详细内容（前10条）

1. ⭐ GSE342671 纵向单细胞和空间转录组学揭示犬边缘区淋巴瘤的肿瘤内异质性、治疗反应和比较价值

• ✍️ 作者：未知作者
• 🏷️ 关键词：lymphoma、single-cell、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Grace E Walker ; Marissa Macchietto ; Kelly Reid ; Lauren E Burt ; Amber Winter ; Sara Pracht ; Michelle Buettner ; Velia Penza ; Caitlin Yung ; Rose Dicovitsky ; Alana Kuzmik ; Daniel A Vallera ; Kim Demos-Davies ; Davis M Seelig ; Antonella Borgatti ; Mike Henson ; Caitlin Feiock ; Jaime F Modiano ; Shruthi Naik ; Aaron L Sarver ; Amy E TreefulSeries Type : OtherOrganism : Canis lupus familiarisDiffuse B-cell lymphomas are the most prevalent canine hematologic malignancies, and their clinical presentation resembles that of human B-cell non-Hodgkin lymphomas (NHLs). However, a lack of a clear subtyping framework perpetuates imprecise treatment approaches that fail to address mechanisms of therapy resistance. Here, we employed deep phenotyping via serial sampling and longitudinal transcriptomics to evaluate intratumoral composition and therapy response in a 6-year-old neutered male goldendoodle with stage 5A marginal zone lymphoma (MZL). Following sequential treatment consisting of a single IV dose of oncolytic vesicular stomatitis virotherapy (VSV) and standard CHOP chemotherapy 30 days later, we performed scRNAseq on seven serial lymph node biopsies and spatial sequencing on a resection taken 10 days post-VSV treatment. B cells (>90%) comprised three transcriptionally distinct and temporally stable subpopulations, with specific copy number profiles and robust spatial organization despite disrupted lymph node architecture. Analysis across subpopulations revealed downregulation of the quiescence program including KLF2, suggesting similarity to KLF2-deficient human MZL. While VSV successfully reached target B cells, downstream transcriptional responses were predominantly localized to the T-cell compartment. T cells (≤6%) showed increased proliferation and upregulation of cytotoxicity markers post-VSV administration, enriching for leukocyte-mediated cytotoxicity pathways consistent with an anti-viral immune response. Ultimately, these results provide an in vivo proof-of-concept for the treatment paradigm in canine lymphoma, while emphasizing the need for improved subtyping frameworks and multidimensional treatment strategies targeting intratumoral heterogeneity.
• 🔗 查看原文

2. ⭐ GSE333300 CD4+ T 细胞激活的 CD8+ T 细胞驱动 MHC-I 阴性 DNA 错配修复缺陷癌症的免疫治疗反应

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、T cell、MHC、regex:immuno(logy|therapy|suppression)
• 📝 描述：Contributors : Marta Requesens ; Luciana Gneo ; Tijana Tomasevic ; Nienke van Rooij ; Annechien Plat ; Mingjia Xi ; Charlotte O’Riordan-Moore ; Katarzyna Kedzierska ; Noelia Che ; Mark Glaire ; Yanshu Cai ; Monika Madrova ; Lai Mun Wang ; Ibrahem Al-Obaidi ; Matthieu Miossec ; Marnix Jansen ; Annabelle Lewis ; Noemi Perujo Holland ; Ian Tomlinson ; Floris Foijer ; Isabela Pedroza-Pacheco ; Hans W. Nijman ; David N. Church ; Marco de BruynSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusDNA mismatch repair deficiency (MMRd) occurs in multiple malignancies including 10–15% of colorectal cancers (CRC), where it causes increased tumor mutational burden (TMB) and T cell response. MMRd CRC display multiple mechanisms of immune evasion, yet are highly sensitive to immune checkpoint blockade (ICB), with underlying mechanisms only partially understood. We generated genetically engineered mouse models (GEMM) of hereditary (Lynch syndrome) and sporadic MMRd CRC, and found that accelerated tumorigenesis was accompanied by universal tumor loss of major histocompatibility class I (MHC-I) expression and exclusion of cytotoxic CD8+ T cells, but not helper CD4+ T cells. MHC-I deletion (MHC-IKO) in a syngeneic MMRd CRC model reduced tumor CD8+ but not CD4+ cell infiltrate, and accelerated tumor growth. MMRd MHC-IKO tumors were resistant to anti-PDL1 ICB, but sensitive to anti-PD1 and anti-CTLA4 combination ICB (cICB) with response dependent on both CD4+ and CD8+ T cells, but not γδ-T cells. cICB resistance caused by CD4+ cell depletion was reversed by CD40 agonism, suggesting a mechanism where CD4+ cells license CD8+ cells to kill cancer cells by MHC-I-independent activity. Multimodal analysis revealed that CD4+ T cell help increases the cytotoxic state of CD8+ T cells, potentially lowering their MHC-I-independent activation threshold against cancer cells. Our results underscore the central role of MHC-I loss in tumor immune evasion, and the cooperative role of CD4+ and CD8+ cells in cICB response of MHC-I negative tumors. Our data suggest that MHC-I status may be useful as a biomarker to stratify for ICB monotherapy versus combination therapy.
• 🔗 查看原文

3. ⭐ GSE330748 CD4+ T 细胞激活的 CD8+ T 细胞驱动 MHC-I 阴性 MMRd 癌症的免疫治疗反应

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、T cell、MHC、regex:immuno(logy|therapy|suppression)
• 📝 描述：Contributors : Luciana Gneo ; David ChurchSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusDNA mismatch repair deficiency (MMRd) causes hypermutation and increased T cell response in multiple tumor types. MMRd colorectal cancers (CRC) display frequent immune evasion, but respond to immune checkpoint blockade (ICB), through uncertain mechanisms. We generated mouse models of MMRd CRC, and found that accelerated tumorigenesis was accompanied by loss of major histocompatibility class I (MHC-I) expression and exclusion of cytotoxic CD8+ T cells, but not helper CD4+ T cells. MHC-I deletion (MHC-IKO) in a syngeneic MMRd CRC model reduced tumor CD8+ but not CD4+ cell infiltrate, and accelerated tumor growth. MMRd MHC-IKO tumors were resistant to anti-PD-L1 ICB, but sensitive to anti-PD1 and anti-CTLA4 combination ICB (cICB) with response dependent on both CD4+ and CD8+ T cells, but not gd-T cells. CD4+ cell depletion-induced cICB resistance was reversed by CD40 agonism, suggesting that CD4+ cells license CD8+ cell cytolysis by MHC-I-independent activity. Investigation of MHC-I status as predictor of cICB vs ICB monotherapy appears worthwhile.
• 🔗 查看原文

4. ⭐ GSE317372 基质导向的肿瘤微环境促进骨内成釉细胞瘤的生长 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、tumor microenvironment、RNA-seq
• 📝 描述：Contributors : Da-Yo Yuh ; Ting-Han ChangSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensAmeloblastoma is a locally aggressive odontogenic epithelial tumor with poorly understood intraosseous pathogenesis due to a lack of physiologically relevant models. Here, we established an orthotopic intraosseous mouse model using ameloblastoma epithelial cells in combination with ameloblastoma-derived mesenchymal stromal cells (AMMSCs) or their secretome. AMMSC-derived extracellular vesicle-enriched secretome enhances stemness, epithelial-mesenchymal transition (EMT) phenotypes, and tumorigenic ability of ameloblastoma epithelial cells. A unique signature of microRNAs in AMMSC-derived secretome is functionally associated with the upregulation of EMT-regulatory transcription factors in tumor epithelial cells. Single-nucleus ATAC and RNA sequencing revealed a dynamic EMT trajectory in primary human AM-derived epithelial cells activated by paired AMMSC-derived secretome. This study suggests that AMMSCs and their secretome drive orthotopic AM tumor development by promoting tumor epithelial cell proliferation, EMT, and vascular formation in the tumor microenvironment. This stromal-oriented orthotopic model provides a clinically relevant platform for dissecting tumor-stroma crosstalk and identifying therapeutic vulnerabilities in ameloblastoma.
• 🔗 查看原文

5. ⭐ GSE342674 抑制磷脂酰丝氨酸外化可克服癌症免疫逃逸并增强免疫疗法

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、regex:immuno(logy|therapy|suppression)
• 📝 描述：Contributors : Johann S Bergholz ; Grace Trombley ; Gwendolyn Cusing ; Zhaoqi Li ; Margaret E Torrence ; Geneva Sganga ; Jennifer Casey ; Shangtao Liu ; Ashley H Choi ; Samuel R Meier ; Tenzing Khendu ; Yi Yu ; Teng Teng ; Binzhang Shen ; Hannah Stowe ; Salam Shaaban ; Jannik N Andersen ; Serge GueroussovSeries Type : OtherOrganism : Homo sapiens ; Mus musculusImmune checkpoint blockade (ICB) has transformed cancer therapy, yet many tumors remain refractory to treatment due to diverse immune evasion mechanisms. To uncover novel drivers of ICB resistance, we performed an in vivo CRISPR-Cas9 screen in mice with increasing levels of immune pressure. This screen identified phosphatidylserine (PS) externalization as a potent mediator of immune escape. Tumors with elevated surface PS exposure prevented reinvigoration of CD8+ T cells upon PD-1 blockade, which was associated with increased recruitment of immunosuppressive myeloid cells. Targeting of PS Synthase 1 (PTDSS1) or either of the scramblases, XKR8 or ANO6, sensitized tumors to ICB in vivo. These findings demonstrate that elevated PS exposure constitutes a mechanism of resistance to ICB, and that targeting regulators of PS externalization represents a promising strategy to enhance the efficacy of immunotherapy in refractory tumors.
• 🔗 查看原文

6. GSE337302 Zfp57 和 Gzf1 相互依赖甲基化的结合在发育重编程过程中保护 Dlk1-Dio3 印记 [bulk RNAseq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNAseq、methylation
• 📝 描述：Contributors : Arik Toren ; Liron Hoffman ; Irina Miodownik ; Yoav Mayshar ; Raz Ben-Yair ; Ayelet-Hashahar Orenbuch ; Hernan Rubinstein ; Aviezer Lifshitz ; Roni Stok Ranen ; Alexander Wainstein ; Daoud Sheban ; Liran Shlush ; Amos Tanay ; Ariel Afek ; Yonatan StelzerSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusGenomic imprinting secures parent-specific gene expression through differential DNA methylation at imprinted control regions (ICRs). However, how unmethylated alleles resist de novo methylation remains unclear. Using an allelic Dlk1-Dio3 ICR methylation reporter and genome-wide loss-of-function screening, we identify the zinc finger protein GZF1 that binds the unmethylated maternal ICR and protects it from de novo methylation via a regulatory element containing GZF1 and ZFP57 motifs that mediates mutually exclusive, methylation-dependent binding. Loss of either factor causes reciprocal imprinting failure: Gzf1 loss induces maternal allele methylation, H3K4me3 depletion, and silencing of maternal transcripts, whereas Zfp57 loss results in maternalization. Remarkably, GZF1 protects the unmethylated ICR from de novo methylation in both oocytes and embryos, and its loss leads to perinatal death consistent with paternalization of the maternal allele. Together, our findings establish a reciprocal mechanism that maintains parental epigenetic asymmetry across both imprint establishment and embryonic reprogramming.
• 🔗 查看原文

7. GSE337143 Zfp57 和 Gzf1 相互的、甲基化依赖性的结合在发育重编程过程中保护 Dlk1-Dio3 印记 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：ChIP-seq、methylation
• 📝 描述：Contributors : Arik Toren ; Liron Hoffman ; Irina Miodownik ; Yoav Mayshar ; Raz Ben-Yair ; Ayelet-Hashahar Orenbuch ; Hernan Rubinstein ; Aviezer Lifshitz ; Roni Stok Ranen ; Alexander Wainstein ; Daoud Sheban ; Liran Shlush ; Amos Tanay ; Ariel Afek ; Yonatan StelzerSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusGenomic imprinting secures parent-specific gene expression through differential DNA methylation at imprinted control regions (ICRs). However, how unmethylated alleles resist de novo methylation remains unclear. Using an allelic Dlk1-Dio3 ICR methylation reporter and genome-wide loss-of-function screening, we identify the zinc finger protein GZF1 that binds the unmethylated maternal ICR and protects it from de novo methylation via a regulatory element containing GZF1 and ZFP57 motifs that mediates mutually exclusive, methylation-dependent binding. Loss of either factor causes reciprocal imprinting failure: Gzf1 loss induces maternal allele methylation, H3K4me3 depletion, and silencing of maternal transcripts, whereas Zfp57 loss results in maternalization. Remarkably, GZF1 protects the unmethylated ICR from de novo methylation in both oocytes and embryos, and its loss leads to perinatal death consistent with paternalization of the maternal allele. Together, our findings establish a reciprocal mechanism that maintains parental epigenetic asymmetry across both imprint establishment and embryonic reprogramming.
• 🔗 查看原文

8. GSE324559 EZH2 与 SREBP2 合作建立表观基因组、转录组和代谢程序以驱动肿瘤发生 [RNA-seq II]

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolic、RNA-seq
• 📝 描述：Contributors : Arum Kim ; Greg WangSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensEnhancer of Zeste Homolog 2 (EZH2) is recurrently overexpressed in cancers, correlating with adverse clinical outcomes. How exactly EZH2 overexpression contributes to tumorigenicity is far from clear. We here report an unexplored tumor-promoting axis involving the EZH2 association with SREBP2, a master regulator of lipid metabolism. EZH2 and SREBP2 act together to potentiate the expression of mevalonate pathway genes, thereby enhancing cholesterol biosynthesis to sustain aggressive tumor growth. The partially disordered transcriptional activation domains (tADs) of EZH2 and SREBP2 directly bind and recruit p300 to mediate the proto-oncogene activation. Additionally, we employed Proteolysis Targeting Chimeras (PROTACs) to block such a noncanonical function of EZH2 in cancer. Independent EZH2-targeting PROTACs degraded EZH2 and SREBP2 both and downregulated the SREBP2-associated gene-expression program, leading to inhibition of tumor growth. Altogether, this study unveils the existence of an EZH2:SREBP2 axis in cancers, which operates to sustain tumorigenesis via promoting cholesterol metabolism, paradigm-shifting the current understanding of EZH2’s oncogenic functions.
• 🔗 查看原文

9. GSE317374 基质导向的肿瘤微环境促进骨内成釉细胞瘤肿瘤生长 [多组学]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、tumor microenvironment
• 📝 描述：Contributors : Da-Yo Yuh ; Jian-Liang Chou ; Ting-Han ChangSeries Type : Genome binding/occupancy profiling by high throughput sequencing ; Expression profiling by high throughput sequencingOrganism : Homo sapiensAmeloblastoma is a locally aggressive odontogenic epithelial tumor with poorly understood intraosseous pathogenesis due to a lack of physiologically relevant models. Here, we established an orthotopic intraosseous mouse model using ameloblastoma epithelial cells in combination with ameloblastoma-derived mesenchymal stromal cells (AMMSCs) or their secretome. AMMSC-derived extracellular vesicle-enriched secretome enhances stemness, epithelial-mesenchymal transition (EMT) phenotypes, and tumorigenic ability of ameloblastoma epithelial cells. A unique signature of microRNAs in AMMSC-derived secretome is functionally associated with the upregulation of EMT-regulatory transcription factors in tumor epithelial cells. Single-nucleus ATAC and RNA sequencing revealed a dynamic EMT trajectory in primary human AM-derived epithelial cells activated by paired AMMSC-derived secretome. This study suggests that AMMSCs and their secretome drive orthotopic AM tumor development by promoting tumor epithelial cell proliferation, EMT, and vascular formation in the tumor microenvironment. This stromal-oriented orthotopic model provides a clinically relevant platform for dissecting tumor-stroma crosstalk and identifying therapeutic vulnerabilities in ameloblastoma.
• 🔗 查看原文

10. GSE317373 基质导向的肿瘤微环境促进骨内成釉细胞瘤的生长 [miRNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、tumor microenvironment
• 📝 描述：Contributors : Da-Yo Yuh ; Ting-Han ChangSeries Type : Non-coding RNA profiling by high throughput sequencingOrganism : Homo sapiensAmeloblastoma is a locally aggressive odontogenic epithelial tumor with poorly understood intraosseous pathogenesis due to a lack of physiologically relevant models. Here, we established an orthotopic intraosseous mouse model using ameloblastoma epithelial cells in combination with ameloblastoma-derived mesenchymal stromal cells (AMMSCs) or their secretome. AMMSC-derived extracellular vesicle-enriched secretome enhances stemness, epithelial-mesenchymal transition (EMT) phenotypes, and tumorigenic ability of ameloblastoma epithelial cells. A unique signature of microRNAs in AMMSC-derived secretome is functionally associated with the upregulation of EMT-regulatory transcription factors in tumor epithelial cells. Single-nucleus ATAC and RNA sequencing revealed a dynamic EMT trajectory in primary human AM-derived epithelial cells activated by paired AMMSC-derived secretome. This study suggests that AMMSCs and their secretome drive orthotopic AM tumor development by promoting tumor epithelial cell proliferation, EMT, and vascular formation in the tumor microenvironment. This stromal-oriented orthotopic model provides a clinically relevant platform for dissecting tumor-stroma crosstalk and identifying therapeutic vulnerabilities in ameloblastoma.
• 🔗 查看原文

💡 该来源还有 45 条内容，详见 文末

详细内容（全部1条）

1. 科学家发现一种细菌能将有毒的铀锁定成稳定的形式。

• ✍️ 作者：未知作者
• 🏷️ 关键词：bacteria、regex:bacter(ia|ial|ium)
• 📝 描述：Deep underground, bacteria may be capable of doing something remarkable: trapping toxic uranium before it spreads. When researchers fed microbes in uranium-contaminated mine water with glycerol, about 95% of the dissolved uranium disappeared within 130 days. The bacteria helped convert it into an unusually stable uranium compound that had rarely been observed before.
• 🔗 查看原文

• GSE271000 EZH2 与 SREBP2 合作建立表观基因组、转录组和代谢程序以驱动肿瘤发生 [RNA-seq I]
• GSE341296 神经元 Nrf/SKN-1B 控制秀丽隐杆线虫探索行为的性二态性神经内分泌通路
• GSE336706 核 GDOWN1 通过触发 Pol II CTD 磷酸酶的过早终止和核输出来促进 RB 激活，从而发挥强大的肿瘤抑制作用 (RNA-seq)
• GSE336705 核 GDOWN1 通过触发 Pol II CTD 磷酸酶的过早终止和核输出来促进 RB 激活，从而发挥强大的肿瘤抑制作用 (ChIP-seq)
• GSE337303 Zfp57 和 Gzf1 相互依赖甲基化的结合在发育重编程过程中保护 Dlk1-Dio3 印记 [CUT&Tag]
• GSE337141 Zfp57 和 Gzf1 相互依赖甲基化的结合在发育重编程过程中保护 Dlk1-Dio3 印记 [CRISPRscreen]
• GSE337139 Zfp57 和 Gzf1 相互依赖甲基化的结合保护发育重编程过程中 Dlk1-Dio3 印记 [亚硫酸氢盐]
• GSE324561 EZH2 与 SREBP2 合作建立表观基因组、转录组和代谢程序以驱动肿瘤发生 [CUT&Tag II]
• GSE324560 EZH2 与 SREBP2 合作建立表观基因组、转录组和代谢程序以驱动肿瘤发生 [CUT&RUN II]
• GSE324367 Zfp57 和 Gzf1 的相互甲基化依赖性结合在发育重编程过程中保护 Dlk1-Dio3 印记 [GZF1_snp]
• GSE324182 Zfp57 和 Gzf1 的相互甲基化依赖性结合在发育重编程过程中保护 Dlk1-Dio3 印记 [GZF1]
• GSE306322 小鼠乳腺异质性 PROCR+ 细胞的单细胞多组学分析 [scATAC-Seq]
• GSE287353 EZH2 与 SREBP2 协同作用，建立表观基因组、转录组和代谢程序，以驱动肿瘤发生 [CUT&Tag I]
• GSE271001 EZH2 与 SREBP2 协同作用，建立表观基因组、转录组和代谢程序，以驱动肿瘤发生 [CUT&RUN I]
• GSE260473 肾脏集合管细胞类型组成受 Notch 信号通过调节 mTORC1 活性进行调控（RNA-Seq）。
• GSE260472 肾脏集合管细胞类型组成受 Notch 信号通路通过调节 mTORC1 活性进行调控 (ChIP-Seq)
• GSE250115 单细胞分析发现 TCF4 和 ID3 是乳腺上皮干细胞分化的分子开关 [hg_scRNAseq]
• GSE250111 单细胞分析发现 TCF4 和 ID3 是乳腺上皮干细胞分化的分子开关 [mm_scRNAseq]
• GSE250110 单细胞分析鉴定出 TCF4 和 ID3 是乳腺上皮干细胞分化的分子开关 [mm_bulkRNAseq]
• GSE330096 解码循环中候选肿瘤-白细胞杂交细胞的基因组身份 [RNA]
• GSE330094 解码循环中候选肿瘤-白细胞杂交细胞的基因组身份 [DNA]
• GSE343068 骨骼肌代谢、核糖体和发育途径的重编程有助于Roux-en-Y胃旁路术诱导的女性适应
• GSE342962 野生型 (WT) 和 TET2KO 小鼠经血管紧张素 II 治疗 28 天后，心脏中部组织转录组分析 (RNA-seq)。
• GSE342961 野生型 (WT) 和 TET2KO 小鼠经血管紧张素 II 治疗 28 天后肺内皮细胞的转录组分析 (RNA-seq)。
• GSE342695 舒尼替尼通过抑制PPARγ诱导巨噬细胞功能障碍和组织再生受损
• GSE342601 水母来源肽水解物可缓解小鼠饮食诱导的肥胖并改善秀丽隐杆线虫的衰老相关健康寿命
• GSE342553 野生型小鼠肝脏经TM治疗后的CHOP CHIP-seq分析
• GSE341409 RNA测序分析H69胆管细胞系经咪唑丙酸酯刺激
• GSE337623 GDF15 通过神经内分泌糖皮质激素信号通路抑制肝脏炎症，且该作用独立于体重减轻。
• GSE337622 GDF15 通过神经内分泌糖皮质激素信号通路抑制肝脏炎症，且该抑制作用独立于体重减轻
• GSE336708 核GDOWN1通过触发Pol II CTD磷酸酶的过早终止和核输出，促进RB激活，从而发挥强大的肿瘤抑制作用。
• GSE336707 核 GDOWN1 通过触发 Pol II CTD 磷酸酶的过早终止和核输出来促进 RB 激活，从而发挥强大的肿瘤抑制作用 (TT-seq)
• GSE336704 核 GDOWN1 通过触发 Pol II CTD 磷酸酶的过早终止和核输出来促进 RB 激活，从而发挥强大的肿瘤抑制作用 (CUT&Tag)
• GSE319584 冷冻损伤后7天成年斑马鱼骨骼肌转录组分析
• GSE315226 基因组导向发现含辛烯的聚醚离子载体可改善糖尿病皮肤伤口愈合
• GSE305118 产生颗粒酶K的旁观者CD8 T细胞在急性髓系白血病中的促炎作用
• GSE305061 中药活性提取物对RAW264.7巨噬细胞转录组谱的调控作用
• GSE301769 脯氨酸代谢紊乱导致新生血管性年龄相关性黄斑变性视网膜下纤维化：脯氨酰-4-羟化酶抑制剂的治疗潜力
• GSE256324 表征纤维脂肪生成祖细胞在胰腺癌恶病质实验模型中的作用
• GSE256323 表征纤维脂肪祖细胞在胰腺癌恶病质实验模型中的作用 [RNASeq_KPC_KPCScr_and_miR-27a-KD]
• GSE256322 表征纤维脂肪祖细胞在胰腺癌恶病质实验模型中的作用 [RNASeq_FAP_KPCScr_and_miR-27a-KD]
• GSE256321 表征纤维脂肪生成祖细胞在胰腺癌恶病质实验模型中的作用 [RNASeq_FAP_timeseries]
• GSE256320 表征纤维脂肪生成祖细胞在胰腺癌恶病质实验模型中的作用 [snRNASeq_whole_muscle]
• GSE337237 用于提高单细胞转录组分析精度的环境RNA去污工具的系统性基准测试
• GSE326418 人类iPS细胞衍生视网膜神经节细胞的RNA测序