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1. ⭐ 最新14+生信，通过单细胞分析识别HLA-DR +肿瘤细胞，并分析其对 CD8+T 细胞及预后的影响，思路新颖！

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

2. ⭐ 最新10+生信，非常务实的文章。肿瘤免疫微环境中关键免疫生物标志物的泛癌空间特征分析

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：肿瘤、免疫、免疫微环境、微生物、生信
• 📝 描述：点击查看详情
• 🔗 查看原文

3. ⭐ 最新14+生信，单细胞识别PLAUR+中性粒细胞塑造免疫抑制微环境，抑制PLAUR 增强抗 PD1 疗效。高分文章经典思路！

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

4. ⭐ Nature首次揭示染色质调节因子：SATB1调控T细胞，为癌症免疫治疗开新挂！

• ✍️ 作者：生信人
• 🏷️ 关键词：癌症、免疫、T细胞、B细胞
• 📝 描述：在慢性病毒感染和癌症中，CD8+ T细胞长期暴露于抗原刺激下会逐渐分化为衰竭T细胞，其特征是功能受损、抑制性受
• 🔗 查看原文

5. ⭐ 单胞可塑 | Nature | 起源基底细胞解析癌症中神经内分泌-簇状细胞谱系可塑性

• ✍️ 作者：BioJournal Link
• 🏷️ 关键词：癌症、T细胞、神经、单细胞
• 🔗 查看原文

6. ⭐ 10.6分非肿瘤干湿结合生信，靶向 CD177 + 中性粒细胞减轻缺血再灌注损伤。适合动物建模测序思路！

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

7. ⭐ 跟着文献学习VisiumHD单细胞空间转录组数据处理，这个大家做的也越来也多了

• ✍️ 作者：生信钱同学
• 🏷️ 关键词：单细胞、空间转录组、转录组
• 📝 描述：好的空间组学代码学习
• 🔗 查看原文

8. ⭐ 《自然·免疫学》：康奈尔团队首次发现，“别吃我”信号分子CD47，竟然还能促进T细胞耗竭，削弱抗肿瘤免疫！

• ✍️ 作者：奇点肿瘤探秘
• 🏷️ 关键词：肿瘤、免疫、T细胞
• 📝 描述：一条调控T细胞耗竭的新通路现身，为改善免疫治疗效果提供了新的探索方向。
• 🔗 查看原文

9. ⭐ Cancer Cell+1！陆军军医大揭示胶质瘤的神经免疫逃逸新机制！

• ✍️ 作者：今日病理
• 🏷️ 关键词：cancer、免疫、神经
• 🔗 查看原文

10. ⭐ 文献分享–空间多组学技术揭示侵袭性前列腺癌特征：肿瘤微环境中促炎性趋化因子活性的关键作用

• ✍️ 作者：单细胞空间交响乐
• 🏷️ 关键词：肿瘤、趋化因子、空间组学
• 📝 描述：文献分享–空间多组学技术揭示侵袭性前列腺癌特征：肿瘤微环境中促炎性趋化因子活性的关键作用
• 🔗 查看原文

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1. ⭐ GSE302715 一种肿瘤相关巨噬细胞靶向免疫细胞因子，利用 T 细胞和 NK 细胞的协同作用进行强效癌症免疫治疗 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、macrophage、NK cell、regex:immuno(logy|therapy|suppression)、scRNA
• 📝 描述：Contributors : Michelle von Locquenghien ; Pascale Zwicky ; Ken Xie ; Diego Jaitin ; Fadi Sheban ; Florian Uhlitz ; Chamutal Gur ; Reut Sharet Eshed ; Eyal David ; Kfir Mazuz ; Jahan Adeeb Rahman ; Noam Solomon ; Roberto Avellino ; Assaf Weiner ; Ido AmitSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTumor-associated macrophages (TAMs) expressing the myeloid checkpoint TREM2 are key immunosuppressive cells in the tumor microenvironment (TME), driving tumor progression and contributing to poor prognosis in cancer patients. Due to their pivotal role, TAMs have emerged as a promising target for immunotherapies. However, current TAM-targeting monotherapies show only modest efficacy in clinical trials in solid tumors . Here, we have developed a new class of cancer immunotherapies: myeloid-targeted immunocytokines and NK-T cell enhancers (MiTEs). MiTEs are trans-acting immunocytokines with tumor-specific activation, allowing dual targeting of TAMs and lymphocytes by TREM2 antagonism and cytotoxic effector cell activation through IL-2. To avoid off-target toxicities, MiTEs contain an IL-2 masking moiety, which is cleaved by a TAM-specific protease. MiTEs demonstrate high efficacy in preclinical tumor models through extensive immune reprogramming spanning TAM, T and NK cell compartments. MiTEs show transformative potential for treating solid-cancers by inducing potent multi-arm anti-tumor immunity and minimizing toxicities.
• 🔗 查看原文

2. ⭐ GSE303870 一种靶向肿瘤相关巨噬细胞的免疫细胞因子，利用T细胞和NK细胞的协同作用，实现强效的癌症免疫治疗

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、macrophage、NK cell、regex:immuno(logy|therapy|suppression)
• 📝 描述：Series Type : Expression profiling by high throughput sequencing ; OtherOrganism : Homo sapiens ; Mus musculusThis SuperSeries is composed of the SubSeries listed below.
• 🔗 查看原文

3. ⭐ GSE303868 一种肿瘤相关巨噬细胞靶向免疫细胞因子，利用 T 细胞和 NK 细胞的协同作用进行强效癌症免疫治疗 [CITE-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、macrophage、NK cell、regex:immuno(logy|therapy|suppression)
• 📝 描述：Contributors : Michelle von Locquenghien ; Pascale Zwicky ; Ken Xie ; Diego Jaitin ; Fadi Sheban ; Florian Uhlitz ; Chamutal Gur ; Reut Sharet Eshed ; Eyal David ; Kfir Mazuz ; Jahan Adeeb Rahman ; Noam Solomon ; Roberto Avellino ; Assaf Weiner ; Ido AmitSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Homo sapiensTumor-associated macrophages (TAMs) expressing the myeloid checkpoint TREM2 are key immunosuppressive cells in the tumor microenvironment (TME), driving tumor progression and contributing to poor prognosis in cancer patients. Due to their pivotal role, TAMs have emerged as a promising target for immunotherapies. However, current TAM-targeting monotherapies show limited efficacy, highlighting the need for strategies engaging multiple immune modalities. Here, we developed a new class of cancer immunotherapies: myeloid-targeted immunocytokines and NK-T cell enhancers (MiTEs). MiTEs are trans-acting immunocytokines with tumor-specific activation, allowing dual targeting of TAMs and lymphocytes by TREM2 antagonism and cytotoxic effector cell activation through IL-2. To avoid off-target toxicities, MiTEs contain an IL-2 masking moiety, which is cleaved by a TAM-specific protease. MiTEs demonstrate high efficacy in preclinical tumor models through extensive immune reprogramming spanning TAM, T and NK cell compartments. MiTEs show transformative potential for treating solid-cancers by inducing potent multi-arm anti-tumor immunity and minimizing toxicities.
• 🔗 查看原文

4. ⭐ GSE281973 肿瘤浸润性 NK 细胞 (tuNK) 与脾脏 NK 细胞 (spNK) 的功能和转录谱比较 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、NK cell、RNA-seq
• 📝 描述：Contributors : Yi Wang ; Li Tang ; Yugang GuoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusNatural killer (NK) cells, a type of potent cytotoxic lymphocytes, are particularly promising for the treatment of cancers that lose or downregulate major histocompatibility complex class I (MHC-I) expression to evade T cell-mediated immunotherapy. However, the hostile and immune suppressive tumor microenvironment (TME) greatly hinders the function of tumor-infiltrating NK cells limiting the therapeutic efficacy against solid tumors. Here, we show that a fusion protein of interleukin-21 (IL-21−Fc), as a direct in vivo intervention, can safely and effectively reprogram NK cell metabolism and enhance their effector function in the TME. Our research demonstrates that combining IL-21−Fc with IL-15 superagonist (IL-15SA) or NK cell transfer leads to the eradication of MHC-I-deficient tumors and confers durable protection in syngeneic and xenograft tumor models. Mechanistically, we uncover that IL-21−Fc enhances NK cell effector function by upregulating glycolysis in a lactate dehydrogenase A (LDHA)-dependent manner. These findings not only underscore the considerable potential of IL-21−Fc as an in vivo therapeutic intervention to bolster NK cell-based immunotherapy, but also unveil an innovative strategy of metabolic reprogramming for NK cell rejuvenation within tumors.
• 🔗 查看原文

5. ⭐ GSE254278 单细胞转录组学揭示亨廷顿病神经退行性变中T细胞的物种依赖性免疫浸润

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、single-cell、transcriptomics
• 📝 描述：Contributors : Jiawei Li ; Yingqi Lin ; Sen YanSeries Type : Expression profiling by high throughput sequencingOrganism : Sus scrofaImmune infiltration of T cells in the brain has been observed in various pathological conditions, but whether this phenomenon occurs in Huntington disease (HD) remains unknown. To address this question, we conducted an investigation using HD knock-in pigs, which exhibit selective neurodegeneration similar to HD patients. Single-cell transcriptomes identified that glial cells are the most abundant cell type in the human and pig striatum, while neurons outnumber glial cells in the mouse striatum. HD knock-in pigs recapitulate the loss of specific types of striatal neurons (iSPN and dSPN) observed in HD patients, a phenomenon not observed in HD knock-in mice. The increased IFN-activated microglia subgroup in HD knock-in pigs was found to secrete CCL8 chemokines to recruit CD8+ T cells. These T cells release perforin and granzyme, leading to the degeneration of striatal neurons. Although HD-KI mouse striatum does not show elevated CCL8, administration of CCL8 resulted in an increase in CD8+ T cells and a reduction in neuronal cells. These findings suggest that species-dependent abundance of glial cells and the effects of mutant huntingtin on glial cells contribute to microglia-driven immune infiltration of CD8+ T cells, ultimately playing a critical role in the selective neurodegeneration in HD.
• 🔗 查看原文

6. ⭐ GSE248419 Zeb1-Cxcl1轴通过诱导乳腺癌中M2巨噬细胞极化来削弱抗肿瘤免疫反应 II

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、macrophage
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusZeb1, a classic epithelial-mesenchymal transition (EMT) regulator, has recently been found to be involved in M2 macrophage polarization in the tumor immune microenvironment, thereby promoting tumor development. However, the underlying mechanism of Zeb1-induced M2 macrophage polarization remains largely unexplored. To identify the potential role of Zeb1 in remodeling the tumor immune microenvironment in breast cancer, we crossed the floxed Zeb1 allele homozygously into PyMT mice to generate PyMT;Zeb1cKO (MMTV-Cre; PyMT;Zeb1fl/fl) mice. We found that the recruitment of M2 macrophages was significantly reduced in tumors from PyMT;Zeb1cKO mice, along with weakening of the tumor suppressive effect. Mechanistically, Zeb1 plays a crucial role in transcriptionally promoting the expression of Cxcl1 in tumor cells and enhancing the secretion of Cxcl1 in serum. Eventually, Cxcl1 activated the JAK-Stat3 signature via Cxcr2 and then induced the M2 polarization of macrophages, which leads to T cell inactivation and impairs the antitumor immune response in breast cancer. Our results revealed the important role of Zeb1 in the remodeling of the breast cancer tumor microenvironment, suggesting a novel therapeutic intervention for the treatment of advanced cancers.
• 🔗 查看原文

7. ⭐ GSE248418 Zeb1-Cxcl1轴通过诱导乳腺癌中M2巨噬细胞极化来损害抗肿瘤免疫反应 I

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、macrophage
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensZeb1, a classic epithelial-mesenchymal transition (EMT) regulator, has recently been found to be involved in M2 macrophage polarization in the tumor immune microenvironment, thereby promoting tumor development. However, the underlying mechanism of Zeb1-induced M2 macrophage polarization remains largely unexplored. To identify the potential role of Zeb1 in remodeling the tumor immune microenvironment in breast cancer, we crossed the floxed Zeb1 allele homozygously into PyMT mice to generate PyMT;Zeb1cKO (MMTV-Cre; PyMT;Zeb1fl/fl) mice. We found that the recruitment of M2 macrophages was significantly reduced in tumors from PyMT;Zeb1cKO mice, along with weakening of the tumor suppressive effect. Mechanistically, Zeb1 plays a crucial role in transcriptionally promoting the expression of Cxcl1 in tumor cells and enhancing the secretion of Cxcl1 in serum. Eventually, Cxcl1 activated the JAK-Stat3 signature via Cxcr2 and then induced the M2 polarization of macrophages, which leads to T cell inactivation and impairs the antitumor immune response in breast cancer. Our results revealed the important role of Zeb1 in the remodeling of the breast cancer tumor microenvironment, suggesting a novel therapeutic intervention for the treatment of advanced cancers.
• 🔗 查看原文

8. GSE310106 DDX6 发生相分离以调节 AML 中的代谢可塑性和耐药性 [CRISPR 筛选]

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolic、resistance
• 📝 描述：Contributors : Rui Su ; Chun-Wei (David) Chen ; Hongjie Bi ; Anthony ChanSeries Type : OtherOrganism : Homo sapiensChemoresistance in acute myeloid leukemia (AML) is a major cause of poor prognosis and frequent relapse among patients. Under stress conditions such as chemotherapy or radiotherapy, processing bodies (PBs) and stress granules (SGs) can sequester essential mRNAs and proteins to modulate leukemia cell survival. However, the precise role(s) of PBs and SGs in AML pathogenesis and chemotherapy response remains unclear. To systematically identify PB/SG-associated genes that are critical for AML survival, we selected 101 genes encoding RNA-binding proteins that are localized within PBs and SGs, and constructed a customized CRISPR library targeting these genes for both in vitro and in vivo CRISPR screening with AML cell line (Mono-Mac-6) and patient-derived xenograft (PDX) cells.
• 🔗 查看原文

9. GSE304762 利用基因条形码和单细胞转录组学解析食管癌前病变中前体细胞的动态变化

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell、transcriptomics
• 📝 描述：Series Type : OtherOrganism : Mus musculusEsophageal preneoplastic cells, despite appearing histologically normal, exhibit early genetic alterations and lineage plasticity, yet their origins and trajectories remain unclear. This study employs genetic barcoding combined with single-cell RNA sequencing to trace the lineage of esophageal preneoplastic cells and identify a distinct progenitor-like population with high plasticity. Through a newly developed scoring system, high-plasticity cells are mapped, revealing their contributions to proliferative and basal cell populations. The study identifies key molecular markers, including Nfib and Qk, that define these precursor cells. These findings provide critical insights into early tumorigenesis, highlighting the potential of precursor cells as biomarkers for early cancer detection and therapeutic targeting. By elucidating the cellular dynamics underlying esophageal cancer initiation, this research lays the foundation for strategies to prevent malignant progression, offering broader implications for improving cancer diagnostics and treatment approaches.
• 🔗 查看原文

10. GSE291689 Pfkfb1 选择性地识别含有胞内生长细菌的巨噬细胞

• ✍️ 作者：未知作者
• 🏷️ 关键词：bacteria、regex:bacter(ia|ial|ium)
• 📝 描述：Contributors : Li Fan ; Yang SunSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThrough releasing virulence molecules into host cells, intracellular bacteria interfere with host cellular functions and grow in the cells that engulf them. To ensure survival and virulence, these pathogens also manipulate host factors, but this process is not fully understood. In this study, we investigated the host molecular mechanisms required for intracellular bacterial growth in macrophages using Salmonella typhimurium (Salmonella) infection model and bacterial division reporter system. Upon Salmonella infection, Protein Phosphatase 6 (Pp6) was significantly reduced in macrophages containing growing bacteria. Conditional knockout of Pp6 increased host susceptibility to Salmonella-mediated killing, which was attributed to the poor resistance in Pp6-deficient macrophages. MicroRNA-31 (miR-31) was identified as a negative regulator of Pp6, and its conditional deletion promoted Salmonella clearance. Moreover, a yeast two-hybrid screening identified 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 1 (Pfkfb1), a key metabolic regulator, as a substrate of Pp6. Pp6-deficient macrophages exhibited elevated Pfkfb1 expression. Furthermore, we found that macrophages containing growing Salmonella exclusively exhibited high Pfkfb1 expression. Pfkfb1 deletion reduced bacterial growth, likely due to increased NO levels, while also downregulating arginase-1 (Arg-1) expression and impairing arginine biosynthesis and metabolism in macrophages. Together, we investigated the role of Pp6-Pfkfb1 axis in orchestrating host metabolic adaptions and intracellular bacterial survival, which may provide therapeutic targets for infectious diseases against intracellular multidrug-resistant bacteria.
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1. Cergutuzumab Amunaleukin 与阿替佐利珠单抗联合治疗癌胚阳性晚期/转移性实体肿瘤患者

• ✍️ 作者：未知作者
• 🏷️ 关键词：肿瘤、抗体
• 📝 描述：Secret hovertext: 目的：Cergutuzumab amunaleukin（CA）是一种免疫细胞因子，由白介素-2 变异形式组成（设计为避免 CD25 结合和 Treg 刺激），融合于致癌胚胎抗原（CEA）靶向抗体。该 Ib 期开放标签、多中心剂量递增与扩展研究（NCT02350673）评估了 CA 加阿替唑珠单抗在晚期/转移性 CEA 阳性实体肿瘤患者的安全性、活性、药代动力学和药效学。患者与方法：患者每 2 周（每 2 周）接受 CA 剂量递增（6–20/25 毫克）与固定剂量阿替唑珠单抗（840 毫克）;或每周递增剂量 CA（10–15/20 毫克）与固定剂量阿替唑珠单抗（1200 毫克）每 3 周（每 3 周）递增剂量。主要目标：最大耐受剂量（MTD）;扩张推荐剂量（RDE）;安全。结果：24 名患者被随机分配为每 2 周接受 CA 加阿替唑珠单抗，45 名患者为 CA QW 加阿替唑珠单抗每 3 周
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2. 复发/难治性大 B 细胞淋巴瘤患者 JULIET 试验五年分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：淋巴、B细胞
• 📝 描述：Secret hovertext: 临床肿瘤学杂志，印刷前。
• 🔗 查看原文

3. 原发性硬化性胆管炎相关胆道癌的临床基因组学特征

• ✍️ 作者：未知作者
• 🏷️ 关键词：基因组
• 📝 描述：Secret hovertext: 目的：胆道癌（BTC）是原发性硬化性胆管炎（PSC）患者的主要死因。与 PSC 相关的 BTC 目前尚不充分，常规和免疫疗法的风险与益处尚不明确。我们的目标是表征 PSC 相关 BTCs 的临床结局和基因组。实验设计：这是一项回顾性队列研究，针对在 MD Anderson 癌症中心（N=46）和玛格丽特公主癌症中心（N=16）接受治疗的基础 PSC 患者的 BTC 患者，与非 PSC 相关 BTC 患者（N=146）进行了对比。我们比较了 PSC 与非 PSC 的结局，以及有无免疫治疗的 PSC 治疗。靶向测序（N=139）、全基因组测序（N=27）及全基因组配对 RNA 测序（N=33）的组合，描绘了 PSC 相关 BTCs 的基因组和转录组格局。结果：在 PSC 相关 BTC 中，将免疫治疗加入化疗与改善一线无进展生存期相关（N=22 对 11，中位 PFS 12.2 对 4.7 个月），
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4. 随着双特异性抗体上升，利妥昔单抗/吉西他滨/奥沙利铂的使用日落：SUNMO 试验

• ✍️ 作者：未知作者
• 🏷️ 关键词：抗体
• 📝 描述：Secret hovertext: 临床肿瘤学杂志，印刷前。
• 🔗 查看原文

5. 胰腺癌中的雌激素生成塑造了抑制肿瘤的基质微环境

• ✍️ 作者：未知作者
• 🏷️ 关键词：肿瘤
• 📝 描述：Secret hovertext: 由于缺乏有效的治疗干预，胰管腺癌（PDAC）是导致癌症相关死亡的主要原因之一。PDAC 肿瘤高度纤维化，间质丰度被假设对患者结局有影响。然而，基质成纤维细胞可能促进肿瘤并抑制肿瘤，这或许能解释基质靶向治疗令人失望的临床结果。我们观察到，女性 PDAC 患者的血清间质生物标志物水平显著高于男性患者。这一观点得到了对实体癌间质丰度的计算机估计，以及磁共振弹性成像和组织染色的支持，这些方法显示女性 PDAC 患者的肿瘤组织更为坚硬。基因表达分析显示，雌激素信号传导指示一个基质成纤维母细胞表型，该表型与相对惰性分子亚型相关，且预后更为良好，而该预后由 C 型凝集素 CLEC3B 的基质表达维持。值得注意的是，雌激素在肿瘤内被检测到，胰腺癌细胞表达了促成雌激素合成的关键酶。PDAC 中的雌激素产生由基质衍生的分支链氨基酸分解作用推动，最终产生类固醇激素前体。这些数据共同揭示了重要的激素驱动因素，通过重编程肿瘤微环境来限制肿瘤进展，并为
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6. 加拿大青少年和青年癌症后跨性别和年龄的收入。

• ✍️ 作者：未知作者
• 🏷️ 关键词：癌症
• 📝 描述：Secret hovertext: 背景 青少年和年轻成人（AYAs）癌症在关键的过渡阶段出现，对财务健康产生持久影响。目前尚不确定 AYAs 中的癌症是否会因性别和诊断年龄随时间在收入上表现出差异。方法 我们将加拿大国家癌症登记处与个人税务记录关联，以识别 1994 年至 2013 年间诊断的 AYA（15-39 岁）。在确诊前一年，幸存者在多个社会人口学特征上与 10 名无癌者进行了变异比匹配。参与者的纵向随访时间最长可追溯至诊断后 10 年或 2015 年。使用双稳健差分估算相对和绝对收入变化。我们将年龄分为三组：青少年（15-17 岁）、新兴青年（18-29 岁）和青年成人（30-39 岁），反映了不同的 AYA 生命阶段。分析按性别和诊断年龄分层。结果：女性幸存者 60,240 人，男性幸存者 33,085 人，分别匹配到无癌者 490,645 人和 274,595 人。总体而言，男性和女性收入减少率分别为 6.9%（95%置信区间：5
• 🔗 查看原文

7. FaceAge 作为大型肿瘤学队列预后和治疗分层的生物标志物。

• ✍️ 作者：未知作者
• 🏷️ 关键词：肿瘤
• 📝 描述：Secret hovertext: 背景：人类衰老速度不同，面部特征可能揭示生物年龄和生理健康状况。FaceAge 是一款通过面部照片估算生物年龄的深度学习系统，已展现出作为癌症预后生物标志物的潜力。本研究探讨了面部年龄与实际年龄（FaceAge-Age）之间极端不一致在预测生存率和早期死亡率中，涵盖 28 种癌症类型的大型临床数据集中的预后价值。方法：分析了 2008 年至 2023 年间接受放疗的 24,556 名年龄≥60 岁的癌症患者的数据。在不同诊断/临床背景下，比较了 FaceAge 估计值与时间年龄，并进行了生存分析。所有测试均为双面测试。结果 FaceAge 在 65%的年龄中比实际年龄更老（中位数为 74 岁对 70 岁）。年轻患者、女性、预后较差且接受缓和意图治疗的患者，脸龄-年龄≥10 岁的可能性更高。面年龄年龄≥10 岁患者存活率显著较低，而面年龄年龄≤-5 岁患者存活率较佳。在多变量分析中，FaceAge-Age≥10
• 🔗 查看原文

8. 肿瘤相关生物类似药的采用：全球使用数据分析。

• ✍️ 作者：未知作者
• 🏷️ 关键词：肿瘤
• 📝 描述：Secret hovertext: 背景生物制剂极大地改善了癌症管理，但成本较高。生物类似药成本较低，且与参考产品相比没有临床意义上的差异。然而，它们并不完全相同，导致临床医生和患者对使用它们持犹豫态度。目的 测量美国及类似监管框架国家中肿瘤相关生物类似药相较于参考产品的采用情况。方法 我们于 2022 年 10 月至 2023 年 9 月期间，在 13 个国家对五种含生物类似药的肿瘤相关生物制剂进行了横断面销售分析：贝伐珠单抗、菲格拉斯汀、呐非格拉斯汀、利妥昔单抗和曲妥珠单抗。我们使用了 IQVIA MIDAS®关于国家层面季度销售量和价值的数据。结果 在 13 个国家中，美国在肿瘤相关生物类似药的采用比例（按销售单位计 75%对中位数 86%）和支出比例（58%对 76%）方面排名第十。美国生物类似药的采用率为：非格瑞司汀 84%（对比 95%），贝伐单抗 83%（对比 86%），利妥昔单抗 75%（对比 93%），曲妥珠单抗
• 🔗 查看原文

详细内容（全部7条）

1. 科学家重新激活疲惫的T细胞，以增强癌症免疫力。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immunity
• 📝 描述：Researchers discovered a way to keep T cells from wearing out during the fight against cancer, and the approach could make immune-based treatments far more powerful. They found that tumors use a particular molecular signal to weaken T cells, and that interrupting this signal helps the cells stay active.
• 🔗 查看原文

2. RNA测序揭示了肌肉干细胞如何引导巨噬细胞促进蝌蚪尾部再生。

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：RNA sequencing reveals how muscle stem cells use c1qtnf3 to shift macrophages toward regeneration, enabling African clawed frog tadpoles to regrow functional tails…
• 🔗 查看原文

3. RNA测序为以往无法确诊的罕见病病例提供了功能性见解和诊断依据。

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：RNA sequencing uncovers hidden splicing and regulatory defects, improving diagnostic clarity for rare disease cases when DNA tests fall short.
• 🔗 查看原文

4. Parse Biosciences公司宣布推出与FFPE兼容的条形码技术，用于全转录组单细胞分析。

• ✍️ 作者：未知作者
• 🏷️ 关键词：transcriptome
• 📝 描述：RNA sequencing of FFPE tissues gains whole transcriptome, single cell resolution through…
• 🔗 查看原文

5. 一种简单的分子在老鼠身上展现出显著的阿尔茨海默病逆转作用

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：Scientists have developed a new molecule that breaks down beta-amyloid plaques by binding to excess copper in the brain. The treatment restored memory and reduced inflammation in rats, while also proving non-toxic and able to cross the blood–brain barrier. Because it’s far simpler and potentially cheaper than existing drugs, researchers are now pursuing partnerships to begin human trials.
• 🔗 查看原文

6. 炎症使骨髓成为疾病滋生的温床。

• ✍️ 作者：未知作者
• 🏷️ 关键词：inflammation
• 📝 描述：Researchers discovered that chronic inflammation fundamentally remodels the bone marrow, allowing mutated stem cell clones to quietly gain dominance with age. Reprogrammed stromal cells and interferon-responsive T cells create a self-sustaining inflammatory loop that weakens blood production. Surprisingly, the mutant cells themselves may not be the main instigators.
• 🔗 查看原文

7. 抗体新突破或将最终减缓多囊肾病的发展

• ✍️ 作者：未知作者
• 🏷️ 关键词：antibody
• 📝 描述：A specially engineered antibody that can infiltrate kidney cysts has shown the ability to block key growth signals driving polycystic kidney disease. Early mouse studies suggest it may halt or even reverse cyst expansion without harming healthy tissue.
• 🔗 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
• 刚刚发表的8.9分生信，除了识别某基因阳性细胞，识别某通路/表型阳性细胞也是发文的好思路！
• 33+生信， 识别从癌前病变到肿瘤不同恶性程度相关的细胞亚型，针对IL-33+内皮细胞促进疾病进展进行实验验证！
• 空间转录组平台怎么选？北大团队5大平台系统性测评Visium HD、Stereo-seq 、CosMx 6K、Xenium 5K
• 使用python读取疑难杂症的单细胞数据（GSM7870858）
• Cell ｜ 华大基因：Stereo-seq V2以单细胞精度重塑FFPE空间全转录宇宙
• Cell技术突破，STAMP让百万单细胞分析不是问题!
• Nature最新！寒门女博士解决国家生物信息学领域50年“卡脖子”技术！前途无量！
• 大规模血浆蛋白质组学分析！郁金泰&谭兰团队首次系统性揭示癫痫发病前血浆蛋白质的变化规律，发现103种与癫痫发病风险显着相关
• HIV感染免疫学无反应者的免疫异质性分析
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• Molecular Cell：监测线粒体翻译的复杂性与动态
• 刚刚发表的14+生信分析，识别MMP11+成纤维细胞进行分析和验证，本文思路新颖，值得认真学习模仿！
• 介绍两个生信热点发文思路
• 从只能活6个月，到生存期延长十余倍！这类肿瘤正迎来治疗曙光
• Cell：多组织器官免疫细胞图谱揭示系统免疫建立与耐受新机制
• 基于R语言的微生物组数据挖掘的最佳流程
• 新分子抗体新纪元｜BPI 2026成都站首批30+领袖就位！共筑抗体药物“第四极”强势崛起！
• 67分巨作，带你用爆火的代谢重编程实现弯道超车
• Nature Medicine：徐兵河院士/马飞教授乳腺癌大作——免疫联合节拍化疗
• 神经退行性疾病新线索：脑血管内皮TDP-43，血脑屏障的“隐形杀手”？
• Nature 背靠背：骆利群院士团队实现神经环路重编程 | 一作之一已回国加入西湖大学
• 转录因子 | Nat.Genet. | 利用scTF-seq解析转录因子剂量对细胞重编程异质性的影响
• 青岛大学×复旦大学合作Cell子刊：揭示癫痫发作相关的血浆蛋白质组
• 西湖大学×北京大学合作Nature子刊：AI从头设计蛋白，实现线粒体基因精准编辑
• 生信数据如何支撑国自然基础研究？
• 如何通过组学数据分析，挖掘国自然思路？
• 菌群移植在神经系统疾病治疗和预防中的作用机理

• GSE289049 利用基因条形码和单细胞转录组学解析食管癌前病变中前体细胞的动态变化
• GSE288193 神经元 GDF-15 递送改变外周 CD4+ T 细胞表型
• GSE282621 5-HT 再摄取阻断破坏基于基因组稳定性的蛋白质稳态，通过重塑组蛋白血清素化诱导细胞焦亡 [RNA-seq]
• GSE282619 5-HT 再摄取阻断破坏基于基因组稳定性的蛋白质稳态，通过重塑组蛋白血清素化诱导细胞焦亡 [ChIP-seq]
• GSE282082 环状RNA circTNK2 促进免疫逃逸，并可作为他莫昔芬耐药ER阳性乳腺癌的纳米治疗靶点
• GSE141341 佐剂、性别和微生物组对恒河猴SIV疫苗诱导免疫和保护效力的影响
• GSE310442 SARS-CoV-2 疫苗接种后抗原反应性 CD4 T 细胞在有或无再次刺激的情况下表现出不同的表型状态 [混合样本]
• GSE310441 SARS-CoV-2 疫苗接种后抗原反应性 CD4 T 细胞在有或无再次刺激的情况下表现出不同的表型状态 [不同样本]
• GSE310364 IL-15 中和作用可减轻脑内急性慢病毒炎症和信号传导
• GSE270194 血小板富集血浆和血小板贫乏血浆中的小细胞外囊泡主要来源于血小板，并能保护滑膜细胞免受IL-1β诱导的炎症损伤
• GSE310491 受体激酶复合物调控拟南芥形成层活性
• GSE307000 肠道巨噬细胞调节帕金森病中的脑突触核蛋白病变
• GSE302403 淡水海绵 Ephydatia muelleri 在光照和黑暗条件下发育过程中藻类内共生体的分子和空间整合
• GSE284163 自身免疫性肝炎小鼠肝脏调节性T细胞的智能RNA测序
• GSE282741 Menin抑制剂DS-1594b与Venetoclax联合使用可促进分化，并在具有MLL1和NPM1重排突变的急性髓系白血病细胞中诱导协同致死作用
• GSE272082 单核多组学揭示散发性早发性阿尔茨海默病三个脑区的调控程序
• GSE285557 新一代测序技术促进了对黑暗或蓝光处理下 B73 和 Zmcryq 突变体转录组的定量分析
• GSE310051 高渗应激诱导 3D 染色质相互作用的大规模重组 [Hi-C]
• GSE310049 高渗应激诱导 3D 染色质相互作用的大规模重组 [RNA-Seq]
• GSE309786 PNPLA3-I148M 基因变异重塑脂质代谢，驱动人类肝细胞程序性细胞死亡
• GSE309785 Tat表达对宿主转录组图谱的影响，以及细胞在潜伏期各阶段的转变
• GSE305126 Lamin A/C 调控的半胱氨酸分解代谢通量通过表观基因组重编程调节干细胞命运 [ES_RNA_seq_G609G_LA_EXP2]
• GSE304993 Lamin A/C 调控的半胱氨酸分解代谢通量通过表观基因组重编程调节干细胞命运 [ES_RNA_seq_G609G_LA_EXP1]
• GSE304972 层粘蛋白 A/C 调控的半胱氨酸分解代谢通量通过表观基因组重编程调节干细胞命运 [ES_H3K9ac_ChIP-seq]
• GSE289309 RNA-seq 分析小鼠肺内皮细胞，以研究 ENG 依赖性和 ENG 非依赖性 BMP9 诱导靶基因。
• GSE287935 CTCF 耦合长程环挤出和扩散来介导多样化的 Igk 库 [ChIP-Seq]
• GSE282121 CT26_b2m-/- 肿瘤浸润 NK (tuNK) 的单细胞水平基因表达谱，接受 IL-21 治疗或 IL-21 和 IL-15 联合治疗。
• GSE281737 独特的DNA甲基化特征可能无法特异性地表征不同遗传变异中的BLBS
• GSE278999 层粘蛋白 A/C 调控的半胱氨酸分解代谢通量通过表观基因组重编程调节干细胞命运 [ES_ChIP_seq_H3K9ac_H3K27ac_LA]
• GSE278998 Lamin A/C 调控的半胱氨酸分解代谢通量通过表观基因组重编程调节干细胞命运 [ES_ChIP_seq_H3K9me3_LA]
• GSE249274 尼非林通过调节多种信号通路改善高血压引起的心脏重塑——心脏
• GSE248534 层粘蛋白A/C调控的半胱氨酸分解代谢通量通过表观基因组重编程调节干细胞命运
• GSE248533 Lamin A/C 调控的半胱氨酸分解代谢通量通过表观基因组重编程调节干细胞命运 [04scRNA_seq_D10]
• GSE248530 Lamin A/C 调控的半胱氨酸分解代谢通量通过表观基因组重编程调节干细胞命运 [bulkPolyA_RNA_seq_LA_ES]
• GSE248421 USP51-GRP78轴通过调节ABCB1的活性促进三阴性乳腺癌细胞对阿霉素的耐药性。