expression were compared
• 🔗 查看原文

10. GSE263810 小鼠慢性 GVHD 期间肝脏和肺中 CD4⁺ Tm 亚群的整合转录组学、表观遗传学和 TCR 克隆性分析 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：ATAC-seq、epigenetic
• 📝 描述：Contributors : Defu Zeng ; Xiwei Wu ; Xiaohui Kong ; Hyejin ChoSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusPathogenic CD4+ T cells perpetuate chronic tissue inflammation, but mechanisms remain largely undefined. Here, with transcriptome, epigenome, and clonal analysis, we compared CD4+Tm subsets among the liver and lung in the No GVHD and cGVHD recipients. Four CD4+Tm subsets identified with Ly108 versus CD69 expression were compared.
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1. Outreachy 2025年6月 Bioconductor实习生

• ✍️ 作者：未知作者
• 🏷️ 关键词：Bioconductor
• 📝 描述：Introduction To a beginner, open source can be one of the best pathways into a fulfilling tech career. It not only provides access to source codes but also connects you with a global community of people from diverse backgrounds and skill sets. … Continue reading: Outreachy June 2025 Interns with Bioconductor
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1. SIDISH——将单细胞信息与批量RNA测序相结合，以识别高风险细胞并指导精准治疗

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：SIDISH merges single cell data with bulk RNA sequencing to identify high risk cells, improve clinical prediction and reveal therapeutic targets
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2. 基因编辑的CAR-T细胞可清除侵袭性T细胞白血病

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia
• 📝 描述：A cutting-edge therapy using base-edited immune cells is offering a major breakthrough for patients with one of the toughest forms of blood cancer, T-cell acute lymphoblastic leukaemia. By precisely rewriting tiny sections of DNA, scientists at UCL and Great Ormond Street Hospital created universal CAR T-cells capable of targeting the cancer without harming themselves—a long-standing challenge in T-cell–based therapies. Early trial results show deep, long-lasting remissions, including in patients who had exhausted standard treatment options.
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3. 即使是适量饮酒，其患癌风险也比你想象的要高。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Researchers found that both how often and how much someone drinks significantly shape their cancer risk, even at moderate levels. Vulnerability varies across groups, with genetics, socioeconomic status, obesity, and lifestyle behaviors amplifying harm. The review also uncovered gender differences, beverage-specific risks, and biological pathways that intensify cancer development.
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4. 神经损伤会引发全身隐匿的免疫变化。

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune
• 📝 描述：Researchers discovered that nerve injuries can alter the immune system throughout the body, and males and females react very differently. Male mice showed strong inflammatory responses, while females showed none, yet both transmitted pain-inducing signals through their blood. These findings reveal previously unknown pathways driving pain, especially in females. The work points toward new opportunities for personalized chronic pain therapies.
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• GSE292715 单细胞测序揭示轻度创伤性脑损伤对海马体的影响
• GSE312946 基质细胞对脂肪酸的代谢适应驱动口腔鳞状细胞癌的转移
• GSE307811 开发靶向L1CAM的抗体药物偶联物以治疗转移性癌症
• GSE287188 活性状态 RAS 抑制对结直肠癌细胞转录组的影响
• GSE285564 对视网膜中髓系细胞在移植人类干细胞衍生神经元和眼损伤后进行单细胞转录组比较，揭示了小胶质细胞活化的可逆性。
• GSE313053 APC 协调 GSK3 对 SETD8 的磷酸化以抑制结直肠癌
• GSE312833 大鼠肺组织Glenn手术或假手术后的单细胞RNA测序
• GSE311758 批量 RNA 测序：Glenn 手术或假手术以及饮食调整后 CD31 分选的肺细胞
• GSE308672 利用单核转录组学解析拟南芥根中离散的、细胞特异性的缺氧反应
• GSE306023 CD8 T 细胞受 HLA-B57 和 HLA-E01 交叉限制，识别 HIV Gag 具有不同的功能特征 [数据集 2]
• GSE306022 CD8 T 细胞受 HLA-B57 和 HLA-E01 交叉限制，识别 HIV Gag 具有不同的功能特征 [数据集 1]
• GSE289039 RXR介导的APP小鼠脑转录和染色质结构重塑：来自整合的单细胞RNA和ATAC分析的启示
• GSE286174 系统方法揭示 SMARCD3 调控子驱动依维莫司耐药乳腺癌细胞的替代生长信号传导和对 MEK 抑制剂的敏感性
• GSE283906 RXR介导的APP小鼠脑转录和染色质图谱重塑：来自整合的单细胞RNA和ATAC分析的启示
• GSE263813 小鼠慢性 GVHD 期间肝脏和肺中 CD4⁺ Tm 亚群的整合转录组学、表观遗传学和 TCR 克隆性分析 [scTCR-seq]
• GSE313474 RNA-seq分析PU.1缺失对CAIA小鼠腹腔巨噬细胞中RELM-a+巨噬细胞的影响
• GSE313368 人类肠道类器官对分泌型微环境因子的反应单细胞分辨率词典
• GSE312155 评估放射动力疗法在人胰腺癌MIA PaCa-2异种移植模型中的疗效
• GSE305165 重新定义 EBV 阳性弥漫性大 B 细胞淋巴瘤和 EBV 阳性经典霍奇金淋巴瘤的谱系
• GSE292127：对轻度创伤性脑损伤后TMSB4X条件性敲除（CKO）小鼠海马神经元进行批量RNA测序
• GSE292126 ATAC-Seq 揭示轻度创伤性脑损伤对海马体的影响
• GSE285889整合转录组学和网络分析揭示了驱动脑膜瘤发病机制和临床结局的核心基因
• GSE313379 人类胚胎干细胞中具有活性的染色质区域的发现 [ChIP-Seq 2]
• GSE313377 HnRNPA2B1 通过 Irgm1 的选择性剪接调节巨噬细胞中的抗分枝杆菌免疫反应
• GSE313376 人类胚胎干细胞中具有活性的染色质区域的发现 [ATAC-seq]
• GSE312824 KMT2C 缺陷通过 H3K27ac 介导的 HIPPO 通路失活促进脑膜瘤进展 [CUT&Tag]
• GSE312822 整合药代动力学、组织分布、RNA测序和网络药理学数据，确定STAT1和SERPINE1是莫斯卡替林治疗肝病的潜在靶点
• GSE312820 斑蝥素钠治疗对 AGS 和 MKN1 胃癌细胞系基因表达的影响（治疗组与未治疗组）
• GSE312810 DUS1L 敲除和野生型 A375 人黑色素瘤细胞的 RNA 测序
• GSE298682 SCD1 敲低导致 UMUC3 和 SW780 细胞中基因表达差异（RNA-seq）
• GSE295226 CUT&RUN 在 SCC-25 亲代细胞和 RARG 敲除细胞中定位 RARγ 结合位点以及 H3K4 和 H3K27 三甲基化的全基因组变化
• GSE293632 霸权 EWSR1::ETS 癌基因在尤文氏肉瘤中凌驾于核心调控回路机制之上。
• GSE288935 人类尿液细胞外囊泡的小RNA测序揭示高钠饮食与肾脏促炎通路之间的关联
• GSE271245 唐氏综合征呼吸道合胞病毒感染期间气道上皮JAK-STAT信号过度激活会损害III型干扰素反应[批量RNA测序]
• GSE271139 唐氏综合征呼吸道合胞病毒感染期间气道上皮JAK-STAT信号过度激活会损害III型干扰素反应[单细胞RNA测序]
• GSE253973 间皮瘤中的成纤维细胞样细胞可能来源于肿瘤细胞
• GSE220752 Hyal1基因敲除小鼠肝脏组织的转录组