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1. ⭐ 最新10+生信，空转+单细胞+H3K18la ChIP-seq+CRISPR+bulk转录组，多组学经典好文，值得收藏！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：ChIP-seq、单细胞、转录组、生信
• 📝 描述：点击查看详情
• 🔗 查看原文

2. ⭐ 【参会提醒】利用单细胞与空间多组学探索微生物组与免疫互作机制

• ✍️ 作者：10x Genomics
• 🏷️ 关键词：免疫、微生物、单细胞、空间组学
• 📝 描述：11月26日直播，与专家共同揭秘 “如何利用单细胞与空间多组学探索微生物组与免疫互作机制”。
• 🔗 查看原文

3. ⭐ 最新10分生信，单细胞+空转多组学进行中性粒细胞亚型分析，识别 CTCF+TAN，靶向CTCF改善免疫治疗疗效！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：免疫、单细胞、生信
• 📝 描述：点击查看详情
• 🔗 查看原文

4. ⭐ 10月最新26+生信，多组学空间免疫谱分析确定了三级淋巴结构（TLS）的亚群并进行深入分析，建议收藏！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：免疫、淋巴、生信
• 📝 描述：点击查看详情
• 🔗 查看原文

5. ⭐ 最新8+生信，多组学识别三级淋巴结构（TLS）结构并进行针对性分析。预测预后及免疫治疗疗效，值得借鉴！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：免疫、淋巴、生信
• 📝 描述：点击查看详情
• 🔗 查看原文

6. ⭐ 单细胞+空转+代谢组，公开数据集找出亮点就能发1区12分

• ✍️ 作者：生信人
• 🏷️ 关键词：代谢、代谢组、单细胞
• 🔗 查看原文

7. ⭐ Cancer Cell重磅：肿瘤竟被自己人背刺！突变引爆免疫治疗

• ✍️ 作者：生信人
• 🏷️ 关键词：肿瘤、cancer、免疫
• 📝 描述：10月16日，Cancer Cell发表了德州大学MD安德森癌症中心Padmanee Sharma教授团队的重
• 🔗 查看原文

8. ⭐ 看看NC生信为主的文章需要多少工作量，单细胞多组学分析学习。发现 IDH1 抑制剂可逆转髓母细胞瘤放疗耐药

• ✍️ 作者：生信钱同学
• 🏷️ 关键词：耐药、单细胞、生信
• 📝 描述：生信文章学习
• 🔗 查看原文

9. pH/ROS响应微针重塑巨噬细胞线粒体功能

• ✍️ 作者：同医济云Medfocus
• 🏷️ 关键词：巨噬细胞、线粒体
• 📝 描述：“代谢免疫重编程”策略，通过级联靶向微针精准调控巨噬细胞线粒体代谢，实现了糖尿病创面的无瘢痕愈合。
• 🔗 查看原文

10. 扬州大学团队聚焦“肠脑轴”精准上分！这套菌群变化-代谢物改变-通路调控的思路，值得推敲！

• ✍️ 作者：神经岛
• 🏷️ 关键词：代谢、通路
• 🔗 查看原文

💡 该来源还有 25 条内容，详见 文末

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1. ⭐ GSE301957 共靶向 EZH2 和 TEAD 通过 Hippo 通路突变癌症中的肿瘤固有免疫信号通路诱导细胞凋亡 - 来自 EZH2 基因破坏的 RNA-seq 数据

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune、RNA-seq、pathway
• 📝 描述：Contributors : Antja-Voy Hartley ; Zhaorong Li ; Matthew Booker ; Nicholas Tourtillot ; Pasi A JänneSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensTEA/TEF-domain [TEAD] inhibitors are being evaluated in clinical trials for cancers with alterations in the Hippo pathway including mesothelioma. We recently developed and showcased the potency of TEAD palmitoylation inhibitors MYF-03-69 and MYF-03-176 in mesothelioma cell lines. However, TEAD inhibition results in cell cycle arrest in cell line models with Hippo pathway alterations without inducing cell death, potentially limiting their long-term clinical efficacy. Using a genome-wide CRISPR/Cas9 screen, we identified EZH2 as a critical modulator of the cellular response to TEAD inhibition. Compared to single agent treatments, EZH2i/TEADi robustly triggered apoptosis and suppressed the growth of Hippo-mutated cells in vitro and in vivo. Mechanistically, EZH2i/TEADi-treated cells exhibited heightened activation of tumor-intrinsic innate immune signaling which resulted in DNA damage and subsequent apoptosis. Taken together, we propose this novel combinatorial strategy as a potential approach to enhancing the anti-tumor efficacy of single agent TEAD targeting therapies in Hippo pathway altered tumors. This GEO accession includes the data series associated with RNA-seq derived from pharmacologic disruption of EZH2.
• 🔗 查看原文

2. ⭐ GSE289248 多梳抑制复合物 2 与 DNA 甲基化之间的串扰介导神经内分泌前列腺癌谱系可塑性 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq、methylation
• 📝 描述：Contributors : Richa Singh ; David S RickmanSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAcquired changes in DNA methylation have been proposed as a mechanism underlying epigenetic plasticity in several cancer types. In prostate cancer, methylation changes are dynamic, with preclinical studies pointing to a tumor suppressor role of the DNA methyltransferase DNMT1 in early stage, in contrast to an oncogenic function of DNMT1 in later stage. The importance of DNA methylation dynamics during normal development and cell lineage fate decisions also points to DNA methylation having a critical function in lineage plasticity, yet the mechanisms by which DNA methylation changes drives lineage transitions in prostate cancer is not well understood. DNA methylation can directly repress gene expression but also cooperate with other epigenetic pathways to modulate downstream transcriptional activity. The enhancer of zeste homolog 2 (EZH2) protein is a subunit of the polycomb repressive complex 2 (PRC2) and catalyzer of the repressive histone 3 lysine 27 tri-methylation (H3K27me3) mark that also acts to suppress downstream transcriptional activity and has also been implicated in lineage plasticity. EZH2 is overexpressed in castration-resistant prostate cancer (CRPC) including NEPC and is an emerging therapeutic target. Although, the compensatory relationship between DNA methylation and EZH2 has been shown in embryonic stem cell studies and in some cancer types during acquired treatment resistance or immune evasion, how DNA methylation and EZH2/PRC2 interact to modulate prostate cancer lineage plasticity has not been characterized. In this study, we address the potential crosstalk between epigenetic pathways in advanced prostate cancer and demonstrate how DNA methylation and H3K27me3 profiles overlap and cooperate to reprogram the epigenome during prostate cancer lineage plasticity. Using both mouse and patient-derived models, we highlight the compensatory roles of these two repressive machineries during progression of CRPC towards a NE-lineage state. We predict their specific impact on NEPC progression by assessing the associated molecular alterations following genetic and pharmacological perturbations of each.
• 🔗 查看原文

3. ⭐ GSE289247 多梳抑制复合物 2 与 DNA 甲基化之间的串扰介导神经内分泌前列腺癌谱系可塑性 [ChIP-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、ChIP-seq、methylation
• 📝 描述：Contributors : Richa Singh ; David S RickmanSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiens ; Mus musculusAcquired changes in DNA methylation have been proposed as a mechanism underlying epigenetic plasticity in several cancer types. In prostate cancer, methylation changes are dynamic, with preclinical studies pointing to a tumor suppressor role of the DNA methyltransferase DNMT1 in early stage, in contrast to an oncogenic function of DNMT1 in later stage. The importance of DNA methylation dynamics during normal development and cell lineage fate decisions also points to DNA methylation having a critical function in lineage plasticity, yet the mechanisms by which DNA methylation changes drives lineage transitions in prostate cancer is not well understood. DNA methylation can directly repress gene expression but also cooperate with other epigenetic pathways to modulate downstream transcriptional activity. The enhancer of zeste homolog 2 (EZH2) protein is a subunit of the polycomb repressive complex 2 (PRC2) and catalyzer of the repressive histone 3 lysine 27 tri-methylation (H3K27me3) mark that also acts to suppress downstream transcriptional activity and has also been implicated in lineage plasticity. EZH2 is overexpressed in castration-resistant prostate cancer (CRPC) including NEPC and is an emerging therapeutic target. Although, the compensatory relationship between DNA methylation and EZH2 has been shown in embryonic stem cell studies and in some cancer types during acquired treatment resistance or immune evasion, how DNA methylation and EZH2/PRC2 interact to modulate prostate cancer lineage plasticity has not been characterized. In this study, we address the potential crosstalk between epigenetic pathways in advanced prostate cancer and demonstrate how DNA methylation and H3K27me3 profiles overlap and cooperate to reprogram the epigenome during prostate cancer lineage plasticity. Using both mouse and patient-derived models, we highlight the compensatory roles of these two repressive machineries during progression of CRPC towards a NE-lineage state. We predict their specific impact on NEPC progression by assessing the associated molecular alterations following genetic and pharmacological perturbations of each.
• 🔗 查看原文

4. ⭐ GSE286958 前列腺腺癌和神经内分泌前列腺癌模型的表观遗传学分析，以了解DNMT-EZH2的相互作用。[RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq、epigenetic
• 📝 描述：Contributors : Venkadakrishnan Varadha Balaji ; Beltran HimishaSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensEZH2-DNMT crosstalk is diverse across prostate adenocarcinoma and neuroendocrine prostate cancer.
• 🔗 查看原文

5. ⭐ GSE310915 染色质可及性和转录组学的单细胞整合揭示卵巢肿瘤浸润适应性NK细胞的调控网络

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、single-cell、transcriptomics
• 📝 描述：Contributors : Yizhe Sun ; Meng Wan ; Solrun Kolbeinsdottir ; Kang Wang ; Shruti Khare ; Okan Gultekin ; Sahar Salehi ; Kaisa Lehti ; Ramanuj Dasgupta ; Theodoros Foukakis ; Martin Enge ; Dhifaf SarhanSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensNatural killer (NK) cells are traditionally recognized for their rapid, non-specific responses against virus-infected or malignantly transformed cells, functioning as key effectors of innate immunity. However, a distinct subset known as adaptive NK (aNK) cells has been shown to acquire memory-like properties following viral infections, indicating their capacity for antigen-specific immune recall. Intriguingly, aNK cells have also been identified within the tumor microenvironment, where they can mediate tumor-specific recall responses. Yet, the regulatory mechanisms managing their function in tumor-infiltrating aNK cells remain largely unknown. In this study, we integrated publicly available multiomics datasets from ovarian cancer, including single-cell chromatin accessibility (scATAC-seq) and single-cell RNA sequencing (scRNA-seq), to identify chromatin-accessible regions and construct transcription factors (TF)-gene regulatory networks. To validate and extend these findings, we performed Smart-seq3 on NK cells isolated from ovarian tumors and applied SCENIC analysis to identify TF-driven gene regulation. By integrating results from both analyses, we identified PRDM1 and STAT2 as key TFs, along with their downstream targets CRCP and MTFP1, specifically enriched in tumor-infiltrating aNK cells. The expression levels of CRCP and MTFP1 positively correlated with NK cell infiltration in ovarian cancer tissues, suggesting their potential functions in supporting tumor-specific NK cell memory responses. In addition, external validation using data from the PROMIX clinical trial demonstrated that PRDM1 and STAT2 expression levels are positively associated with both overall survival and aNK cell-associated transcriptional features.
• 🔗 查看原文

6. ⭐ GSE293929 IPSC衍生的CAR-NK细胞外囊泡重塑巨噬细胞免疫并增强肿瘤清除

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immunity、macrophage
• 📝 描述：Contributors : Hao Zhang ; Peng Xia ; Bin Jin ; Minghe Zhang ; Jie LiuSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusChimeric antigen receptor (CAR) cell therapy has revolutionized the treatment of hematological malignancies; however, its efficacy in solid tumors remains limited due to dense stromal barriers and the immunosuppressive tumor microenvironment (TME), which hinder immune cell infiltration and persistence. To overcome these challenges, we propose an innovative strategy utilizing induced pluripotent stem cell (iPSC)-derived CAR-NK extracellular vesicles (CAR-iNEV), engineered from iPSC-differentiated NK cells. Unlike conventional CAR-NK cell therapies that rely on immortalized NK92 cell lines, our approach leverages iPSC-derived NK cells, reducing tumorigenic risk and enhancing CAR transduction efficiency. Additionally, we incorporate nanobody-based CAR constructs in place of traditional single-chain variable fragments (scFv), significantly improving CAR stability and expression efficiency. Beyond direct cytotoxicity, CAR-iNEV offers superior therapeutic advantages, including reduced systemic toxicity and enhanced drug delivery capabilities compared to CAR-iNK cells. In vivo studies demonstrate that CAR-iNEV exhibits exceptional safety and potent antitumor activity across multiple solid tumor xenograft and patient-derived xenograft (PDX) models in humanized mice. Mechanistically, CAR-iNEV not only directly eliminates tumor cells but also reprograms the TME by activating macrophage-derived nitric oxide synthase (NOS2), amplifying host antitumor immunity. These findings establish CAR-iNEV as a promising platform for solid tumor immunotherapy, particularly in relapsed and metastatic settings, providing a novel and effective strategy that bridges direct tumor targeting with immune microenvironment remodeling. This study lays the foundation for future clinical translation, advancing the next generation of cell-free CAR-based immunotherapies.
• 🔗 查看原文

7. ⭐ GSE221608 CRC患者正常肠黏膜组织、配对的原发性CRC组织和肝转移病灶的转录组测序

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、transcriptome、regex:intestin(e|al)
• 📝 描述：Contributors : Wen Ni ; Su Yao ; Jianming LiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensTo investigate the key regulators in CRC progression, we carried out transcriptome sequencing in normal intestinal mucosal tissues, paired primary CRC tissues and liver metastases lesions in participants of CRC.We then performed gene expression profiling analysis using data obtained from RNA-seq of tissues.
• 🔗 查看原文

8. GSE311014 细胞因子驱动的糖鞘脂代谢调节原代人肾小球系膜细胞内质网钙稳态

• ✍️ 作者：未知作者
• 🏷️ 关键词：cytokine、metabolism
• 📝 描述：Contributors : Mariia Stefanenko ; Tessa M Ortiz ; Sandra G Mungaray ; Mykhailo Fedoriuk ; Oleg Palygin ; Stefano Berto ; Drew Moore ; Tamara K NowlingSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensGlycosphingolipids (GSLs), including hexosylceramides (HexCers), lactosylceramides (LacCers), and gangliosides composed of one or more sugar residues attached to ceramide, are essential components of cell membranes. Dysregulated GSL metabolism has been implicated in various inflammatory and autoimmune diseases, including lupus nephritis; however, its contribution to renal cell dysfunction remains largely unexplored. In this study, we demonstrate that in primary human renal mesangial cells (hRMCs), proinflammatory cytokines relevant to lupus elicit significant upregulation and secretion of inflammatory mediators that parallel intracellular and extracellular accumulation of HexCers and elevated cytosolic calcium (Ca2+) levels. The increase in cytosolic Ca2+ was attributed to a decrease in endoplasmic reticulum (ER) Ca2+ store capacity. Pharmacological inhibition of GSL synthesis with eliglustat significantly reduced HexCers levels and restored ER Ca2+ stores, but did not impact cytokine-induced cytokine/chemokine secretion or cell viability/proliferation. Together, these data suggest that elevated GSL synthesis modulates cytokine-induced ER Ca²⁺ dysregulation in mesangial cells and may play a role in the pathogenesis of lupus nephritis.
• 🔗 查看原文

9. GSE295902 EBF1 和 PAX5 对 T 细胞谱系潜能发挥剂量依赖性的表观遗传抑制作用 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：ATAC-seq、epigenetic
• 📝 描述：Contributors : Johanna Tingvall-Gustafsson ; Kim Hellerstedt ; Jonas Ungerbäck ; Mikael SigvardssonSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusB-lymphocyte development is dependent on the coordinated action of transcription factors controlling the expression of stage and lineage specific genes. To better understand gene regulation and changes in the epigenetic landscape in early B-cell development, we conducted combined SC-RNA/ATAC seq analysis of bone marrow progenitor populations, allowing us to build a developmental trajectory based on changes in epigenetic accessibility. This analysis identified a rapid shift in DNA accessibility, where T-lineage primed progenitors gained the epigenetic landscape of B-lymphocytes. The epigenetic switch correlated well with initiation of EBF1 and PAX5 transcription as well as their functional activity. As ectopic expression of EBF1 in Pax5-/- pro-B cells was not sufficient to mediate either the full activation of the B-lineage program of silencing of T-lineage associated genes, we conclude that PAX5 and EBF1 are independently essential for the establishment of the epigenetic landscape in normal B-cell development. This idea was supported by the finding that pro-B cells from mice with combined heterozygote deletion of the Ebf1 and Pax5 genes, carried a non-differentiated epigenetic landscape and expressed T-lineage associated genes. The importance of epigenetic silencing for the preservation of B-cell fate was supported by the finding that inhibition of the histone methylases EZH1 and EZH2 in pro-B cells, allowed for the activation of T-lineage genes and generation of T-lineage cells in response to Notch signaling. Hence, B-lymphoid commitment is associated with a transcription factor dose dependent epigenetic switch, silencing an inherent T-lineage potential in early lymphoid progenitors.
• 🔗 查看原文

10. GSE295900 EBF1 和 PAX5 对 T 细胞谱系潜能发挥剂量依赖性的表观遗传抑制作用 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、epigenetic
• 📝 描述：Contributors : Johanna Tingvall-Gustafsson ; Kim Hellerstedt ; Jonas Ungerbäck ; Mikael SigvardssonSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusB-lymphocyte development is dependent on the coordinated action of transcription factors controlling the expression of stage and lineage specific genes. To better understand gene regulation and changes in the epigenetic landscape in early B-cell development, we conducted combined SC-RNA/ATAC seq analysis of bone marrow progenitor populations, allowing us to build a developmental trajectory based on changes in epigenetic accessibility. This analysis identified a rapid shift in DNA accessibility, where T-lineage primed progenitors gained the epigenetic landscape of B-lymphocytes. The epigenetic switch correlated well with initiation of EBF1 and PAX5 transcription as well as their functional activity. As ectopic expression of EBF1 in Pax5-/- pro-B cells was not sufficient to mediate either the full activation of the B-lineage program of silencing of T-lineage associated genes, we conclude that PAX5 and EBF1 are independently essential for the establishment of the epigenetic landscape in normal B-cell development. This idea was supported by the finding that pro-B cells from mice with combined heterozygote deletion of the Ebf1 and Pax5 genes, carried a non-differentiated epigenetic landscape and expressed T-lineage associated genes. The importance of epigenetic silencing for the preservation of B-cell fate was supported by the finding that inhibition of the histone methylases EZH1 and EZH2 in pro-B cells, allowed for the activation of T-lineage genes and generation of T-lineage cells in response to Notch signaling. Hence, B-lymphoid commitment is associated with a transcription factor dose dependent epigenetic switch, silencing an inherent T-lineage potential in early lymphoid progenitors.
• 🔗 查看原文

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1. Camrelizumab 加 rivoceranib 与 sorafenib 作为不可切除肝细胞癌（CARES-310）的一线治疗：一项随机、开放标签、国际三期临床研究的最终分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：B细胞
• 📝 描述：Secret hovertext:
• 🔗 查看原文

2. 癌症革命：科学、创新与希望

• ✍️ 作者：未知作者
• 🏷️ 关键词：癌症
• 📝 描述：Secret hovertext:
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3. 癌症与喜剧：三场单口喜剧特别节目回顾

• ✍️ 作者：未知作者
• 🏷️ 关键词：癌症
• 📝 描述：Secret hovertext:
• 🔗 查看原文

4. IDH 突变胶质瘤神经外科切除范围增加：转化为标准实践的问题

• ✍️ 作者：未知作者
• 🏷️ 关键词：神经
• 📝 描述：Secret hovertext:
• 🔗 查看原文

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1. 伦敦基因组学与生物数据节

• ✍️ 作者：未知作者
• 🏷️ 关键词：genomics
• 📝 描述：The Festival of Genomics and Biodata 2026 offers two days of cutting edge science, technology and networking, bringing together researchers, clinicians and innovators across more than sixteen content theatres…
• 🔗 查看原文

• 最新8分生信，空转多组学分析揭示CAF-癌细胞通讯介导 PARPi 耐药的全新机制，内容很少，优势在于自测数据！
• 《自然》：肠癌靠“变身”逃生！科学家首次证实，肠癌可利用上皮细胞可塑性对MAPK通路抑制剂耐药
• python单细胞学习（三）：batch2数据读取与处理
• Nature Genetics | 终结变异致病性评分“通胀”！首个全蛋白质组校准模型popEVE重塑致病性预测标准
• 顶刊里程碑突破！哈佛团队绘 170 万 T 细胞图谱，生信注释有了 “黄金标尺”
• 新角色！重庆大学附属肿瘤医院发文：ICIs免疫治疗的潜在联合治疗靶点
• Cell Stem Cell：逆转溶酶体功能障碍，让衰老造血干细胞恢复年轻态
• 刚刚发表的7.5分生信，一种用于精准泛癌分类的多表征深度学习框架！只要有技术，还做什么实验！
• 淋巴循环（建议收藏）
• 从心梗到全身炎症，都指向同一关键蛋白！靶向药物有望改写治疗格局
• Sci Tra Med | 实验性胶质母细胞瘤试验结果有望推动患者监测与疗法的革新
• Nat Biotech | 最新肿瘤芯片技术：助力实体瘤CAR-T疗法研发
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• 中国科学院北京基因组研究所郝亚静团队诚招特别研究助理（博士后）
• Nature：scWGS+scRNA解密全基因组倍增的演化动态
• 别傻了！多组学只做关联和通路？这波血亏！
• 腾讯登26.6分Nature子刊，只有你想不到的蛋白质！没有这个模型预测不了的
• 机体稳态的免疫调节——苏冰教授与Immunity对话录 | Cell Symposia摘要征集中
• 为省经费，导师喊大家手搓抗体？但我两个月都没拿到阳性克隆
• 成功逆转老年痴呆！四川大学华西医院发现：注射 2 小时，清除近 50% 大脑「垃圾」，记忆恢复持续半年
• 临床试验结果发布！北京协和医院曾小峰团队领衔新型抗CD38单克隆抗体在系统性红斑狼疮治疗中表现出良好安全性和显着疗效
• 脑科学 | Nature | 全皮层原位测序揭示输入依赖的区域身份
• 综述 | Brief.Bioinform. | 细胞间通信推断的研究进展与挑战：工具、资源及未来方向的全面综述
• Nature Neuroscience：李明/肖潇/朱峰/方贻儒合作揭示双相情感障碍遗传特征和细胞机制
• 线粒体自噬

• GSE289249 多梳抑制复合物 2 与 DNA 甲基化之间的串扰介导神经内分泌前列腺癌谱系可塑性 [RRBS]
• GSE287164 ISG20 缺失对 EMT6 小鼠乳腺癌细胞基因表达的影响（RNA-Seq）。
• GSE286954 前列腺腺癌和神经内分泌前列腺癌模型的表观遗传学分析，以了解DNMT-EZH2的相互作用。[Cut&Run]
• GSE273769 PLK1 抑制剂 Onvansertib 与 FOLFIRI 和 Bevacizumab 联合用于 KRAS 突变转移性结直肠癌的二线治疗：一项单臂 II 期试验。
• GSE266604 先兆子痫胎盘组织的空间转录组分析
• GSE251960 Beckwith-Wiedemann 综合征和大后代综合征涉及甲基化组、转录组和染色质构型的改变 [RNA-Seq]
• GSE310509 SREBP信号通路调节肺部驻留记忆B细胞代谢以维持过敏记忆
• GSE311170 CDK12 和 BAF 抑制剂联合使用可协同抑制三阴性乳腺癌细胞系的存活。
• GSE311157 区域均衡化归一化以改善表观遗传信号的对齐
• GSE300112 宫颈阴道微生物组与人类宫颈外上皮和黏膜下层中空间受限的宿主转录特征相关
• GSE297099 恢复机械表型可逆转富含细胞外基质的声带癌的恶性特征
• GSE289681 拟南芥花发育早期阶段花诱导系统 (FIS) 中 leunig_homolog (luh) 和 leunig (lug) 突变体的转录组分析
• GSE278894 Sox9f/f 和 Sox9HKO 小鼠原代肝细胞转录组的 RNA-seq 分析
• GSE310962 EGFR突变型小细胞肺癌存在肿瘤内异质性，可通过MEK抑制剂联合疗法进行靶向治疗。
• GSE296748 Dp16 肝脏转录组
• GSE296500 Crnic研究所人类三体计划 - 21三体模型图谱：来自成年野生型和Dp16小鼠肝脏组织（±高脂饮食）的PolyA RNA测序
• GSE296449 Crnic研究所人类三体计划 - 21三体模型图谱：来自人类iPSC衍生肝细胞样细胞的PolyA RNA测序
• GSE296420 Crnic研究所人类三体计划 - 21三体模型图谱：来自成年野生型和Dp16小鼠肝脏组织的PolyA RNA测序
• GSE295901 EBF1 和 PAX5 对 T 细胞谱系潜能发挥剂量依赖性的表观遗传抑制作用 [ChIPmentation]
• GSE295899 EBF1 和 PAX5 对 T 细胞谱系潜能发挥剂量依赖性的表观遗传抑制作用 [scMultiome]
• GSE195997 HIF抑制剂32-134D联合抗PD-1疗法可阻断小鼠肝细胞癌生长并根除肿瘤
• GSE311367 对表达野生型 RUNX1 和嵌合蛋白 RUNX11-299-SPI11-102 的 293T 细胞进行 DNA 甲基化分析
• GSE303684 YAP1功能障碍促进与乳腺癌易感性相关的分子特性
• GSE251961 Beckwith-Wiedemann综合征和大后代综合征涉及甲基化组、转录组和染色质构象的改变
• GSE251959 Beckwith-Wiedemann 综合征和大后代综合征涉及甲基化组、转录组和染色质构型的改变 [WGBS]
• GSE311458 一项评估西达米德联合维奈托克、阿扎胞苷、阿克拉霉素、阿糖胞苷和粒细胞集落刺激因子治疗难治性/复发性急性髓系白血病的 I 期研究：临床安全性、有效性和相关性分析
• GSE311175 单细胞多组学分析揭示 CTCF 是肺形态发生和祖细胞维持的关键调控因子 I
• GSE311050 抗体多样性产生的染色质折叠原理
• GSE306856 Venetoclax 通过脂肪酸氧化增强复发性急性髓系白血病中 γδT 细胞的抗白血病活性。
• GSE283418 杏仁核神经元的空间分子谱分析实现了针对疼痛不适的精准药理学治疗
• GSE283060 人源化单酰甘油酰基转移酶 2 小鼠在喂食高脂饮食后会变得肥胖并发展为代谢功能障碍相关的脂肪肝疾病
• GSE282984 基于网络药理学和转录组学探索芥酸的抗流感机制
• GSE282864 阻塞性睡眠呼吸暂停患者血浆外泌体microRNA的差异表达谱
• GSE270116 淋巴毒素α是急性髓系白血病的内源性抑制因子