详细内容（前10条）

1. ⭐ GSE292421 基于泛癌免疫和基因组特征的肿瘤微环境和免疫治疗耐药性分类

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immune、tumor microenvironment、regex:immuno(logy|therapy|suppression)、resistance
• 📝 描述：Contributors : Yiming Zhao ; Pei Wang ; Zhiren Han ; Zixuan Qiu ; Hai Hu ; Man-Li LuoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe tumor microenvironment (TME) profoundly influences responses to immune checkpoint blockade (ICB) therapies, however characterizing its complexity has been challenging. While the immune-inflamed, immune-excluded, and immune-desert T cell immunophenotypes are commonly used to classify the TME, their association with clinical outcomes to ICBs remains inconsistent. Here we demonstrated that integrating T cell immunophenotypes and tumor mutational burden (TMB) enables a more precise stratification of tumors into five distinct subtypes: immune-inflamed phenotype with high TMB (TMB-H), immune-inflamed phenotype with low TMB (TMB-L), TMB-H excluded phenotype, TMB-L excluded phenotype, and desert phenotype. Subsequently, we revealed the underlying mechanisms of tumor resistance to ICBs of each phenotype within the novel classification and elucidate several combination treatment approaches aiming at overcoming these inherent resistance mechanisms. Our study suggested that tailored combination therapy regimens addressing distinct patterns of immune resistance in different TME subtypes hold promise for enhancing immunotherapy efficacy
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2. ⭐ GSE306326 嵌合抗原受体-巨噬细胞外囊泡重编程免疫微环境用于癌症治疗。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、macrophage、antigen
• 📝 描述：Contributors : Peng Xia ; MInghe Zhang ; Yufeng YuanSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiens ; Mus musculusImmunotherapy has become a new milestone in cancer treatment, with chimeric antigen receptor (CAR)-T cell therapy proven to be an effective method for treating hematologic malignancies. However, its efficacy in solid tumors remains limited. Macrophages, the most infiltrative innate immune cells in the tumor microenvironment, are being genetically engineered to express CARs, rapidly emerging as a promising new therapy for non-hematologic malignancies. Yet, CAR- Macrophages therapy is associated with unique acute toxicities and is susceptible to immunosuppressive mechanisms. Here, we propose using CAR macrophages-derived extracellular vesicles (CAR-MEVs) as an optimization of CAR-Ms therapy. Compared to CAR-Ms cells, CAR-MEVs exhibit lower toxicity and enhanced drug delivery capabilities. In an in vivo liver cancer model, CAR-MEVs administration proved safer than CAR-Ms therapy, reducing tumor burden and prolonging overall survival. In a humanized mouse model, CAR-MEVs further demonstrated the ability to induce a pro-inflammatory tumor microenvironment and enhance anti-tumor T cell activity. Mechanistically, CAR-MEVs target tumor cells, inducing immunogenic cell death (ICD) and subsequently leading to neutrophil infiltration in tumor tissues. We demonstrated that the anti-tumor effects of CAR-MEVs depend on neutrophils and are partially reliant on inducible nitric oxide synthase (iNOS). This study supports the potential of macrophage extracellular vesicles as a novel therapeutic approach for solid tumors.
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3. ⭐ GSE261890 癌细胞自身构建的物理屏障促进获得性免疫治疗耐药性[空间]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、regex:immuno(logy|therapy|suppression)、resistance、spatial
• 📝 描述：Contributors : Xiangyu Pan ; Manli Wang ; Yu Liu ; Chong ChenSeries Type : OtherOrganism : Mus musculusDrug resistance is the principal challenge of cancer therapies, including recently developed immunotherapy. More and more popular use of immunotherapy, especially treatments with immune checkpoint inhibitors (ICIs), witnesses explosively increasing cases of both primary and acquired immunotherapy resistance. While primary resistance has been extensively studied, mechanisms underlying acquired resistance of immunotherapy are less understood. Here we reported that tumor cells could develop acquired resistance to ICI treatment through self-built collagen-containing physical barriers in non-small cell lung cancer (NSCLC). We found that tumor cells expressed high levels of multiple collagen genes, including COL3A1 and COL6A1, and were fully covered with collagen fibers. COL3A1 formed a castle-like structure of a cluster of tumor cells and prevented the infiltration of T cells, while COL6A1 seemed to be an armor-like structure of each tumor cell and protected them from attack by cytotoxic T cells. Genetic or pharmaceutic disruption of these collagens, by warfarin, a commonly used medicine, significantly reversed the acquired resistance. Thus, our data reveal an unprecedented tumor cell-intrinsic mechanism, mediated by collagen-containing physical barriers, of acquired immunotherapy resistance, which immediately suggests a treatment option for patients.
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4. ⭐ GSE331374 胶质瘤内在的 MAPK/ERK 信号通路通过 T 细胞浸润和干扰素反应促进免疫疗法疗效

• ✍️ 作者：未知作者
• 🏷️ 关键词：T cell、glioma、regex:immuno(logy|therapy|suppression)
• 📝 描述：Series Type : Expression profiling by high throughput sequencing ; OtherOrganism : Homo sapiensGlioblastoma (GBM) remains a formidable challenge in neuro-oncology, with immune checkpoint blockade (ICB) only showing efficacy in some patients, while the mechanisms governing therapeutic responsiveness are poorly defined. Although MAPK/ERK signaling correlates with survival following ICB, its causal role and mechanisms underlying tumor immunogenicity remain unclear. Here, we perform in vivo kinome-wide CRISPR/Cas9 screens in murine gliomas where we identify RAF-MEK-ERK axis as the strongest modulators of glioma susceptibility to anti-programmed cell death protein 1 (anti-PD-1) therapy and CD8+ T cell recognition. Experimentally-induced ERK phosphorylation (p-ERK) enhances survival after anti-PD-1 and anti-CLTA4, leading to durable antitumor immunity upon rechallenge. Additionally, glioma cell p-ERK promotes increased interferon responses and T cell infiltration. Notably, BRAF/MEK inhibition disrupts interferon programs and tumor-microglia interactions in BRAFV600E ex vivo in human GBM/brain slice cultures. Our findings elucidate that tumor-intrinsic MAPK/ERK promotes immunotherapy response, interferon responses, T cell tumor infiltration, and GBM cell-microglia interactions.
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5. ⭐ GSE313451 LeishDog：犬利什曼病进展过程中外周血免疫细胞的单细胞转录组图谱

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、single-cell、transcriptome
• 📝 描述：Contributors : Daniel J Holbrook ; Danielle P Uhl ; Max Waugh ; Shoumit Dey ; Najmeeyah Brown ; Karen I Cyndari ; Jacob J Oleson ; Paul M Kaye ; Christine A PetersenSeries Type : Expression profiling by high throughput sequencingOrganism : Canis lupus familiarisControlling visceral leishmaniasis (VL) requires not only addressing human disease but also targeting animal reservoirs, particularly domestic dogs, which are critical hosts that sustain zoonotic Leishmania infantum transmission. Although considerable advances have been made, the immune mechanisms underlying the transition from asymptomatic infection to symptomatic disease remain ill-defined, both in humans and dogs. To address this unresolved question, we generated a comprehensive atlas of peripheral immune cells from naturally-infected dogs and uninfected controls. The LeishDog Atlas captures the cellular and transcriptional complexity underlying canine visceral leishmaniosis (CanL), tracing shifts in immune composition and gene expression across progressive, well-defined disease stages. Notably, we identified distinct myeloid, CD4+ and CD8+ T cell phenotypes associated with severe disease. This resource provides a valuable framework for understanding systemic immune dysregulation in CanL, and establishes a foundation for comparative, translational, and mechanistic studies of CanL immunopathology.
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6. GSE332549 过表达具有增强的 GTPase 活性的 KRAS-Q25A 突变体可抑制 KRAS-G12D 结直肠癌的进展

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、KRAS
• 📝 描述：Contributors : Juncheng Su ; Xuehan Yan ; Yingjie Xu ; Zheng WangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe high mutation rate of KRAS in cancers leads to consistent activation of downstream signaling and eventually promoting malignancy. While restoring GTP hydrolysis in KRAS-mutant tumors represents a promising therapeutic strategy, its mechanistic basis remains unclear. Our previous finding that mutation of the KRAS P4 pocket exhibited elevated intrinsic GTPase activity of KRAS, and therefore presented a promising new strategy to intervene KRAS mutated cancer. This exciting potential has now been verified in the current work. We explored how P4 mutants impact the progression of colorectal cancer, and found KRAS-Q25A, a P4 mutant with the most significant elevated GTPase activity, can inhibit the progression of CT26 cell, a commonly used colorectal cell line with KRAS-G12D mutation. Moreover, this inhibitory effect of KRAS-Q25A is depended on its GTP hydrolysis process. To assess the impact of KRAS-Q25A overexpression on the overall cellular state, we performed RNA sequencing on CT26 cells overexpressing either KRAS-WT or KRAS-Q25A.
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7. GSE307998 基于连续DNA甲基化反卷积的慢性淋巴细胞白血病B细胞分化状态替代指标

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、methylation
• 📝 描述：Contributors : Jeffrey Hage ; Lauren Wainman ; Fiyinfoluwa Kolawole ; Fred Kolling IV ; Pauline Patzke ; Daniel Schoolcraft ; Sarah Spracklin ; Prabhjot Kaur ; Brock ChristensenSeries Type : Methylation profiling by arrayOrganism : Homo sapiensChronic Lymphocytic Leukemia (CLL) is clinically divided into IGHV mutated (M-CLL) and IGHV unmutated (U-CLL) subtypes, which are thought to arise from distinct cells of origin along the B-cell differentiation pathway. We measured genome-scale DNA methylation in purified CLL samples (n=89) and utilized reference-based cell deconvolution techniques to develop a continuous metric of epigenetic similarity across a B-naive-like to B-memory-like scale (B-Index). B-Index accurately classifies CLL into clinical subtypes (98.8%), has a stronger epigenetic signal than IGHV gene percent identity, and demonstrates additional epigenetic signal within the M-CLL subgroup. We demonstrate that U-CLL is epigenetically more similar to B-memory than B-naive cells and reconcile previous reports of a B-naive-like epigenetic signal. The B-memory-like program of U-CLL is enriched for binding sites of transcription factors related to the germinal center activation pathway. Our findings provide epigenetic evidence for discerning CLL mechanisms of initiation and cell of origin. We also identified an epigenetic signal associated with tumor burden, which may have some relation to viral infections such as Epstein-Barr-Virus. Our cell-type deconvolution-based approach to developing a continuous metric for CLL epigenetic differentiation state can be applied to other tumors with multiple subtypes across differentiation stages.
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8. GSE233554 肾癌和肺癌细胞系在 GSK-J4 刺激前后的 mRNA 测序

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、sequencing
• 📝 描述：Contributors : Montse Sanchez-Cespedes ; Octavio R Ferraro ; Andrea V PortaSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensWe performed RNA sequencing to assess changes in gene expression in two models of SMARCB1 deficient cells. Total RNA was extracted from the cells, before and after treatment with GSK-J4 and before and after the ectopic exoresion recovery of the gene, using standard approaches. RNA-sequencing data performed in this work was performed and analyzed at Novogene.
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9. GSE204966 嗅觉丧失是衰老的早期标志，并且与C57BL6/J小鼠的炎症和DNA损伤有关

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、inflammation
• 📝 描述：Contributors : Xiuli Dan ; Beimeng Yang ; Ross McDevitt ; Samuel Gray ; Xixia Chu ; Quia Claybourne ; David M Figueroa ; Yongqing Zhang ; Deborah L Croteau ; Vilhelm A BohrSeries Type : Expression profiling by arrayOrganism : Mus musculusOlfactory dysfunction (loss of the ability to detect odors) is a prevalent symptom and an early marker of age-related neurodegenerative diseases in humans, including Alzheimer’s Disease and Parkinson’s Disease. However, as olfactory dysfunction also is a common symptom of normal aging, it is important to identify associated behavioral and mechanistic changes that underlie olfactory dysfunction in nonpathological aging. In the present study, we systematically investigated age-related behavioral changes in four specific domains of olfaction and the molecular basis in C57BL6/J mice. Our results show that selective loss of odor discrimination is the earliest smelling behavioral change with aging, followed by a decline in odor sensitivity and identification. Compared to behavioral changes related with memory and motor functions, smelling loss is among one of the earliest biomarkers of aging. During aging, metabolites related with of oxidative stress, osmolytes and infection become dysregulated in the olfactory bulb, and G protein coupled receptor related signaling was significantly down regulated in olfactory bulb of aged mice. Poly ADP-ribosylation levels and protein expressions of DNA damage markers and inflammation increased significantly in the olfactory bulb of older mice in which a lower NAD+ level was also detected. Supplementation of NAD+ through NR in water improved longevity and partially enhanced olfaction in aged mice.
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10. GSE332846 一例MMR缺陷型前列腺癌患者对免疫疗法完全缓解，伴有NK样和CD4+CD8+ T细胞

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、regex:immuno(logy|therapy|suppression)
• 📝 描述：Contributors : Alexander K Tsai ; John R Lozada ; Philippa R Kennedy ; David Moline ; Rachana Pandey ; Riley C Lyons ; Christine Luo ; Ali T Arafa ; Elise L Femino ; Sarah Zipkowitz ; Andrew Elliott ; Paari Murugan ; Martin Felices ; Nicholas A Zorko ; Badrinath Konety ; Scott M Dehm ; Jeffrey S Miller ; Stephen Shen ; Elizabeth A Thompson ; Laura A Sena ; Justin Hwang ; Emmanuel S AntonarakisSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Homo sapiensMismatch repair deficiency (dMMR) and microsatellite instability (MSI-H) are rare in prostate cancer, occurring in 2-4% of cases. These defects result in increased genomic instability and elevated tumor mutational burden (TMB), which can support responses to immune checkpoint inhibitors (ICIs). Here, we report a patient with locally-advanced Gleason 5+5=10 prostatic adenocarcinoma harboring MSH2 and MSH6 genomic deletions with ultrahigh TMB (>250 mutations/megabase) in whom pembrolizumab resulted in a striking complete radiographic, pathologic, and molecular response. Using digital-spatial microscopy, single-cell RNA/TCR-sequencing, and multiplex cytometry, we identify atypical tumor-infiltrating T-cells with natural killer-like phenotypes and CD4+CD8+ (double-positive) lymphocytes. These unique and clonal T-cell populations expand preferentially following ICI and adopt terminally-differentiated and cytotoxic profiles that may drive clinical response. Similar T-cells are also present in diverse cancers and expand exclusively in ICI-responsive patients. These findings inform on cellular mechanisms by which immunotherapies may mediate profound responses in patients with dMMR solid tumors.
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1. 科学家发现一种可能导致癌症和关节炎的两阶段衰老过程

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、aging
• 📝 描述：A new theory suggests many age-related diseases may actually start decades before symptoms appear. Researchers say early-life damage — from infections, injuries, or genetic mutations — can remain hidden until aging weakens the body’s ability to keep it under control. This could explain why conditions like cancer, osteoarthritis, and shingles suddenly emerge later in life.
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2. miND规范了用于生物标志物发现的小RNA测序分析。

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：RNA sequencing with the miND pipeline supports standardized small RNA analysis for biomarker discovery across tissues, plasma, extracellular vesicles, and other sample types…
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3. 牛津纳米孔公司和龙沙公司联合推出用于GMP mRNA质量控制的直接RNA测序解决方案

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：RNA sequencing combined with nanopore technology and machine learning may streamline GMP quality control testing for mRNA therapeutics within a single workflow…
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4. 科学家发现数百种癌症突变体共有的隐藏弱点

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Scientists have unveiled a powerful new tool called PerturbFate that could change how researchers tackle diseases driven by huge numbers of genetic mutations, including cancer and Alzheimer’s. Instead of trying to target every faulty gene individually, the system tracks how different mutations reshape cells over time and identifies the hidden “control hubs” where those pathways converge.
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5. 像Wegovy这样的热门减肥药也可能针对关节炎炎症。

• ✍️ 作者：未知作者
• 🏷️ 关键词：inflammation
• 📝 描述：Researchers have discovered that the GLP-1 hormone targeted by drugs like Wegovy is present in very low amounts inside the joints of arthritis patients. That finding suggests high-dose GLP-1 medications could potentially reach the joints and influence inflammation directly, not just help through weight loss. Scientists say this could open the door to a completely new approach to arthritis treatment.
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6. “僵尸细胞”并非总是坏事，这可能会彻底改变抗衰老医学。

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging
• 📝 描述：Scientists are uncovering a surprising truth about aging cells: some may damage the body, while others help protect it. The discovery is fueling a new wave of precision anti-aging therapies aimed at removing only the harmful “zombie” cells without disrupting the body’s natural repair systems.
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• GSE161154 胶质瘤亚型的差异性迁移机制和免疫反应
• GSE331257 组蛋白琥珀酰化直接抑制 Jumonji 结构域去甲基化酶并稳定抑制性染色质状态 [RNA-Seq]
• GSE331233 限制蛋氨酸饮食对小鼠高级别胶质瘤（3xCr）染色质可及性的影响 [scATAC-seq]
• GSE331215 IL1R1阻断增强CD40激动剂介导的胰腺癌免疫
• GSE298125 阿托伐他汀调节肝脏转录组 PXR 依赖性，但与孕烯醇酮 16α-腈不同，并且不诱导 PXR 介导的肝脂肪变性 [ATAC-seq]
• GSE332729 成纤维细胞介导的促纤维增生反应通过YAP-CTRB1驱动的竞争适应性抑制胃癌
• GSE332708 混合体内乳腺癌模型揭示了癌症随年龄进展的转录组学见解
• GSE331492 成年果蝇雌性雌激素相关受体 (ERR) 敲除的转录组分析
• GSE328089 靶向肝星状细胞中的 AREL1 可减轻 MASH 相关肝纤维化 [RNA-Seq]
• GSE327949 靶向肝星状细胞中的 AREL1 可减轻 MASH 相关肝纤维化 [scRNA-seq]
• GSE323364 EZH2 的催化功能和非经典功能的协调作用可增强肿瘤对 CAR-T 细胞疗法的敏感性
• GSE315793 五味子素B通过诱导胰腺癌细胞铁死亡发挥抗增殖作用
• GSE300268 链霉菌 WblA 调控子的鉴定揭示了其对发育和特化代谢的显著影响
• GSE331259 组蛋白琥珀酰化直接抑制 Jumonji 结构域去甲基化酶并稳定抑制性染色质状态 [CUT&Tag]
• GSE331221 FK506结合蛋白OsFKBP57和OsFKBP73通过SOS途径赋予水稻耐盐性并维持籽粒蛋白质含量。
• GSE319763 急性髓系白血病肺浸润和呼吸衰竭的炎症免疫调节因子
• GSE284747 急性髓系白血病肺浸润和呼吸衰竭的炎症免疫调节因子
• GSE269045 急性髓系白血病肺浸润和呼吸衰竭的炎症免疫调节因子