详细内容（前10条）

1. ⭐ GSE276542 弥漫性大B细胞淋巴瘤免疫肿瘤微环境生态系统的空间转录组学特征

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、lymphoma、immune、tumor microenvironment、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Alba Diaz Herrero ; Pierre TonnerreSeries Type : OtherOrganism : Homo sapiensThis dataset comprises spatial transcriptomic profiles from 10 tissue samples of Diffuse Large B-cell Lymphoma (DLBCL) the most common subtype of non-Hodgkin’s lymphoma and secondary lymphoid organ controls (SLO). The diffuse nature of DLBCL challenges the analysis of cellular organization within the immune tumor microenvironment (TME). We employed spatial transcriptomics to map spatially-resolved gene expression patterns. The analysis led to the identification of six cellular ecosystems (Cell-Eco) that differ in cellular composition, functional patterns, and neighborhood characteristics. The spatially-resolved Cell-Eco signatures provided prognostic scores that stratified patients with different overall survival rates. We also found that C1q+ tumor-associated macrophages are the primary cells interacting with malignant B cells and influencing the spatial architecture of the TME. This resource offers valuable insights into the spatial complexity of the DLBCL microenvironment and its potential prognostic significance.
• 🔗 查看原文

2. ⭐ GSE328719 癌细胞内在的 SSBP4 通过促进胆固醇生物合成实现肿瘤免疫逃逸 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immune、RNA-seq
• 📝 描述：Contributors : Ou Peiqi ; Eres Ittai ; Zhao Junjie ; Han Chia-Jung ; Oh Jaehak ; Kim Aeryon ; Dong Jiayi ; Zhou Hong ; Yamawaki Tracy ; Li Chi-Ming ; Rankin Andrew ; Noubade Rajkumar ; Yu XinSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe immunosuppressive tumor microenvironment (TME) contributes to resistance against checkpoint inhibitors. However, the precise factors that shape the immune contexture of the TME remain elusive. Here, we report that Single-Stranded DNA Binding Protein 4 (SSBP4), a previously uncharacterized protein, suppresses intratumoral T-cell activation by promoting excessive cholesteryl ester production in tumor cells. Overexpression of SSBP4 in tumor cells decreased T-cell infiltration and accelerated tumor growth in murine syngeneic tumor models. Conversely, genetic ablation of SSBP4 in tumor cells enhanced T-cell infiltration and inhibited tumor growth in a CD8+ T cell–-dependent manner. Mechanistically, SSBP4 upregulated cholesterol synthesis genes, leading to increased production of cholesterol and cholesteryl esters in tumor cells, which directly suppressed CD8+ T-cell activation and function. Furthermore, SSBP4 abrogation significantly improved the efficacy of anti-PD-1 treatment. Thus, in this study, we have identified SSBP4 as a cancer cell–intrinsic regulator of cholesterol metabolism that contributes to tumor immune evasion.
• 🔗 查看原文

3. ⭐ GSE328718 癌细胞内在的 SSBP4 通过促进胆固醇生物合成实现肿瘤免疫逃逸 [ATAC-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immune、ATAC-seq
• 📝 描述：Contributors : Ou Peiqi ; Eres Ittai ; Zhao Junjie ; Han Chia-Jung ; Oh Jaehak ; Kim Aeryon ; Dong Jiayi ; Zhou Hong ; Yamawaki Tracy ; Li Chi-Ming ; Rankin Andrew ; Noubade Rajkumar ; Yu XinSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusThe immunosuppressive tumor microenvironment (TME) contributes to resistance against checkpoint inhibitors. However, the precise factors that shape the immune contexture of the TME remain elusive. Here, we report that Single-Stranded DNA Binding Protein 4 (SSBP4), a previously uncharacterized protein, suppresses intratumoral T-cell activation by promoting excessive cholesteryl ester production in tumor cells. Overexpression of SSBP4 in tumor cells decreased T-cell infiltration and accelerated tumor growth in murine syngeneic tumor models. Conversely, genetic ablation of SSBP4 in tumor cells enhanced T-cell infiltration and inhibited tumor growth in a CD8+ T cell–-dependent manner. Mechanistically, SSBP4 upregulated cholesterol synthesis genes, leading to increased production of cholesterol and cholesteryl esters in tumor cells, which directly suppressed CD8+ T-cell activation and function. Furthermore, SSBP4 abrogation significantly improved the efficacy of anti-PD-1 treatment. Thus, in this study, we have identified SSBP4 as a cancer cell–intrinsic regulator of cholesterol metabolism that contributes to tumor immune evasion.
• 🔗 查看原文

4. ⭐ GSE322620 原发性口腔鳞状细胞癌和淋巴结转移病变的单细胞转录组分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、lymph、regex:lymph(o|atic)?、single-cell
• 📝 描述：Contributors : Yichao Xia ; Yongsheng LiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapienswe performed single-cell RNA sequencing (scRNA-seq) on tumor tissues from five patients with primary OSCC and five patients lymph node metastatic lesions.
• 🔗 查看原文

5. ⭐ GSE307285 BRD2 上调作为泛癌对 BET 抑制的适应性耐药机制 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、resistance、ChIP-seq
• 📝 描述：Contributors : Suyakarn Archasappawat ; Chang-il HwangSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusBromodomain and extraterminal motif (BET) inhibitors, such as JQ1, are promising cancer therapeutics that target epigenetic regulators, particularly BRD4. However, resistance to BET inhibitors (BETi) limits their clinical utility, necessitating a better understanding of adaptive mechanisms. We identified BRD2 upregulation as a conserved response to BET inhibition across multiple cancer types and hypothesized that BRD2 compensates for BRD4 loss, sustaining essential transcriptional programs during treatment. Consistent with this, BRD2 knockdown sensitized cancer cells to BETi in vitro, and combining BRD2 depletion and JQ1 treatment significantly impaired tumor growth in vivo. At the chromatin level, BRD2 and BRD4 ChIP-seq analysis of pancreatic cancer cells showed consistent BRD4 loss from chromatin after JQ1 treatment, while BRD2 displacement differed by sensitivity. Resistant cells maintained higher BRD2 occupancy than sensitive cells, suggesting a link between BRD2 retention and drug response. To dissect the underlying mechanism of BRD2 upregulation upon BET inhibition, we analyzed co-expression networks and observed that NFYA is co-expressed with BRD2 across diverse tissues and cancer types. Consistently, NFYA binds the BRD2 promoter. NFYA depletion abrogated BRD2 upregulation upon BETi treatment, indicating that NFYA is required for BRD2 induction following BET inhibition. Collectively, our findings establish BRD2 as a critical mediator of adaptive resistance to BETi in pan-cancer and identify NFYA as a novel transcriptional regulator of this process. Co-targeting BRD2 or its regulatory network offers a rational strategy to enhance the durability and efficacy of BET-based therapies.
• 🔗 查看原文

6. ⭐ GSE307284 BRD2 上调作为泛癌适应性抗 BET 抑制机制 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、resistance、RNA-seq
• 📝 描述：Contributors : Suyakarn Archasappawat ; Chang-il HwangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusBromodomain and extraterminal motif (BET) inhibitors, such as JQ1, are promising cancer therapeutics that target epigenetic regulators, particularly BRD4. However, resistance to BET inhibitors (BETi) limits their clinical utility, necessitating a better understanding of adaptive mechanisms. We identified BRD2 upregulation as a conserved response to BET inhibition across multiple cancer types and hypothesized that BRD2 compensates for BRD4 loss, sustaining essential transcriptional programs during treatment. Consistent with this, BRD2 knockdown sensitized cancer cells to BETi in vitro, and combining BRD2 depletion and JQ1 treatment significantly impaired tumor growth in vivo. At the chromatin level, BRD2 and BRD4 ChIP-seq analysis of pancreatic cancer cells showed consistent BRD4 loss from chromatin after JQ1 treatment, while BRD2 displacement differed by sensitivity. Resistant cells maintained higher BRD2 occupancy than sensitive cells, suggesting a link between BRD2 retention and drug response. To dissect the underlying mechanism of BRD2 upregulation upon BET inhibition, we analyzed co-expression networks and observed that NFYA is co-expressed with BRD2 across diverse tissues and cancer types. Consistently, NFYA binds the BRD2 promoter. NFYA depletion abrogated BRD2 upregulation upon BETi treatment, indicating that NFYA is required for BRD2 induction following BET inhibition. Collectively, our findings establish BRD2 as a critical mediator of adaptive resistance to BETi in pan-cancer and identify NFYA as a novel transcriptional regulator of this process. Co-targeting BRD2 or its regulatory network offers a rational strategy to enhance the durability and efficacy of BET-based therapies.
• 🔗 查看原文

7. ⭐ GSE328971 癌细胞内在的SSBP4通过促进胆固醇生物合成使肿瘤免疫逃逸。

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immune
• 📝 描述：Contributors : Ou Peiqi ; Eres Ittai ; Zhao Junjie ; Han Chia-Jung ; Oh Jaehak ; Kim Aeryon ; Dong Jiayi ; Zhou Hong ; Yamawaki Tracy ; Li Chi-Ming ; Rankin Andrew ; Noubade Rajkumar ; Yu XinSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe immunosuppressive tumor microenvironment (TME) contributes to resistance against checkpoint inhibitors. However, the precise factors that shape the immune contexture of the TME remain elusive. Here, we report that Single-Stranded DNA Binding Protein 4 (SSBP4), a previously uncharacterized protein, suppresses intratumoral T-cell activation by promoting excessive cholesteryl ester production in tumor cells. Overexpression of SSBP4 in tumor cells decreased T-cell infiltration and accelerated tumor growth in murine syngeneic tumor models. Conversely, genetic ablation of SSBP4 in tumor cells enhanced T-cell infiltration and inhibited tumor growth in a CD8+ T cell–-dependent manner. Mechanistically, SSBP4 upregulated cholesterol synthesis genes, leading to increased production of cholesterol and cholesteryl esters in tumor cells, which directly suppressed CD8+ T-cell activation and function. Furthermore, SSBP4 abrogation significantly improved the efficacy of anti-PD-1 treatment. Thus, in this study, we have identified SSBP4 as a cancer cell–intrinsic regulator of cholesterol metabolism that contributes to tumor immune evasion.
• 🔗 查看原文

8. ⭐ GSE314048 人乳头瘤病毒 (HPV) 感染的上皮细胞和 FBLN1+ 纤维网状细胞调控 HPV 相关口咽鳞状细胞癌的免疫原性肿瘤微环境

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、carcinoma、tumor microenvironment
• 📝 描述：Series Type : OtherOrganism : Homo sapiensOPSCC can occur through either the exposure to carcinogens such as alcohol and/or tobacco or high-risk human papillomavirus (HPV) infection. We used single cell RNA sequencing (scRNA-seq) to analyze the tumor microenvironment (TME) of HPV-positive OPSCC exhibits distinctive features, with relevance to the interaction between cancer cells and adjacent stromal cells.
• 🔗 查看原文

9. ⭐ GSE311100 通过单核和空间转录组学解码H19在胆汁淤积性肝损伤中的细胞类型和空间作用

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Grayson W Way ; Huiping ZhouSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Mus musculusDespite recent advances, Primary Sclerosing Cholangitis (PSC)-a chronic obstructive biliary disease-still lacks effective therapies to prevent disease progression or the need for liver transplantation. Long non-coding RNA H19 (H19) has been implicated in promoting PSC disease progression. However, the underlying cell-specific and molecular mechanisms by which H19 contributes to PSC pathogenesis remain incompletely understood. Here we used single nucleus RNA sequencing (snRNAseq) and spatial transcriptomics to elucidate the cell- and spatial-specific expression alterations associated with H19 in the Mdr2KO PSC mouse model.
• 🔗 查看原文

10. ⭐ GSE299323 单细胞RNA测序结果显示HCM小鼠存在心脏纤维化和免疫微环境激活。

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、cardiac、scRNA
• 📝 描述：Contributors : Nianwei Zhou ; Wenjun Wang ; Luman Wang ; Xianhong ShuSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusHypertrophic cardiomyopathy (HCM), the most prevalent inherited cardiovascular disorder, confers elevated risks of stroke, progressive heart failure, and sudden cardiac death. Emerging evidence suggests that myocardial inflammation may contribute to the progression and complications of HCM. While colchicine has demonstrated therapeutic potential in reducing adverse cardiovascular events through its pleiotropic anti-inflammatory mechanisms in other cardiac conditions, its efficacy profile in HCM populations have not been investigated. Our study offered preclinical evidence suggesting that colchicine may exhibit potential therapeutic efficacy in the treatment of HCM, thereby presenting a theoretical foundation for the application of colchicine in HCM.
• 🔗 查看原文

💡 该来源还有 80 条内容，详见 文末

详细内容（全部5条）

1. ⭐ 新的肺癌模型揭示了肿瘤位置如何影响免疫反应

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immune
• 📝 描述：RNA sequencing combined with spatial transcriptomics reveals how immune cells reorganize within lung tumors, providing deeper insight into tumor microenvironment dynamics and potential therapeutic targets…
• 🔗 查看原文

2. PreludeDx公司基于AidaBREAST® RNA-seq技术的早期浸润性乳腺癌检测方法获得FDA突破性医疗器械认定。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq
• 📝 描述：RNA sequencing integrated with multi-omic analysis enables AidaBREAST to predict recurrence risk and radiation therapy benefit, supporting personalized treatment decisions…
• 🔗 查看原文

3. 利用 AutoRNAseq 实现 RNA 测序分析自动化

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：RNA sequencing workflows like AutoRNAseq automate data processing, improving reproducibility and consistency across experiments while simplifying gene expression analysis for large-scale datasets…
• 🔗 查看原文

4. 科学家通过阻断一种阿尔茨海默病蛋白来恢复记忆。

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：Researchers have identified a new potential weapon against Alzheimer’s: blocking a protein called PTP1B. In mice, this approach boosted memory and helped brain immune cells clear harmful plaque buildup. Since PTP1B is also linked to diabetes and obesity—both risk factors for Alzheimer’s—it could offer a broader treatment strategy.
• 🔗 查看原文

5. 首个3D视图揭示了杀伤性T细胞如何摧毁癌细胞

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：The body’s “killer” T cells don’t just attack—they strike with astonishing precision, forming a tiny, highly organized contact zone that lets them destroy dangerous cells without harming their neighbors. Now, scientists have captured this process in unprecedented detail, revealing a hidden world of molecular choreography.
• 🔗 查看原文

• GSE297394 配对突变检测和空间转录组学鉴定出决定结肠炎肿瘤结局的细胞邻域
• GSE295070 小鼠胰腺肿瘤中抗原呈递癌相关成纤维细胞通过 CXCL9 和 CCL22 差异性地调控调节性 T 细胞表型和功能
• GSE294512 eIF4G2介导的组蛋白修饰酶翻译起始对于肠道干细胞的维持和分化至关重要[RNA-seq]
• GSE294071 PCSK9 通过促进肿瘤内胆固醇积累和增强免疫抑制性肿瘤微环境来促进前列腺癌的发生发展
• GSE288786 人乳头瘤病毒 (HPV) 感染的上皮细胞和 FBLN1+ 纤维网状细胞调控 HPV 相关口咽鳞状细胞癌的免疫原性肿瘤微环境
• GSE263916 缺氧条件下 METTL3 介导的 m6A RNA 甲基化稳定 RIPOR3 mRNA 驱动乳腺肿瘤生长和转移 [RNA-seq]
• GSE298602 先兆子痫和健康胎盘的单细胞 RNA-Seq 数据
• GSE328821 U2AF1 突变挽救 KRAS 突变引起的有害外显子跳跃 [RNA-Seq]
• GSE328098 3’UTR 导向的激酶近端 mRNA 降解抑制 C/EBPβ 磷酸化/激活，从而抑制肿瘤细胞衰老
• GSE329266 Nanostring nCounter 小鼠泛癌免疫谱分析小鼠肿瘤组织
• GSE329124 小鼠小肠经静脉注射免疫球蛋白（IVIg）治疗后接受全腹部照射的 RNA-seq 分析
• GSE326534 罗伊氏乳杆菌介导的肉鸡肠黏膜炎症损伤修复机制：来自肠道巨噬细胞-干细胞相互作用的启示
• GSE325201 UHRF1在KRAS突变型胰腺癌细胞中的作用
• GSE318069 eIF4G2介导的组蛋白修饰因子翻译起始对于肠道干细胞的维持和分化至关重要
• GSE318068 eIF4G2介导的组蛋白修饰酶翻译起始对于肠道干细胞的维持和分化至关重要[多组学]
• GSE318066 eIF4G2介导的组蛋白修饰酶翻译起始对于肠道干细胞的维持和分化至关重要 [CUT&Tag]
• GSE316603 HDAC3抑制作为通过TYK2-STAT1-BCL2信号通路治疗T细胞急性淋巴细胞白血病的一种策略
• GSE298361：甲羟戊酸激酶缺乏症小鼠模型外周血单核细胞的单细胞RNA测序分析
• GSE294863 雷帕霉素靶蛋白/血液检测屏障机制介导环境因素加速精子表观遗传衰老。
• GSE293546 EZH2抑制剂SHR2554通过STAT1增强HDAC抑制剂西达米德在T细胞淋巴瘤中的抗肿瘤疗效
• GSE264577 靶向 LMO2 诱导的自分泌 FLT3 信号以克服早期 T 细胞前体急性淋巴细胞白血病的化疗耐药性 [RNA-seq]
• GSE264576 靶向 LMO2 诱导的自分泌 FLT3 信号以克服早期 T 细胞前体急性淋巴细胞白血病的化疗耐药性 [ChIP-seq]
• GSE264572 靶向 LMO2 诱导的自分泌 FLT3 信号以克服早期 T 细胞前体急性淋巴细胞白血病的化疗耐药性 [ATAC-seq]
• GSE235391 靶向 PCDH7 的单克隆抗体可抑制非小细胞肺癌的肿瘤生长并增强靶向治疗反应
• GSE178413 RNA-Seq 分析人乳腺癌细胞中 c-MYC 诱导性敲低
• GSE175617 RNA-Seq 分析 p53 敲低和敲除的人类癌细胞
• GSE329336 广泛的转录记忆塑造癌症和干细胞的遗传状态和功能异质性 [scRNA-seq]
• GSE329159 广泛的转录记忆塑造癌症和干细胞的遗传状态和功能异质性 [RNA-Seq]
• GSE303732 配对的原发-转移患者来源类器官和鼠模型揭示了阑尾癌腹膜转移的表型演变和药物靶向依赖性
• GSE302859 多层信号传导和表观基因组重编程驱动与脱髓鞘相关的小胶质细胞炎症状态和功能 [ChIP-seq]
• GSE302858 多层信号传导和表观基因组重编程驱动与脱髓鞘相关的小胶质细胞炎症状态和功能 [ATAC-seq]
• GSE302857 多层信号传导和表观基因组重编程驱动与脱髓鞘相关的小胶质细胞炎症状态和功能 [RNA-seq]
• GSE267967 Foxp3 和 BATF 协同指导 Treg 细胞功能分化的顺式调控程序和基因表达 [RNA-seq]
• GSE328804 U2AF1突变可挽救KRAS突变引起的有害外显子跳跃
• GSE311739 PRMT5抑制可使B细胞非霍奇金淋巴瘤细胞对内在和外在凋亡细胞死亡均更加敏感
• GSE295472 NOD2驱动肠上皮细胞的再生性胎儿样重编程
• GSE329267 Nanostring nCounter 髓系固有免疫分析：用条件培养基培养的 CD8 T 细胞
• GSE329123 体外诱导的由野生型和Cd4-Cre Rpa1fl/fl CD8+ T细胞产生的虚拟记忆T细胞的单细胞转录组学和单细胞ATAC分析
• GSE329120 草鱼肠道和全身对维罗尼气单胞菌感染的分子调控机制的新见解
• GSE329009 白化美洲牛蛙体内系统性氧化应激和黑色素生成基因的矛盾性上调：来自多组织转录组学和 UVB 照射的启示
• GSE328605 流感相关肺曲霉病中的髓系细胞状态受铁过载和代谢重编程的影响
• GSE328273 颈交感神经干切断术可能通过抑制大鼠模型中的转录组谱和钙信号传导来改善肺动脉高压
• GSE328199 柠檬苦素可改善小鼠代谢功能障碍相关性脂肪性肝炎
• GSE328052 全基因组鉴定MYB家族并分析EpMYB71作为紫草素生物合成关键调控因子的功能
• GSE327824 染色质连接状态的单分子、单细胞分析 [Single_cell_CUT&Tag]
• GSE327821 染色质连接状态的单分子、单细胞分析 [Single_cell_CoCUT&Tag]
• GSE327819 染色质连接状态的单分子、单细胞分析 [Bulk_CoCUT&Tag]
• GSE327816 染色质连接状态的单分子、单细胞分析 [Bulk_CUT&Tag]
• GSE327575 TET2_x001E_介导的PTPN6去甲基化导致烧伤后免疫麻痹，而靶向PTPN6的AAV_x001E_CRISPRi可改善继发性血流感染的预后
• GSE326585 Peersim [RNA-Seq]
• GSE325134 肉牛小母牛妊娠状态相关的转录组学特征
• GSE322735 CD28靶向酶响应构象转换肽自组装用于选择性T细胞急性淋巴细胞白血病（T-ALL）治疗
• GSE319524 转录偶联修复去除细胞毒性DNA甲基化损伤并促进胶质瘤中的突变链不对称性
• GSE318877 从人类胸主动脉获得的微区域批量 RNA 测序数据
• GSE316905 lncBCAS1-4_1，CYP24A1 的功能同源物，通过糖酵解和上皮间质转化减弱 1,25(OH)₂D₃ 在肺癌中的抗癌功效
• GSE314814 Myc 维持果蝇肠道中区域性和性别偏向的器官分区
• GSE312944 STC-15 对 METTL3 的抑制诱导 RNA 错误加工，导致双链 RNA 形成并激活先天免疫
• GSE301904 基因工程小鼠模型中胰腺癌细胞和组织的转录组分析
• GSE296064：利用RNAi干扰Hsp90aa1和Hsp90ab1表达后，对小鼠乳腺癌模型MMTV-PyMT中正常乳腺成纤维细胞（NFs）和癌相关成纤维细胞（CAFs）的基因表达进行分析
• GSE295955 METTL16 缺失对 HPMVEC 基因表达的影响 [RNA-Seq]
• GSE295752 一项随机对照试验，比较静脉注射免疫球蛋白与标准治疗在肾移植受者慢性活动性抗体介导排斥反应中的疗效 (VIPAR)
• GSE295302 利用小分子将小鼠成肌细胞转化为肌肉干细胞 [RNA-Seq]
• GSE295091 利用小分子将小鼠成肌细胞转化为肌肉干细胞 [scRNA-Seq]
• GSE294454 KO-2806 和卡博替尼治疗对 KI-12-0073 透明细胞肾细胞癌 (ccRCC) 异种移植瘤基因表达的影响
• GSE293956 hDF-EVs 对成纤维细胞和角质形成细胞的作用机制 [RNA-seq]
• GSE293684 胡桃和补骨脂联合治疗大鼠双侧卵巢切除术后骨质疏松症的潜在机制转录组分析
• GSE288618 利用DMS-FIRST-seq构建的长读长转录组范围RNA结构图谱
• GSE279444 烟酰胺N-甲基转移酶作为紫杉烷类耐药去势抵抗性前列腺癌的治疗靶点
• GSE266241 脊髓缺血后抑制性信号传导减少和C-C基序趋化因子配体的选择性诱导
• GSE263254 韩牛牛背最长肌中与牛肉品质相关的年龄相关转录组变化
• GSE248584 由 FOSL1 驱动的保守上皮伤口样转录程序是胰腺导管腺癌恶性进展的基础（scRNA-Seq）
• GSE248583 由 FOSL1 驱动的保守上皮伤口样转录程序是胰腺导管腺癌恶性进展的基础 (ATAC-Seq)
• GSE231854 肝细胞癌和混合型肝细胞胆管癌的异质性分析
• GSE231700 miRNA表达变化在慢性心脏压力负荷小鼠中的作用
• GSE231698 circRNA表达变化在慢性心脏压力负荷小鼠中的作用
• GSE183445 RNA-Seq 分析高脂饮食或生酮饮食喂养的 NSG 小鼠中，抑制人 A375 黑色素瘤肺转移瘤生长的抑制剂组合
• GSE329335 广泛的转录记忆塑造癌症和干细胞的遗传状态和功能异质性 [RRBS]
• GSE329158 广泛的转录记忆塑造了癌症和干细胞的遗传状态和功能异质性
• GSE263653 利用人类小脑类器官研究髓母细胞瘤的发病机制和治疗。[甲基化]
• GSE263652 利用人类小脑类器官研究髓母细胞瘤的发病机制和治疗。[scRNA-Seq]