详细内容（前10条）

1. ⭐ GSE288142 巨噬细胞中的 tRNA m1A 修饰促进干扰素通路基因的翻译，从而增强 CD8+ T 细胞介导的抗肿瘤免疫 [CAR-iMACs RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immunity、T cell、RNA-seq、pathway
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe involvement of tRNA m1A modification in the anti-tumoral tumor-associated macrophages (TAMs) has been validated in our study that macrophage-specific knockout of m1A “writer” enzymes TRMT61A leads to increased infiltration of TAMs, impaired CD8+ T cell function, and enhanced tumor growth. Since we observed that tumor-derived components suppresses tRNA m1A modification in macrophages, we sought to identify which component in the TME induces the down-regulation of tRNA m1A modification. Here, we performed bulk RNA-seq using TRMT61AOE-CAR-iMACs and CAR-iMACs to ensure the effect of human Trmt61a overexpression on CAR-iMACs. Kyoto encyclopedia of genes and genomes (KEGG) analysis showed that signal transduction is the most up-regulated pathway in CAR-iMACs after human Trmt61a overexpression.
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2. ⭐ GSE320505 脑转移瘤微环境中癌症相关成纤维细胞的单细胞和空间测序分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、tumor microenvironment、sequencing、spatial
• 📝 描述：Contributors : Thomas Simon ; David N Buckley ; Zeyi Yang ; Chikako Matsuba ; Ben Y Tew ; Gerald C Gooden ; Kyle Hurth ; Steven A Toms ; David D Tran ; Gabriel Zada ; Matthew P Salomon ; Bodour SalhiaSeries Type : OtherOrganism : Homo sapiensBrain metastasis (BM) remains largely incurable. Cancer-associated fibroblasts (CAFs) can either support or inhibit tumor growth in the tumor microenvironment (TME), yet their roles in BM remain under-described. Here we report a single-cell and spatial sequencing analysis of human BM tissues and define four transcriptionally distinct CAF subpopulations. BM CAF subpopulations are characterized by either extracellular matrix (ECM), immune, contractile, or neural features, and show distinct spatial distributions within the BM TME. Further analyses reveal that BM CAFs engage extensively in cell-cell communication and adopt distinct cell states, including an ECM CAF cell state marked by high levels of immunoglobulin superfamily containing leucine rich repeat expression (ISLR-CAFs). Functionally, ISLR-CAFs reduce BM tumor cell viability in vitro, consistent with a tumor-inhibitory role. These findings highlight the heterogeneity and plasticity of CAFs in BM, emphasizing the importance of precision in defining stromal contributions to disease progression and therapeutic response.
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3. ⭐ GSE292434 基于AAV的新抗原癌症疫苗的异源初免-加强免疫可诱导抗肿瘤免疫，从而抑制肿瘤生长和复发

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immunity、vaccine
• 📝 描述：Contributors : Chi-Hsien Huang ; Hsin-Yu Chang ; Jhen-Yu Chen ; Wei-Ze Hong ; Yi-Wen Jiang ; Chien-Yueh Lee ; Chia-Hsin Wu ; Chia-Hisn Wu ; Yu-Sen Lin ; Yuan-Yao Tsai ; Wei-Ling Kao ; K. S. Clifford Chao ; Kevin Chih-Yang HuangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTherapeutic cancer vaccines, which induce anti-tumor immunity by targeting specific antigens, constitute a promising approach to cancer therapy. Our previous work developed a novel engineered adenovirus-associated virus (AAV)-based tumor-specific (neoantigen) cancer vaccine to boost antitumor immunity in combination with radiotherapy, resulting in tumor regression and less distant metastasis. However, the therapeutic efficacy of constitutive vector-based vaccination may be limited by poor immunogenicity, pre-existing vector-specific immunity, and vaccine-induced vector-specific immunity. Here, we examined the combinational therapeutic efficacy of AAV-based cancer vaccine, local radiotherapy and immune checkpoint blockade (ICB) in two poor immunogenic cancer animal models. We found that administration with AAV-based neoantigen vaccine significantly increased the response to radiotherapy and ICB, and decreased the risk of distant metastasis. Furthermore, we evaluated a heterologous prime-boost immunization strategy using two optimized AAV serotype vaccines to amplify tumor-specific immunity to neoantigens. These optimized AAV2/AAV6 neoantigen vaccine displayed strong immunogenicity with potent induction of CD8+ T cells. As combined with local radiotherapy, the prime-boost vaccine induced superior tumor clearance and survival compared with other groups. Remarkably, optimized AAV2/AAV6 vaccination promoted CD8+ T-cell infiltration in the tumors, and elicited the enrichment of T cell clones. Furthermore, exhausted T cell marker expression was significantly decreased in the tumor-infiltrating CD8+ T cells. Taken together, these results highlight the synergistic potency of engineered AAV2/AAV6 vaccines combined with local radiotherapy for poor immunogenic cancers.
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4. ⭐ GSE316844 CRISP3 是一种潜在的肿瘤抑制因子，它通过调节 PI3K/AKT 通路抑制高级别浆液性卵巢癌的进展。

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、carcinoma、pathway
• 📝 描述：Contributors : Mingjun Ma ; Xiu Tian ; Weiwei Cao ; Chao Wang ; Yue Zhang ; Jiani Yang ; Shanshan Cheng ; Sijia Gu ; Jianxiao Li ; Yaqian Zhao ; Yaodi Shao ; Chao Huang ; Shuo Shi ; Renhao Xue ; Chen Chu ; Jindan Sheng ; Yu WangSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBackground: Ovarian cancer (OC) remains the most common cause of gynecological cancer-related death, and about 70% of the deaths are from advanced high-grade serous ovarian cancer (HGSOC). Cysteine-rich secretory protein 3 (CRISP3) is related to various human diseases, however, the roles and mechanisms of CRISP3 in HGSOC remain unclear. Methods: The clinical significance of CRISP3 in patients with OC was analyzed using The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus databases. CRISP3 ex-pression in OC tissues was validated by RNA-sequencing (RNA-seq), quantitative PCR, and immuno-histochemistry. Furthermore, we explored the effect of CRISP3 expression modulation on the biological be-havior of HGSOC through CCK-8, EdU, and transwell assays in vitro and the differences of CRISP3 during the progression of HGSOC in vivo. We utilized RNA-seq, GSEA and Western blotting to detect CRISP3’s regulatory mechanisms. Finally, we employed data from the IMvigor210 cohort and TCGA to assess the correlation of CRISP3 with clinical response to immunotherapy, and the landscape of immune cell infiltra-tion. Results: CRISP3 expression was markedly reduced in HGSOC. In vitro studies demonstrated that CRISP3 knockdown significantly enhanced proliferation, migration, and invasion of HGSOC cells, whereas its overexpression suppressed these malignant phenotypes. Moreover, CRISP3 expression was found to be downregulated during OC progression in vivo. Mechanistically, CRISP3 acted as a tumor suppressor through the PI3K/AKT signaling pathway to inhibit the progression and metastasis of HGSOC. Addition-ally, we observed an association between CRISP3 expression and CD8⁺ T cells, macrophages, neutrophil and Th1 cells infiltration. Conclusions: We demonstrate that CRISP3 suppresses tumorigenesis in HGSOC by regulating the PI3K/AKT pathway, and that its expression alterations correlate with disease progression, supporting its utility as a biomarker.
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5. ⭐ GSE303578 JUN 是 KRAS 突变型胰腺导管腺癌中 MAPK 通路抑制耐药性的主要介质。

• ✍️ 作者：未知作者
• 🏷️ 关键词：resistance、pathway、KRAS
• 📝 描述：Contributor : Sara MainardiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensPancreatic ductal adenocarcinoma (PDAC) is often driven by KRAS mutations, but inhibitors targeting the most frequent KRAS substitutions in PDAC are not yet approved in the clinic. We previously discovered that KRAS-mutant PDAC are sensitive to the combination of SHP2 and ERK inhibitors, recently investigated in the Phase I/Ib clinical trial NCT04916236. Lately, RAS(ON) multi-selective inhibitors have entered clinical development, representing a promise for mono or combination therapies in PDAC. However, resistance may arise even for combination therapies. Here, we aimed at anticipating mechanisms of resistance to SHP2 plus ERK or RAS(ON) multi-selective inhibitors. Through unbiased CRISPR-based screenings, we identified mTOR and JUN hyperactivation as interconnected mechanisms that overcome MAPK suppression. Functional genetic and pharmacological experiments pointed at JUN as the most downstream resistance mediator, and indirect therapeutic target, using MAP2K4 inhibitors. Alterations in the PI3K/AKT/mTOR and JUN pathways may serve as biomarkers for sensitivity/resistance in clinical trials testing MAPK inhibitors combinations in KRAS-mutant PDAC.
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6. ⭐ GSE299711 克隆动力学揭示癌症耐药性源于适应性程序 [scRNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、resistance、scRNA
• 📝 描述：Contributors : Haiyin Li ; Yeqing Chen ; Jessica Kaster ; Maggie Dunne ; Min Xiao ; Ling Li ; Monzy Thomas ; Nazifa Promi ; Dylan Fingerman ; Gregory S Brown ; Xingyue Zhu ; Meenhard HerlynSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensMost advanced cancers initially respond to targeted therapies but eventually relapse1. Rather than acquiring new mutations, resistance is driven by drug-tolerant persister cells (DTP) that enter a reversible drug-refractory state and sustain minimal residual disease2. Here, we developed MeRLin, a high-resolution barcoding platform combining single-cell RNA sequencing, RNA fluorescence in situ hybridization, and computational analyses to track clonal and transcriptional dynamics of melanoma cells during targeted therapy. Clonal tracking reveals that dominant resistant clones arise from minor pre-treatment subpopulations. The pre-treatment melanoma populations diversify into phenotypically distinct DTP subpopulations, marked by stress-like, lipid metabolism, PI3K signaling, and extracellular matrix remodeling programs associated with adaptive resistance. Spatial transcriptomics revealed the co-localization of lipid metabolism and PI3K signaling programs near the tumor boundaries, and a complex network of autocrine and paracrine interactions among DTP subpopulations. Using barcoded RNA fluorescence in situ hybridization, we identified a dominant persister subpopulation in resistant tumors marked by SLC2A1 expression. Thus, MeRLin provides a robust framework to dissect melanoma heterogeneity and uncover vulnerabilities in persister populations to improve long-term treatment efficacy.
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7. ⭐ GSE239606 tRNA m1A 修饰通过促进关键干扰素相关基因的翻译增强巨噬细胞的抗肿瘤免疫力 [TAMs 批量 RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immunity、RNA-seq
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTumor-associated macrophages (TAMs) play a crucial role in tumor progression through their recruitment, polarization, and interaction with T cells in the tumor microenvironment (TME). However, the mechanisms underlying the post-transcriptional and translational regulation of TAMs in the TME remain largely unknown. In this study, we investigate the role of tRNA N1-methyladenosine (m1A) modification in controlling the behavior of macrophages in response to TME stimuli. We demonstrate that the m1A “writer” enzymes TRMT61A is highly enriched in the anti-tumoral and phagocytotic TAM subset, and TRMT61A is rapidly downregulated in macrophages upon stimulation with multiple TME components. Macrophage-specific knockout of TRMT61A leads to increased infiltration of TAMs, impaired CD8+ T cell function, and enhanced tumor growth. To further explore the biological effects of m1A deficient macrophages, we performed RNA sequencing analysis of TRMT61A-KO and WT TAMs derived from tumor bearing Trmt61af/fLysmCre and Trmt61af/f mice. The Gene ontology (GO) and Gene set enrichment analysis (GSEA) documented that the interferon response and the STAT1/IL-12 signaling pathway were impaired in TAMs upon TRMT61A deletion, indicating that TRMT61A is critical for macrophages to control interferon responses and exert anti-tumor effect in the TME.
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8. ⭐ GSE239601 tRNA m1A 修饰通过促进关键干扰素相关基因的翻译增强巨噬细胞的抗肿瘤免疫力 [BMDM 批量 RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immunity、RNA-seq
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe involvement of tRNA m1A modification in the anti-tumoral tumor-associated macrophages (TAMs) has been validated in our study that macrophage-specific knockout of m1A “writer” enzymes TRMT61A leads to increased infiltration of TAMs, impaired CD8+ T cell function, and enhanced tumor growth. Since TRMT61A-derived tRNA m1A modification mainly enhances translation efficiency, we reasoned that the loss of TRMT61A in macrophages would result in the downregulation of a group of protein levels without affecting their mRNA levels. To assess the impact of TRMT61A deficiency on mRNA transcript levels in macrophages, we collected TRMT61A-KO and WT BMDMs derived from Trmt61af/fLysmCre and Trmt61af/f mice to perform bulk RNA sequencing. Of total 22173 genes, the mRNA expression of 22054 genes remain unchanged in macrophages upon TRMT61A deletion, suggesting that TRMT61A did not contribute to mRNA transcriptional regulation in macrophages.
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9. ⭐ GSE322707 9-PAHSA 调控 TCR-T 细胞命运以增强抗肿瘤免疫力 [KPC]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immunity、T cell
• 📝 描述：Contributor : Xiaozhen ZhangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusWe identify the endogenous lipid 9-PAHSA as a potent enhancer of T cell anti-tumor function and stemness, validated in murine models and a clinical trial. Mechanistically, we identify ICAM2 as a direct surface sensor for 9-PAHSA and delineate a downstream signaling axis whereby the ICAM2-Ezrin-mTORC2 cascade drives FOXO1 O-GlcNAcylation at S318, facilitating its nuclear translocation to enact a stem-like transcriptional program. Translating this discovery, we engineered armored human TCR-T cells with potentiated ICAM2 expression, which achieve superior tumor control through their enhanced intrinsic efficacy and a remarkable ability to ignite a coordinated and durable host anti-tumor immune response. Our work establishes a new paradigm of metabolite-sensing in T cell biology and provides a compelling therapeutic strategy to potentiate cellular immunotherapy for intractable cancers.
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10. GSE309883 预测I期肝癌患者1年生存率的多基因特征：整合临床前数据和TCGA数据

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、TCGA
• 📝 描述：Contributors : Ritam Adhikari ; Bhaskar Kallakury ; Chiranjeev Dash ; Rabindra RoySeries Type : Expression profiling by arrayOrganism : Rattus norvegicusThis study used the Long Evans Cinnamon (LEC) rat model of Wilson’s Disease and Hepatocellular Carcinoma (HCC), along with data from The Cancer Genome Atlas (TCGA) human database, to create a novel biomarker panel. We generated and analyzed a rat microarray gene expression profile by comparing liver tumor tissues with adjacent normal tissues from the same animals, covering approximately 30,000 genes. The microarray results were translated into a five-gene panel that predicts 1-year survival probability in Stage I liver cancer patients using TCGA data in combination with machine learning and bioinformatics approaches.The 5-year panel of five genes demonstrated robust performance throughout validation, particularly in predicting 1-year survival in Stage I patients.
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1. Alithea Genomics完成690万瑞士法郎种子轮融资，所得资金将用于解锁工业规模的RNA测序技术，以进行药物初步筛选和毒理学研究。

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、genomics
• 📝 描述：Alithea Genomics raises new funding to scale RNA sequencing with 1536-well DRUG-seq kits…
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2. HIV-seq 提高了利用 RNA 测序检测 HIV 转录细胞的能力

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：A new RNA sequencing approach called HIV-seq improves detection of rare HIV-transcribing cells and reveals distinct gene expression patterns during active infection and antiretroviral therapy suppression…
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3. 数百万人服用阿司匹林来预防结肠癌。但一项重要研究表明，不要指望它能起到预防作用。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Daily aspirin does not reliably prevent bowel cancer in people at average risk, according to a major new review. Any potential protective effect may take more than a decade to appear — if it appears at all — and the evidence for that benefit is weak. In contrast, the risk of serious bleeding begins right away, even with low-dose aspirin. Experts warn that prevention decisions should be individualized, not automatic.
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• GSE305244 TNF-α 缺乏是结直肠癌中 NK 细胞功能障碍的根本原因
• GSE299867 中华绒螯蟹蜕皮期肌肉的ATAC-seq和RNA-seq分析
• GSE295467 人类外周血单核细胞暴露于CPMV的单细胞测序
• GSE295196 m6A RNA 甲基化在维持 X 染色体失活和早期胚胎发生中 X 染色体与常染色体剂量补偿中的作用 [RNA-Seq]
• GSE271043 普通脱硫弧菌鞭毛蛋白通过LRRC19/TRAF6/TAK1通路诱导结直肠癌上皮-间质转化
• GSE317588 以单细胞分辨率解码骨关节炎和地方性骨关节炎中的转录、代谢和细胞死亡特征
• GSE294640 新型干细胞模型揭示巨噬细胞介导的人类 II 型肺泡上皮细胞抗病毒免疫和修复机制
• GSE322703 IRF1 rs2057656 多态性通过等位基因特异性表观遗传抑制调控 IRF1-AS1 转录和 ARDS 中的免疫功能障碍
• GSE320572 SCIMP 的一种非典型功能限制 JAK1 活性以对抗膀胱癌的免疫逃逸
• GSE227004 衰老诱导的 Cirbp 抑制会损害 DHODH 介导的铁死亡防御，并减弱心脏移植期间的低温心脏保护作用 [RNA-seq]
• GSE227003 衰老诱导的 Cirbp 抑制会损害 DHODH 介导的铁死亡防御，并减弱心脏移植期间的低温心脏保护作用 [ChIP-seq]
• GSE321693 使用模拟HCMV病毒感染样本的2倍梯度稀释液，比较SE-SPTM-PCR和miRNA深度测序的诊断性能
• GSE320546 SP1 作为缺氧相关骨质疏松症的潜在治疗靶点：来自多组学 [RNA-seq] 的证据
• GSE320545 SP1 作为缺氧相关骨质疏松症的潜在治疗靶点：来自多组学的证据 [ATAC-seq]
• GSE309650 糖皮质激素受体活性的上下文依赖性效应影响卵巢癌细胞的可塑性和治疗反应
• GSE288154 ST2信号通路调节肾损伤中的先天免疫反应
• GSE263411 年龄依赖性自噬功能障碍通过 ULK1 减少增加阿尔茨海默病风险
• GSE318337 SIRT6 抑制在黑色素瘤中发挥抗增殖作用的机制：多组学分析 [RNA-Seq A375]
• GSE318193 高流速胁迫对东方三鳃鳗能量代谢和转录水平的影响
• GSE316633 TGF-β介导自身免疫炎症中CD8阳性T细胞与CD39阳性诱导型Treg细胞之间的相互作用
• GSE315903 HEK293T细胞转录组节律的时间动态和功能注释
• GSE315667 狼疮相关免疫复合物诱导人类单核细胞中共享的促炎转录程序
• GSE315218 低氧通过HlF1aa-ATGL-PPARy通路协调脂肪细胞肥大和增生，使草鱼能够快速健康地储存能量
• GSE314180 高血压中DNA甲基化和炎症蛋白生物标志物的整合分析
• GSE312974 缺氧模拟线粒体应激通过非经典先天免疫激活途径触发 APOBEC3A 介导的 DNA 损伤
• GSE308849 利用 CRISPR-Cas9 碱基编辑消除 PKCα 磷酸化级联可挽救心力衰竭 [RNA-Seq]
• GSE308811 时间分辨分析揭示 FEN1 是 HEK 293T 细胞昼夜节律转录组动态和核心细胞稳态的关键因子
• GSE307944 人类 THP-1 巨噬细胞感染黏附侵袭性大肠杆菌 (AIEC) 菌株的 RNA 测序
• GSE306340 异常 EZH2 在肝母细胞瘤发生发展中的致癌作用
• GSE304383 基因定位鉴定 Homer1 为注意力发育调节因子 [scRNA-seq]
• GSE298942 发现一种新型 DNMT1 抑制剂，可提高治疗 β-地中海贫血的疗效 [RNA-seq]
• GSE298941 发现一种新型 DNMT1 抑制剂，可提高治疗 β-地中海贫血的疗效 [ATAC-seq]
• GSE296524 新型脓肿分枝杆菌 MmpL3 抑制剂的作用机制和耐药性定义
• GSE296178 腔内转录因子层级结构定义了雄激素受体顺式调控组，并在神经内分泌前列腺癌中丢失
• GSE295197 m6A RNA 甲基化在维持 X 染色体失活和早期胚胎发生中 X 染色体与常染色体剂量补偿中的作用 [MeRIP-Seq]
• GSE291245 慢性内质网应激诱导的细胞表面分子伴侣作为CAR细胞治疗急性髓系白血病的靶点
• GSE286998 高分辨率多尺度胚胎生殖细胞样细胞衍生分析揭示人类多能性状态转变 [RNA-Seq]
• GSE286500 喂养时间改变肠道菌群和短链脂肪酸可能诱导卵巢IL-17的昼夜波动并影响青春期生长兔的卵泡发育
• GSE282700 衰老样肌纤维在杜氏肌营养不良症中促进抗再生细胞因子信号传导
• GSE253889 对引导和非引导前脑类器官的多组学分析揭示了细胞组成和代谢谱的差异
• GSE242413 低分子量肝素对体外肺癌细胞和癌症患者生存率具有不同的影响。
• GSE322652：精氨酸限制条件下RKO结直肠癌细胞的tRNA测序分析
• GSE319843 转移相关伤口修复促进肺上皮细胞的相互激活和乳腺癌转移灶的生长
• GSE297308 端粒保护 1b 通过调节 ROS 稳态来保护拟南芥基因组
• GSE322487 研究发现，印迹基因 SLC22A18 的表观遗传改变通过 β-catenin-Ascl2 轴途径导致先天性“过敏-矮小-脂肪肝”综合征。
• GSE314970 小鼠和大鼠衰老的多组织、多时间点转录组图谱 [大鼠]
• GSE314817 小鼠和大鼠衰老的多组织、多时间点转录组图谱 [小鼠]
• GSE299074 野生型和 MZwnt11/slb 斑马鱼胚胎的 scRNA-seq
• GSE295634 地西他滨预处理的 CAR T 细胞疗法治疗复发/难治性非霍奇金淋巴瘤：一项 1/2 期临床研究显示疗效增强和生存期延长
• GSE287747 布鲁氏菌 tRNA 衍生片段 tRF-Leu-CAG 通过上调 IL13RA1 表达重编程巨噬细胞极化以促进其胞内生存
• GSE276034 一种AAV变体可在体内实现人类T细胞工程改造
• GSE227005 衰老诱导的 Cirbp 抑制会损害 DHODH 介导的铁死亡防御并减弱心脏移植期间的低温心脏保护作用
• GSE173547 BAP1 缺失与 TP53 缺陷协同作用，转化共同的髓系-红系祖细胞（ChIP-seq - 小鼠）
• GSE171815 BAP1 缺失与 TP53 缺陷协同作用，转化共同的髓系-红系祖细胞（RNA-seq - 小鼠）