详细内容（前10条）

1. ⭐ GSE322766 谱系和器官信号依次构建器官固有神经系统 [空间转录组学]

• ✍️ 作者：未知作者
• 🏷️ 关键词：nervous、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : I-Uen Hsu ; Rui B Chang ; Le ZhangSeries Type : OtherOrganism : Mus musculusOrgan intrinsic nervous systems (OINSs) are critical components of the body–brain axis, coordinating visceral organ function with systemic physiological control. Despite their importance, how these distinct neural architectures arise from a common neural crest cell (NCC) origin has remained unclear. Here, we present a systems-level, cross-organ analysis of OINS development, integrating lineage tracing, 3D imaging, single-cell transcriptomics, and genetic perturbations across heart, pancreas, intestine, and lungs. We show that differences in NCC migratory trajectories prefigure the spatial architecture of OINSs, laying the foundation for organ-specific patterning. In contrast, molecular identity emerges largely in response to local environments, indicating that extrinsic cues play a major instructive role. Using in vitro co-cultures, we demonstrate that organ-derived cues reprogram intrinsic neurons toward organ-specific transcriptional profiles and direct neuronal differentiation, with extracellular matrix (ECM) contact identified as a central mediator. In vivo, ECM–integrin signaling supports intrinsic cardiac neuron neurogenesis, while ECM crosslinking stabilizes their stereotyped ganglionic organization. Together, these findings reveal that OINS diversity arises through a dual logic: lineage programs prefigure spatial frameworks, while organ-specific cues instruct final molecular identities and architectural precision. This work establishes a conceptual paradigm for how organs actively build their own nervous systems, illuminating principles that underpin body–brain integration.
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2. ⭐ GSE274160 全基因组加倍驱动乳腺肿瘤进化的机制 [scATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、scATAC、genome
• 📝 描述：Contributors : Pierre Foidart ; Zheqi Li ; Marco Seehawer ; Kornelia PolyakSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusWhole genome doubling (WGD) is one of the most common genetic alterations in human cancer generally associated with poor clinical outcome, yet the underlying mechanisms have not been delineated. Here we developed an experimental model of WGD using murine mammary tumor cell lines in immunocompetent mice and found that WGD triggers immune evasion characterized by reduced infiltration of CD8+ T cells. Via comprehensive cellular and molecular characterization of WGD+ and WGD- tumors at the single cell level, we determined that WGD+ cancer cells have diminished antigen presentation due to muted response to IFN stimulation in part due to epigenetic silencing of transcriptional regulators of MHCI genes via the PRC2 complex. WGD+ tumors also have lower alpha-ketoglutarate/succinate ratio that might lead to the observed increase in histone H3 lysine 27 trimethyl levels associated with repressive chromatin. Lastly, WGD+ tumors are more responsive to anti-PD-L1 blockade and to EED inhibitors and this is associated with increased antigen presentation and CD8+ T cell infiltration. Our results have important implications for the treatment of patients with WGD+ breast cancer.
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3. ⭐ GSE274140 全基因组加倍驱动乳腺肿瘤进化的机制 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、scRNA、genome
• 📝 描述：Contributors : Pierre Foidart ; Zheqi Li ; Marco Seehawer ; Kornelia PolyakSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusWhole genome doubling (WGD) is one of the most common genetic alterations in human cancer generally associated with poor clinical outcome, yet the underlying mechanisms have not been delineated. Here we developed an experimental model of WGD using murine mammary tumor cell lines in immunocompetent mice and found that WGD triggers immune evasion characterized by reduced infiltration of CD8+ T cells. Via comprehensive cellular and molecular characterization of WGD+ and WGD- tumors at the single cell level, we determined that WGD+ cancer cells have diminished antigen presentation due to muted response to IFN stimulation in part due to epigenetic silencing of transcriptional regulators of MHCI genes via the PRC2 complex. WGD+ tumors also have lower alpha-ketoglutarate/succinate ratio that might lead to the observed increase in histone H3 lysine 27 trimethyl levels associated with repressive chromatin. Lastly, WGD+ tumors are more responsive to anti-PD-L1 blockade and to EED inhibitors and this is associated with increased antigen presentation and CD8+ T cell infiltration. Our results have important implications for the treatment of patients with WGD+ breast cancer.
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4. ⭐ GSE273031 全基因组加倍驱动乳腺肿瘤进化的机制 [批量 RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、RNA-seq、genome
• 📝 描述：Contributors : Pierre Foidart ; Zheqi Li ; Marco Seehawer ; Kornelia PolyakSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTriple-negative breast cancers (TNBC) account for 10-15% of all breast cancers. The combination of chemotherapy and Immunotherapy (ICI: immune checkpoint inhibitor) is now a standard in stages II-III TNBC while this regimen is used only in a subset of advanced TNBC tumors presenting a high expression of PD-L1. However, whole exome sequencing of tumors in clinical trials investigating ICI for treatment of various solid tumors other than breast cancer indicate that tumors which undergone a WGD (whole genome doubling) are more sensitive to immune checkpoints inhibitors. Almost all human cells are diploid. Nevertheless, a WGD happens when regulation system maintaining the diploid status fail. The WGD+ cells are tetraploid, oncogenic and facilitate tumorigenesis. The WGD occurs in 44% of breast cancers and has been correlated to advanced cases, lower survival and higher resistance to chemotherapies and targeted therapies. Therefore it is crucial todefine the role of WGD towards the immune escape/control of TNBC and response to ICI. The first step of this work was to generate different cells line in both WGD- and WGD+ status. Using a technique of membrane homofusion of parentals cells, we obtained a WGD in three different basal murine mammary tumor cell lines (67NR, 168fARN, TA3Hauschka) and one human TNBC cell (SUM 159). The acquisition of WGD was then confirmed by flow cytometry (FACS) (DNA quantity by Hoechst staining) and karyotyping. The TA3Hauschka cell line is of particular interest since it is the only murine cell line which is diploid in parental state. By injection of WGD+ or parental DP cells in mammary fat pads of syngeneic immunocompetent strain or immunocompromised (NSG) mice, we observed a plateau of tumoral growth only for immunocompetent mice injected with WGD- cells while the WGD+ tumors escaped to spontaneous immune control. No difference of growth was seen in NSG mice between WGD- and WGD+ tumors. On tumor sections, a much more pronounced necrosis was seen in WGD- tumors comparatively to WGD+ tumors in syngeneic mice while the necrosis was mild and similar for both WGD+ and WGD- tumors in NSG mice. Immunofluorescence staining demonstrated an important neutrophilic infiltration of WGD+ while the WGD- tumors had strong T-cell lymphoid infiltrates frankly superior to the lymphoid infilt…
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5. ⭐ GSE322708 PPAR-γ 通过控制脂质代谢途径抑制巨噬细胞衰老和过敏性气道炎症

• ✍️ 作者：未知作者
• 🏷️ 关键词：macrophage、inflammation、metabolic
• 📝 描述：Contributors : Wenjing Gu ; Rongjun Wan ; Zhifeng Chen ; Wenshen Wang ; Shaobing Xie ; Chuangli Hao ; Guangshu Liu ; Mei Wan ; Peisong GaoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusBackground: Cellular senescence has emerged as a key contributor to the pathogenesis of chronic lung diseases. Peroxisome proliferator-activated receptor gamma (PPAR-γ), a nuclear transcription factor, regulates senescence across multiple cell types. However, the role of PPAR-γ in allergic airway inflammation, particularly through regulation of macrophage senescence, remains poorly defined.Methods: Cellular senescence was evaluated in an allergic asthma mouse model using single-cell RNA sequencing (scRNA-seq). Senescent cells were selectively eliminated with dasatinib and quercetin (D&Q) to assess their contribution to disease pathogenesis. Macrophage-lineage-specific PPAR-γ conditional knockout model (PpargΔCD11c) were generated to define the role of macrophage PPAR-γ in senescence and allergic airway inflammation. PPAR-γ activity was further examined in isolated alveolar macrophages and in vivo using rosiglitazone, including macrophage-targeted delivery via phosphatidylserine-modified liposomes (PSL-ROSI).Findings: scRNA-seq analysis revealed enhanced senescence signatures in mononuclear phagocytes (MNPs), characterized by increased SenMayo scores and elevated Cdkn2a (p16) expression. Clearance of senescent cells significantly reduced airway inflammation and Th2 cytokine levels (IL-4, IL-5). Correlation analysis identified PPAR-γ as a key transcriptional regulator inversely associated with cellular senescence. Macrophage-lineage–specific deletion of PPAR-γ (PpargΔCD11c) exacerbated airway inflammation and increased cellular senescence. In vitro, rosiglitazone reduced allergen-induced senescence and suppressed proinflammatory mediators (IL-6, ICAM-1, CCL4, CCL5, TIMP-1, TNF-α) in alveolar macrophages. In vivo, rosiglitazone and inhaled PSL-ROSI attenuated cockroach allergen-induced airway inflammation, with PSL-ROSI effectively bypassing the airway mucus barrier to deliver rosiglitazone to lung macrophages. Integrated chromatin binding and transcriptomic analyses demonstrated that PPAR-γ promotes macrophage lipid metabolic programs (e.g., CD36, Fabp4).Interpretation: These findings identify macrophage senescence as a pathogenic driver of allergic airway inflammation and establish PPAR-γ as a critical regulator of macrophage senescence…
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6. ⭐ GSE291830 一种用于分离和单细胞表征疾病特异性循环肿瘤细胞的灵活富集策略

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、single-cell、enrichment
• 📝 描述：Contributors : Zachary R Garrison ; Rosalyn M Fey ; Terri Clister ; Connor M Hall ; Khanh L Doan ; Rajan P KulkarniSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBackground: Circulating tumor cells (CTCs) are cells that have broken off from a primary solid tumor, entered the blood stream, and have the potential to metastasize to nearby tissues. Thus, CTCs represent an important biomarker to monitor cancer progression and patient outcome. The isolation, identification and characterization of CTCs are critical for this goal. We previously developed a method for the detection and isolation of melanoma CTCs from peripheral blood through negative and positive antibody enrichment. Methods: Here we show that this protocol is easily applied to other cancers; in this case we expand and validate this method to include prostate cancer. Results: We show that this combined negative and positive enrichment protocol successfully isolates CTCs for characterization using single cell RNA sequencing and have updated the protocol to include a newer version of single cell library preparation, Smart-seq3. In our analysis, cells prepared for sequencing with Smart-seq3, which uses unique molecular identifiers (UMIs), showed no considerable difference compared to those prepared using the previous iteration of the protocol, Smart-seq2. Conclusion: This study demonstrates a robust and flexible method for the isolation and characterization of CTCs from various cancers for potential use as biomarkers for disease management and for characterization with single cell RNA-seq.
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7. GSE319473 PPP1CA 和 RPSA 双重抑制通过破坏 AR-V7/RANKL 信号通路抑制前列腺癌的去势抵抗和骨转移

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、resistance
• 📝 描述：Contributors : Wenshuo Liu ; Wei Liu ; Jing Wan ; Tingting Zhou ; Renlong Zou ; Xiaobei Zhou ; Wensu LiuSeries Type : OtherOrganism : Homo sapiensAndrogen is important in the formation, development and progress of prostate cancer, and deprivation of androgen, which is also named castration, is an effective way in prostate cancer therapies. For patients undergoing castration therapies, castration was gradually becoming ineffective in prostate cancer treatment and therefore resulting in castration-resistance for prostate cancer. Co-IP mass spectrometry, Ribo-seq, RNA-seq and system biology methods were applied to detect castration resistance drivers. Ribosomal drivers were found to be highly expressed and promoting invasion and migration in castration resistant prostate cancer cells and also in bone metastasis prostate cancer cells. Within these ribosomal drivers, RPSA played central roles in promoting castration resistance in assistance of RPL28, RPL4X, RPL11 and RPL23A. RPSA promotes castration resistance through interacting with PPP1CA and AR-V7 to form PPP1CA-RPSA-AR-V7 axis. This axis is bind by RPL23A and RPL28 and assisted by RPL4X. IGF-1 is also engaged in the process of promoting castration resistance and bone metastasis by PPP1CA-RPSA-AR-V7 axis. RPSA inhibitors plus PPP1CA inhibitors have also been proven to significantly restore castration resistance and bone metastasis for prostate cancer. This effect can be reversed by IGF-1 and retinoid acid. For these reasons, we propose that dual inhibition of PPP1CA and RPSA significantly inhibit castration resistance and bone metastasis for prostate cancer.
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8. GSE274224 全基因组加倍驱动乳腺肿瘤进化的机制 [scMultiomic-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、genome
• 📝 描述：Contributors : Pierre Foidart ; Zheqi Li ; Marco Seehawer ; Kornelia PolyakSeries Type : Expression profiling by high throughput sequencing ; Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusWhole genome doubling (WGD) is one of the most common genetic alterations in human cancer generally associated with poor clinical outcome, yet the underlying mechanisms have not been delineated. Here we developed an experimental model of WGD using murine mammary tumor cell lines in immunocompetent mice and found that WGD triggers immune evasion characterized by reduced infiltration of CD8+ T cells. Via comprehensive cellular and molecular characterization of WGD+ and WGD- tumors at the single cell level, we determined that WGD+ cancer cells have diminished antigen presentation due to muted response to IFN stimulation in part due to epigenetic silencing of transcriptional regulators of MHCI genes via the PRC2 complex. WGD+ tumors also have lower alpha-ketoglutarate/succinate ratio that might lead to the observed increase in histone H3 lysine 27 trimethyl levels associated with repressive chromatin. Lastly, WGD+ tumors are more responsive to anti-PD-L1 blockade and to EED inhibitors and this is associated with increased antigen presentation and CD8+ T cell infiltration. Our results have important implications for the treatment of patients with WGD+ breast cancer.
• 🔗 查看原文

9. GSE273087 全基因组加倍驱动乳腺肿瘤进化的机制

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、genome
• 📝 描述：Series Type : Genome binding/occupancy profiling by high throughput sequencing ; Expression profiling by high throughput sequencingOrganism : Mus musculusThis SuperSeries is composed of the SubSeries listed below.
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10. GSE273085 全基因组加倍驱动乳腺肿瘤进化的机制 [CUT&Run]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、genome
• 📝 描述：Contributors : Pierre Foidart ; Zheqi Li ; Marco Seehawer ; Kornelia PolyakSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusTriple-negative breast cancers (TNBC) account for 10-15% of all breast cancers. The combination of chemotherapy and Immunotherapy (ICI: immune checkpoint inhibitor) is now a standard in stages II-III TNBC while this regimen is used only in a subset of advanced TNBC tumors presenting a high expression of PD-L1. However, whole exome sequencing of tumors in clinical trials investigating ICI for treatment of various solid tumors other than breast cancer indicate that tumors which undergone a WGD (whole genome doubling) are more sensitive to immune checkpoints inhibitors. Almost all human cells are diploid. Nevertheless, a WGD happens when regulation system maintaining the diploid status fail. The WGD+ cells are tetraploid, oncogenic and facilitate tumorigenesis. The WGD occurs in 44% of breast cancers and has been correlated to advanced cases, lower survival and higher resistance to chemotherapies and targeted therapies. Therefore it is crucial todefine the role of WGD towards the immune escape/control of TNBC and response to ICI. The first step of this work was to generate different cells line in both WGD- and WGD+ status. Using a technique of membrane homofusion of parentals cells, we obtained a WGD in three different basal murine mammary tumor cell lines (67NR, 168fARN, TA3Hauschka) and one human TNBC cell (SUM 159). The acquisition of WGD was then confirmed by flow cytometry (FACS) (DNA quantity by Hoechst staining) and karyotyping. The TA3Hauschka cell line is of particular interest since it is the only murine cell line which is diploid in parental state. By injection of WGD+ or parental DP cells in mammary fat pads of syngeneic immunocompetent strain or immunocompromised (NSG) mice, we observed a plateau of tumoral growth only for immunocompetent mice injected with WGD- cells while the WGD+ tumors escaped to spontaneous immune control. No difference of growth was seen in NSG mice between WGD- and WGD+ tumors. On tumor sections, a much more pronounced necrosis was seen in WGD- tumors comparatively to WGD+ tumors in syngeneic mice while the necrosis was mild and similar for both WGD+ and WGD- tumors in NSG mice. Immunofluorescence staining demonstrated an important neutrophilic infiltration of WGD+ while the WGD- tumors had strong T-cell lymphoid infiltrates frankly superior to the l…
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详细内容（全部3条）

1. ⭐ 麻省理工学院科学家发现一种肠道蛋白质，可以捕获并杀死危险细菌。

• ✍️ 作者：未知作者
• 🏷️ 关键词：bacteria、regex:bacter(ia|ial|ium)、gut、regex:gut(-?microbiome)?
• 📝 描述：Scientists at MIT have discovered that a little-known protein called intelectin-2 plays a powerful double role in defending the gut. The protein strengthens the mucus layer that lines the gastrointestinal tract while also trapping and disabling harmful bacteria that try to break through. By binding to sugars on both mucus molecules and bacterial surfaces, intelectin-2 forms a protective barrier and can even destroy microbes, including some that resist antibiotics.
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2. 细胞感知距离比预期远10倍，这或许可以解释癌症的扩散。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、10x
• 📝 描述：Scientists have discovered that cells can sense far beyond the surfaces they touch. While individual cancer cells can probe about 10 microns ahead by tugging on surrounding collagen fibers, clusters of normal epithelial cells can combine forces to detect layers as far as 100 microns away. This long-range “depth sensing” helps cells decide where to migrate. Understanding how it works could reveal new targets to stop cancer from spreading.
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3. 科学家研制出一种能照亮肿瘤的癌症手电筒

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Researchers have developed a tiny antibody that can find a common cancer protein and make tumors light up during PET scans. In tests with mice, tumors containing the protein EphA2 glowed clearly when the antibody was used. This could help doctors quickly identify patients who may benefit from new targeted cancer treatments. The method may also provide a faster and less invasive alternative to traditional testing.
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• GSE324690 DPM1 调控内质网应激传感器 IRE1 的活性以及结直肠癌中的抗肿瘤免疫
• GSE324459 RNA测序分析A498肾癌细胞在敲低ELOVL2和ELOVL5后的变化
• GSE324441 非功能性垂体腺瘤（NFPA，整体甲基化组）的单细胞表观遗传景观、微环境相互作用和基因调控模块
• GSE322764 谱系和器官信号依次构建器官固有神经系统 [scRNA-seq]
• GSE296329 非功能性垂体腺瘤的单细胞表观遗传景观、微环境相互作用和基因调控模块（非疾病对照、snMultiome、多重分析）
• GSE296139 非功能性垂体腺瘤的单细胞表观遗传景观、微环境相互作用和基因调控模块（非疾病对照、snMultiome、单样本）
• GSE295840 无功能性垂体腺瘤的单细胞表观遗传景观、微环境相互作用和基因调控模块
• GSE295449 非功能性垂体腺瘤（非疾病对照，bulkRNAseq）的单细胞表观遗传景观、微环境相互作用和基因调控模块
• GSE295046 无功能性垂体腺瘤 (NFPA) 的单细胞表观遗传景观、微环境相互作用和基因调控模块
• GSE292150 单细胞分辨率下的抗原交叉呈递
• GSE281364整合功能基因组学揭示代谢性肝病风险等位基因的转录调控功能
• GSE241071 早期接触孟鲁司特通过损害神经元视黄酸信号传导导致自闭症谱系障碍 [scRNA-Seq]
• GSE232669 早期接触孟鲁司特通过损害神经元视黄酸信号传导导致自闭症谱系障碍 [RNA-seq 和 Ribo-seq]
• GSE290367 单细胞多组学整合揭示患病人类心脏中广泛存在的、细胞类型可分辨的胎儿再激活现象
• GSE265927 肝炎病毒相关纤维化和肝细胞癌的感染性小鼠模型
• GSE324662 COX2-PGE2-PKA信号通路通过抑制胞质线粒体DNA依赖的STING激活来抑制抗病毒先天免疫。
• GSE324602 环境相关微塑料吸入通过 FABP5–FOXK2–PDGFA 巨噬细胞轴驱动肺纤维化
• GSE324503：对感染假感染和肺炎链球菌的幼鼠鼻腔灌洗液样本进行RNA测序
• GSE324502 仿生线粒体靶向单原子纳米酶通过重编程干细胞能量代谢增强骨再生
• GSE316766 在正常生长条件下和热激期间，用戊酸抑制组蛋白去乙酰化酶后拟南芥 (Col-0) 的转录组变化。
• GSE309559 韧皮部蛋白质组学鉴定拟南芥中可能在开花时间控制中发挥作用的小型开放阅读框（sORF）编码肽
• GSE281367 人类代谢功能障碍相关脂肪肝疾病样本的单核染色质可及性分析
• GSE277378 先天免疫信号传导指导瞬时位点特异性拷贝数增加程序
• GSE277317：用poly(I:C)或dsDNA处理的人成纤维细胞和视网膜色素上皮细胞的PolyA RNA-seq
• GSE241074 早期接触孟鲁司特通过损害神经元视黄酸信号传导导致自闭症谱系障碍
• GSE298651 Clec3b+门静脉成纤维细胞通过KLF4/骨膜蛋白轴在胆汁淤积性肝损伤中作为门静脉周围纤维化的关键贡献者[ChIP-Seq]