详细内容（前10条）

1. ⭐ GSE298394 受饮食信号驱动的肠道驻留T-bet表达Tr1细胞主导小肠免疫环境 IV

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、gut、regex:gut(-?microbiome)?、regex:intestin(e|al)
• 📝 描述：Contributors : Eduard Ansaldo ; Daniel Yong ; Nathan Carrillo ; Taryn McFadden ; Mahnoor Abid ; Dan Corral ; Claudia Rivera ; Taylor Farley ; Nicolas Bouladoux ; Inta Gribonika ; Yasmine BelkaidSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusIntestinal immunity provides defense against enteric pathogens, mediates symbiotic relationships with the resident microbiota, and provides tolerance to food antigens, safeguarding critical nutrient absorption and barrier functions of this mucosal tissue. Despite the large abundance of tissue resident activated T cells, how T cell immunity contributes to these various roles remains poorly understood. Here we describe a previously uncharacterized dominant T-bet expressing Tr1 T cell population in the small intestine lamina propria present at homeostasis. Importantly, this IL-10 secreting CD4^+^T-bet^+^ T cell population appears in the small intestine at the time of weaning independently of the resident microbiota, presenting similar accumulation, functional capacity, and TCR repertoire in germ free conditions. Instead, small intestinal T-bet^+^ Tr1 T cells respond to dietary signals driving their accumulation, suppressive program, and clonal selection; and depend on cDC1s, IL-27 signaling, and T-bet, but not IL-12. Altogether, this work uncovers a previously unappreciated dominant player in homeostatic small intestinal immunity with the potential to play critical suppressive roles in oral tolerance to dietary antigens, raising important implications for the understanding of food allergy and celiac disease.
• 🔗 查看原文

2. ⭐ GSE298386 受饮食信号驱动的肠道驻留T-bet表达Tr1细胞主导小肠免疫环境 III

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、gut、regex:gut(-?microbiome)?、regex:intestin(e|al)
• 📝 描述：Contributors : Eduard Ansaldo ; Daniel Yong ; Nathan Carrillo ; Taryn McFadden ; Mahnoor Abid ; Dan Corral ; Claudia Rivera ; Taylor Farley ; Nicolas Bouladoux ; Inta Gribonika ; Yasmine BelkaidSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusIntestinal immunity provides defense against enteric pathogens, mediates symbiotic relationships with the resident microbiota, and provides tolerance to food antigens, safeguarding critical nutrient absorption and barrier functions of this mucosal tissue. Despite the large abundance of tissue resident activated T cells, how T cell immunity contributes to these various roles remains poorly understood. Here we describe a previously uncharacterized dominant T-bet expressing Tr1 T cell population in the small intestine lamina propria present at homeostasis. Importantly, this IL-10 secreting CD4^+^T-bet^+^ T cell population appears in the small intestine at the time of weaning independently of the resident microbiota, presenting similar accumulation, functional capacity, and TCR repertoire in germ free conditions. Instead, small intestinal T-bet^+^ Tr1 T cells respond to dietary signals driving their accumulation, suppressive program, and clonal selection; and depend on cDC1s, IL-27 signaling, and T-bet, but not IL-12. Altogether, this work uncovers a previously unappreciated dominant player in homeostatic small intestinal immunity with the potential to play critical suppressive roles in oral tolerance to dietary antigens, raising important implications for the understanding of food allergy and celiac disease.
• 🔗 查看原文

3. ⭐ GSE298374 受饮食信号驱动的肠道驻留T-bet表达Tr1细胞主导小肠免疫环境 II

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、gut、regex:gut(-?microbiome)?、regex:intestin(e|al)
• 📝 描述：Contributors : Eduard Ansaldo ; Daniel Yong ; Nathan Carrillo ; Taryn McFadden ; Mahnoor Abid ; Dan Corral ; Claudia Rivera ; Taylor Farley ; Nicolas Bouladoux ; Inta Gribonika ; Yasmine BelkaidSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusIntestinal immunity provides defense against enteric pathogens, mediates symbiotic relationships with the resident microbiota, and provides tolerance to food antigens, safeguarding critical nutrient absorption and barrier functions of this mucosal tissue. Despite the large abundance of tissue resident activated T cells, how T cell immunity contributes to these various roles remains poorly understood. Here we describe a previously uncharacterized dominant T-bet expressing Tr1 T cell population in the small intestine lamina propria present at homeostasis. Importantly, this IL-10 secreting CD4^+^T-bet^+^ T cell population appears in the small intestine at the time of weaning independently of the resident microbiota, presenting similar accumulation, functional capacity, and TCR repertoire in germ free conditions. Instead, small intestinal T-bet^+^ Tr1 T cells respond to dietary signals driving their accumulation, suppressive program, and clonal selection; and depend on cDC1s, IL-27 signaling, and T-bet, but not IL-12. Altogether, this work uncovers a previously unappreciated dominant player in homeostatic small intestinal immunity with the potential to play critical suppressive roles in oral tolerance to dietary antigens, raising important implications for the understanding of food allergy and celiac disease.
• 🔗 查看原文

4. ⭐ GSE298371 受饮食信号驱动的肠道驻留T-bet表达Tr1细胞主导小肠免疫环境 I

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、gut、regex:gut(-?microbiome)?、regex:intestin(e|al)
• 📝 描述：Contributors : Eduard Ansaldo ; Daniel Yong ; Nathan Carrillo ; Taryn McFadden ; Mahnoor Abid ; Dan Corral ; Claudia Rivera ; Taylor Farley ; Nicolas Bouladoux ; Inta Gribonika ; Yasmine BelkaidSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusIntestinal immunity provides defense against enteric pathogens, mediates symbiotic relationships with the resident microbiota, and provides tolerance to food antigens, safeguarding critical nutrient absorption and barrier functions of this mucosal tissue. Despite the large abundance of tissue resident activated T cells, how T cell immunity contributes to these various roles remains poorly understood. Here we describe a previously uncharacterized dominant T-bet expressing Tr1 T cell population in the small intestine lamina propria present at homeostasis. Importantly, this IL-10 secreting CD4^+^T-bet^+^ T cell population appears in the small intestine at the time of weaning independently of the resident microbiota, presenting similar accumulation, functional capacity, and TCR repertoire in germ free conditions. Instead, small intestinal T-bet^+^ Tr1 T cells respond to dietary signals driving their accumulation, suppressive program, and clonal selection; and depend on cDC1s, IL-27 signaling, and T-bet, but not IL-12. Altogether, this work uncovers a previously unappreciated dominant player in homeostatic small intestinal immunity with the potential to play critical suppressive roles in oral tolerance to dietary antigens, raising important implications for the understanding of food allergy and celiac disease.
• 🔗 查看原文

5. ⭐ GSE293372 嵌合抗原受体协调肿瘤抗原摄取和树突状细胞活化。[RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、dendritic cell、antigen、RNA-seq
• 📝 描述：Contributors : Nadine Fournier ; Yahya Mohammadzadeh ; Michele De PalmaSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusEffective anti-tumor immunity requires dendritic cells (DCs) to internalize, process and present tumor antigens to T cells. Adoptive transfer of DCs loaded ex vivo with tumor antigens has been shown to stimulate anti-tumor immunity in patients with cancer, but clinical responses have been mixed. To address limitations of traditional DC-based therapies, we constructed and functionally screened a panel of chimeric antigen receptors (CARs) optimized for expression and activity in DCs. Through this screening, we identified key functional components that informed the design of an inducible platform centered on an instructive chimeric antigen receptor (iCAR). This platform enables the DCs to (i) recognize a surface molecule present on cancer cells or their extracellular vesicles (EVs), such as GD2 and HER2, thereby promoting the acquisition of tumor-derived material that contains putative tumor antigens; (ii) undergo immunostimulatory activation to prime antigen-specific T cells via both cross-dressing and cross-presentation; and (iii) transactivate the expression of a therapeutic gene (IL-12) in response to antigen uptake. The iCAR converted melanoma-derived EVs from immune-suppressive to stimulatory cues for DCs. Moreover, systemic administration of iCAR-DCs enhanced antigen-specific T cells, expanded low-frequency T cell clonotypes, and delayed tumor growth in immunotherapy-resistant melanoma models without the need for ex vivo antigen loading or cell maturation. iCAR-DCs provide a platform for antigen-agnostic cancer immunotherapy that integrates antigen uptake with programmable DC activation.
• 🔗 查看原文

6. ⭐ GSE305725 卡罗莱纳子宫内膜癌患者的阴道和肠道微生物组试点研究

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、gut、regex:gut(-?microbiome)?
• 📝 描述：Contributors : Hazel B Nichols ; Mu JinSeries Type : OtherOrganism : metagenomeCharacterization of the microbiome in vaginal and stool samples self-sampled from endometrial cancer survivors enrolled in the Carolina Endometrial Cancer Study.
• 🔗 查看原文

7. ⭐ GSE300199 赖氨酸去甲基酶 Kdm4C 是一种致癌驱动因子，并调节 KRAS 突变胰腺导管腺癌中的 ERK 活性 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：regex:onco(logy|logist|gene|genic)、ChIP-seq、KRAS
• 📝 描述：Contributors : Mennatallah Shaheen ; Sarah Dhebat ; Kimal I Rajapakshe ; Bidyut Ghosh ; Benson C Selvanesan ; Shariq Ansari ; Cara Haymaker ; Dorsay Sadeghian ; Huamin Wang ; Haoqiang Ying ; Anirban MaitraSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensDeregulation of proteins involved in chromatin regulation is common in pancreatic ductal adenocarcinoma (PDAC). Lysine demethylase 4C (Kdm4C) is one of the chromatin-modifying proteins frequently overexpressed across multiple solid cancers and is linked to chromatin instability, increased cell proliferation, and enhanced stem cell-like behavior. We observed upregulation of Kdm4C protein in a panel of human PDAC cell lines and patient samples compared to non-neoplastic controls. CRISPR/Cas9-mediated deletion of KDM4C in human and murine PDAC cells reduced proliferation, clonogenicity and increased survival of orthotopically implanted murine PDAC allografts. Transcriptomic and proteomics analyses revealed that loss of Kdm4C in both human and murine PDAC cell lines was associated with reduction of activated phospho-Erk, a pivotal effector downstream of mutant Ras. Using proximity labeling, we identified the histone deacetylase SIRT1 as a novel interacting protein with Kdm4C via the latter’s Tudor reader domain. SIRT1-mediated deacetylation leads to repression of downstream targets, including the dual specificity phosphatase DUSP2, which is known to inactivate Erk via dephosphorylation. In vitro propagation of KDM4C-null PDAC lines eventually led to adaptation and restitution of Erk signaling via compensatory upregulation of other KDM4 family members. To bypass this genetic compensation, we tested a preclinical pan-KDM4 inhibitor TACH107 and confirmed its efficacy in in vitro and in vivo PDAC models including those resistant to the covalent KRASG12D inhibitor MTRX1133. Our studies identify Kdm4C as an oncogenic molecule that sustains Erk signaling in KRAS-mutant PDAC and can be broadly targeted via small molecule inhibitors.
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8. ⭐ GSE300083 赖氨酸去甲基酶 Kdm4C 是一种致癌驱动因子，并调节 KRAS 突变胰腺导管腺癌中的 ERK 活性 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：regex:onco(logy|logist|gene|genic)、RNA-seq、KRAS
• 📝 描述：Contributors : Mennatallah Shaheen ; Sarah Dhebat ; Kimal I Rajapakshe ; Bidyut Ghosh ; Benson C Selvanesan ; Shariq Ansari ; Cara Haymaker ; Dorsay Sadeghian ; Huamin Wang ; Haoqiang Ying ; Anirban MaitraSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensDeregulation of proteins involved in chromatin regulation is common in pancreatic ductal adenocarcinoma (PDAC). Lysine demethylase 4C (Kdm4C) is one of the chromatin-modifying proteins frequently overexpressed across multiple solid cancers and is linked to chromatin instability, increased cell proliferation, and enhanced stem cell-like behavior. We observed upregulation of Kdm4C protein in a panel of human PDAC cell lines and patient samples compared to non-neoplastic controls. CRISPR/Cas9-mediated deletion of KDM4C in human and murine PDAC cells reduced proliferation, clonogenicity and increased survival of orthotopically implanted murine PDAC allografts. Transcriptomic and proteomics analyses revealed that loss of Kdm4C in both human and murine PDAC cell lines was associated with reduction of activated phospho-Erk, a pivotal effector downstream of mutant Ras. Using proximity labeling, we identified the histone deacetylase SIRT1 as a novel interacting protein with Kdm4C via the latter’s Tudor reader domain. SIRT1-mediated deacetylation leads to repression of downstream targets, including the dual specificity phosphatase DUSP2, which is known to inactivate Erk via dephosphorylation. In vitro propagation of KDM4C-null PDAC lines eventually led to adaptation and restitution of Erk signaling via compensatory upregulation of other KDM4 family members. To bypass this genetic compensation, we tested a preclinical pan-KDM4 inhibitor TACH107 and confirmed its efficacy in in vitro and in vivo PDAC models including those resistant to the covalent KRASG12D inhibitor MTRX1133. Our studies identify Kdm4C as an oncogenic molecule that sustains Erk signaling in KRAS-mutant PDAC and can be broadly targeted via small molecule inhibitors.
• 🔗 查看原文

9. ⭐ GSE310031 肠道菌群促进母胎界面免疫耐受

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、gut、regex:gut(-?microbiome)?
• 📝 描述：Contributors : Julia A Brown ; Mohammed Amir ; Shui Yu ; Daniel S Wong ; Jinghua Gu ; Uthra Balaji ; Christopher Parkhurst ; Seunghee Hong ; Lucy R Hart ; Hannah C Carrow ; Mamadou Bah ; Aparna Ananthanarayanan ; Katherine Z Sanidad ; Mengze Lyu ; Anisa Siddikova ; Marina Lima Silva Santos ; Inna Serganova ; Gretchen E Diehl ; Josef Anrather ; Naohiro Inohara ; Gregory F Sonnenberg ; Virginia Pascual ; Melody Y ZengSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusImmune tolerance at the maternal-fetal interface is required for fetal development. Excessive maternal interferon gamma (IFNγ) and interleukin-17 (IL-17) is linked to pregnancy complications, but the regulation of maternal IFNγ and IL-17 at the maternal-fetal interface (MFI) is poorly understood. Here we demonstrate a gut-placenta immune axis in pregnant mice in which the absence or perturbation of gut microbiota dysregulates maternal IFNγ and IL-17 responses at the MFI, resulting in fetal resorption. Microbiota-dependent tryptophan derivatives suppress IFNγ+ and IL-17+ T cells at the MFI by priming myeloid-derived suppressor cells (MDSCs) and gut-derived RORγt+ Tregs, respectively. The tryptophan derivative indole-3-carbinol, or tryptophan-metabolizing Lactobacillus murinus, rebalances the T cell response at the MFI and reduces fetal resorption in germ-free mice. Furthermore, MDSCs, RORγt+ Tregs, and microbiota-dependent tryptophan derivatives are dysregulated at the MFI in human recurrent miscarriage cases. Together, our findings identify microbiota-dependent immune tolerance mechanisms that promote fetal development.
• 🔗 查看原文

10. ⭐ GSE293373 嵌合抗原受体协调肿瘤抗原摄取和树突状细胞活化。[TCR-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、dendritic cell、antigen
• 📝 描述：Contributors : Nadine Fournier ; Rachel Marcone ; Yahya Mohammadzadeh ; Michele De PalmaSeries Type : OtherOrganism : Mus musculusEffective anti-tumor immunity requires dendritic cells (DCs) to internalize, process and present tumor antigens to T cells. Adoptive transfer of DCs loaded ex vivo with tumor antigens has been shown to stimulate anti-tumor immunity in patients with cancer, but clinical responses have been mixed. To address limitations of traditional DC-based therapies, we constructed and functionally screened a panel of chimeric antigen receptors (CARs) optimized for expression and activity in DCs. Through this screening, we identified key functional components that informed the design of an inducible platform centered on an instructive chimeric antigen receptor (iCAR). This platform enables the DCs to (i) recognize a surface molecule present on cancer cells or their extracellular vesicles (EVs), such as GD2 and HER2, thereby promoting the acquisition of tumor-derived material that contains putative tumor antigens; (ii) undergo immunostimulatory activation to prime antigen-specific T cells via both cross-dressing and cross-presentation; and (iii) transactivate the expression of a therapeutic gene (IL-12) in response to antigen uptake. The iCAR converted melanoma-derived EVs from immune-suppressive to stimulatory cues for DCs. Moreover, systemic administration of iCAR-DCs enhanced antigen-specific T cells, expanded low-frequency T cell clonotypes, and delayed tumor growth in immunotherapy-resistant melanoma models without the need for ex vivo antigen loading or cell maturation. iCAR-DCs provide a platform for antigen-agnostic cancer immunotherapy that integrates antigen uptake with programmable DC activation.
• 🔗 查看原文

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1. ⭐ Durvalumab 单独及与 Tremelimumab 或 Bevacizumab 联合治疗不可切除肝细胞癌的 T 细胞受体与免疫基因表达药效学

• ✍️ 作者：未知作者
• 🏷️ 关键词：免疫、T细胞、B细胞、单细胞
• 📝 描述：Secret hovertext: 目的：在 I/II 期第 22（NCT02519348）试验中，STRIDE（单次特雷美单抗常规间期 Durvalumab）的客观缓解率为 24.0%，durvalumab 加 bevacizumab（D+B）21.3%，durvalumab（D）单用治疗为 11.5%，适用于不可切除肝细胞癌（uHCC）。增殖率增加的 CD8+ T 细胞与 STRIDE 单用治疗相比 D 单用治疗的疗效提升相关。本研究分析了外周血中 T 细胞克隆扩增和基因表达特征（GES）的变化，以探讨 STRIDE 和 D+B 单用治疗抗癌活性的作用机制。患者及方法：组组参与者为 uHCC 且无免疫检查点抑制剂治疗的参与者。从基线及第一轮治疗周期结束时采集的外周血中分离出 DNA 和 RNA。测量了治疗组间 T 细胞克隆性和 GES 基线值及基线变化，并评估了与放射学反应的关联。结果：治疗组间 T 细胞的基线丰富度或辛普森克隆性方面无显著差异。STRIDE
• 🔗 查看原文

2. ⭐ 脂质代谢重编程在塑造肿瘤免疫微环境中的多重作用

• ✍️ 作者：未知作者
• 🏷️ 关键词：肿瘤、免疫、免疫微环境、代谢
• 📝 描述：Secret hovertext: 脂质代谢重编程调节肿瘤微环境（TME），并改变免疫细胞的功能，包括肿瘤浸润淋巴细胞（TILs）。虽然脂质可以增强整体 T 细胞活性，但 TME 中高脂质含量可能抑制效应 T 细胞的抗肿瘤功能，并增强调控 T 细胞的免疫抑制作用。此外，脂质代谢重编程极大影响 TILs 与 TME 中其他免疫细胞之间的交互作用，包括树突状细胞、巨噬细胞和骨髓系来源的抑制细胞。通过讨论针对 TILs 脂质代谢的潜在治疗策略，以及化疗免疫疗法、纳米医学和采纳细胞移植疗法的联合方法，我们旨在为癌症患者有效治疗的推进奠定基础。
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3. ⭐ BRUIN 313 和 314 试验为非共价布鲁顿酪氨酸激酶抑制作为慢性淋巴细胞白血病的初始治疗打开了大门。

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

4. ⭐ BRUIN CLL-313：皮托布替尼与苯达莫司汀加利妥昔单抗在未治疗慢性淋巴细胞白血病/小淋巴细胞淋巴瘤患者中的随机 III 期试验。

• ✍️ 作者：未知作者
• 🏷️ 关键词：淋巴、B细胞、单细胞
• 📝 描述：Secret hovertext: 目的 BRUIN CLL-313 是一项随机、开放标签、全球三期临床试验，比较了高选择性非共价布鲁替尼（BTKi）与苯达莫司汀加利妥昔单抗（Bendamustine plus rituximab，一种常见的一线化疗免疫疗法）在治疗经验未受的慢性淋巴细胞白血病/小淋巴细胞淋巴瘤（CLL/SLL）患者中的疗效和安全性。方法 未治疗 CLL/SLL 且无 del（17p）的患者被随机 1：1 随机分配为持续吡托布鲁替尼单用药物或 BendaR，按免疫球蛋白重链基因突变状态和 Rai 分层。主要终点为独立评审委员会（IRC）评估的无进展生存期（PFS）;次要终点包括总体生存期（OS）、研究者评估的 PFS、安全性和耐受性。结果总体而言，282 名患者被随机分配接受吡托布鲁替尼（n=141）或苯达 R（n=141）。IRC 评估的 PFS 在吡布鲁替尼与 BendaR 治疗下显著改善（风险比[HR]，0
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5. ⭐ 大 B 细胞淋巴瘤一线治疗后循环肿瘤 DNA 可测量残留疾病的前瞻性验证

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

6. 针对癌症免疫治疗的吞噬检查点。

• ✍️ 作者：未知作者
• 🏷️ 关键词：癌症、免疫
• 📝 描述：Secret hovertext: 巨噬细胞通过吞噬作用消灭癌细胞的能力受到促吞噬和抑制性吞噬受体的严格控制。促吞噬受体如 Fc 受体、巨噬细胞 1 抗原（MAC-1;也称为 CD11b/CD18）和信号传导淋巴细胞激活分子家族成员 7（SLAMF7）已被证明在临床前模型中促进肿瘤细胞的消除，而 Fc 受体已被认定对临床上多种单克隆抗体的抗肿瘤疗效至关重要。临床前和早期临床研究还强调，阻断抑制性吞噬检查点，尤其是信号调控蛋白α（SIRPα）及其配体 CD47，是癌症治疗的有前景方法。然而，近期临床试验中对有限疗效和毒性的担忧导致对该方法的热情减弱。本综述探讨了支持吞噬检查点作为癌症治疗靶点的证据，同时强调了该治疗策略当前面临的挑战。我们还提出了提升该方法在未来工作中有效性和安全性的建议。
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7. 关注表达：佐剂腺病毒介导单纯疱疹病毒胸苷激酶给药可改善晚期肝细胞癌患者的肝移植效果。

• ✍️ 作者：未知作者
• 🏷️ 关键词：激酶、单细胞
• 📝 描述：Secret hovertext:
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8. Drp1 与 BIP 的相互作用维持线粒体动态平衡，促进鼻咽癌中 Anoikis 的耐药性和转移

• ✍️ 作者：未知作者
• 🏷️ 关键词：线粒体、耐药
• 📝 描述：Secret hovertext: Anoikis 耐药性是指细胞在锚固无关条件下存活的现象，这对癌细胞的传播和转移至关重要。为寻找克服 anoikis 耐药性的策略，我们采用了结合蛋白质组筛选的 3D 悬浮培养模型，发现了类似 dynamin 的蛋白 Drp1 与鼻咽癌（NPC）中 anoikis 耐药性的关系。Drp1 通过调控裂变和线粒体吞噬，促进新线粒体的生成和损伤线粒体的清除，从而使肿瘤细胞能够克服异眼体。此外，在阿诺伊基斯耐药性期间，Drp1 与 BIP 的相互作用增强，这促进了线粒体相关内质网膜（MAMs）的形成，以维持线粒体动态平衡。从机制上看，CaMKKβ通过 O-GlcNAcylation 修饰激活 AMPK-MFF-Drp1 和 AMPK-mTOR-Drp1 通路，从而招募 Drp1 到 MAMs 中。值得注意的是，Drp1-BIP 复合物作为 NPC 临床结局和转移风险的预后指标。综合来看，这些结果阐明了
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9. 对免疫疗法治疗实体肿瘤中 ctDNA 动态的超灵敏分析的广泛应用

• ✍️ 作者：未知作者
• 🏷️ 关键词：肿瘤、免疫
• 📝 描述：Secret hovertext: 目的：先前研究表明，血浆来源 ctDNA 在接受免疫检查点抑制剂治疗的癌症患者中具有生物标志物潜力。本研究探讨了 ctDNA 在接受免疫疗法治疗的晚期癌症患者队列中预测无进展和总体生存的能力。实验设计：为了表征超灵性 ctDNA 检测在这些患者管理中的潜在作用，我们进行了肿瘤全基因组测序——知情的超灵敏 ctDNA 分析——在回顾性队列（n=136）和前瞻性验证队列（n=66）中，涵盖 24 种癌症类型，均仅使用免疫检查点抑制剂或双特异性抗体或免疫性免疫药物治疗细胞联动者。结果：分析 1455 个纵向样本，我们发现 ctDNA 分子反应在治疗开始后 3 周内测量，与无进展期和总体生存期的改善相关，而任何时候的 ctDNA 清除率与放射反应和延长生存期高度相关。此外，ctDNA 动力学区分了真实进展与伪进展，并预测了接受初期进展后持续免疫治疗患者的结局。结论：本研究强调了超敏感 ctDNA
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10. 接受 PD-1/L1 抗体及联合抗病毒预防药物治疗的肝细胞癌患者 HBV 再活化：前瞻性观察性研究

• ✍️ 作者：未知作者
• 🏷️ 关键词：抗体
• 📝 描述：Secret hovertext: 目的：肝细胞癌（HCC）中免疫检查点抑制剂（ICIs）相关试验因 HBV 再活化对 HBV DNA 负荷有严格限制。本研究旨在比较接受 ICI 和抗病毒治疗的低或高 HBV DNA 负荷 HCC 患者的 HBV 再活化情况。患者与方法：本前瞻性观察性研究（NCT04680598）招募了接受联合抗病毒治疗并进行 ICI 治疗的 HBsAg 阳性 HCC 患者。参与者被分为 HBV DNA 低组（≤500 IU/ml）组和 HBV DNA 高组（> 500 IU/ml 组）。主要终点是 HBV 的再激活率。结果：2020 年 12 月 25 日至 2024 年 2 月 23 日期间，356 至 659 名参与者被分组为 HBV DNA 低组和高组。HBV DNA 高组中，HBeAg 阳性患者比例显著较高（24.1%对 7.0%，p < 0.001）、ALBI 等级 2-3（49.9%对 33.7%，p
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💡 该来源还有 9 条内容，详见 文末

详细内容（全部4条）

1. ⭐ 用于单细胞长读长测序的生物信息学框架：解锁异构体水平分辨率

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell、bioinformatics
• 📝 描述：New long-read RNA sequencing methods capture full-length transcripts at single-cell resolution, revealing isoform diversity, cell-type specific splicing and roles in health and disease…
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2. 利用伪批量方法控制单细胞RNA测序中的噪声

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell
• 📝 描述：Removing unwanted variation improves accuracy in pseudobulk single-cell RNA sequencing, enhancing differential expression analysis and controlling false discoveries across challenging experimental conditions…
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3. 一种预防牙龈疾病而不破坏有益菌的新方法

• ✍️ 作者：未知作者
• 🏷️ 关键词：bacteria、regex:bacter(ia|ial|ium)
• 📝 描述：Scientists are uncovering a surprising way to influence bacteria—not by killing them, but by changing how they communicate. Researchers studying oral bacteria found that disrupting chemical signals used in bacterial “conversations” can shift dental plaque toward healthier, less harmful communities. The discovery could open the door to new treatments that prevent disease by maintaining a balanced microbiome rather than wiping bacteria out entirely.
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4. 结肠癌在年轻人中发病率激增，医生们对此感到担忧。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Cases of colorectal cancer in younger adults are climbing worldwide, driven by lifestyle changes and inherited genetic risks. Diet, obesity, and lack of early screening are playing a major role in this shift. New genetic tests offer hope for earlier detection, but access and awareness lag behind. Health experts say urgent action is needed to reverse the trend.
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• GSE266100 通过嵌合抗原受体协调肿瘤抗原摄取和树突状细胞活化。
• GSE300200 赖氨酸去甲基酶 Kdm4C 是一种致癌驱动因子，并在 KRAS 突变型胰腺导管腺癌中调节 ERK 活性
• GSE289850 犬淋巴瘤病例全血细胞的全基因组亚硫酸氢盐测序
• GSE314028 早期 NAD⁺ 缺乏通过表观遗传下调透明质酸合成来调控骨骼肌衰老
• GSE307561 Dis3l2 介导的 RNA 监视和细胞外囊泡包装可防止异常细胞 RNA 激活先天免疫 [RNA-seq]
• GSE303185 下丘脑室旁细胞类型的空间和投影转录组图谱（10X Chromium v​​3）
• GSE303083 下丘脑室旁细胞类型的空间和投影转录组图谱（10X Chromium v​​3 多重分析）
• GSE291833 基于转录组学的肝细胞癌筛选和新型化合物
• GSE313929 B细胞受体类别转换对淋巴瘤细胞的影响
• GSE313548 小于胎龄儿追赶性生长过程中代谢特征的多组学分析及HBEGF介导的代谢调控机制验证
• GSE313218 缺氧增强的足蛋白定义的肿瘤可塑性驱动CCR7介导的乳腺癌淋巴转移
• GSE311637 PHF8 在神经发生过程中对丝氨酸生物合成的表观遗传调控 [ChIP-Seq H3K9me3]
• GSE308660 斯瓦尔巴岩雷鸟光周期时间测量相关组织中VA视蛋白转录本变体的差异表达
• GSE283228 工程化去核间充质干细胞调节免疫微环境并促进伤口愈合
• GSE229124 上皮细胞WNT分泌驱动胃癌的微环境逃逸
• GSE312125 体内 CRISPR 筛选鉴定出 SAGA 复合物成员是造血的关键调节因子 [scRNA]
• GSE311765 体内筛选揭示了 Hippo 通路组分在发育和再生中的特定作用
• GSE311378 利用 Trikine 免疫疗法从细胞表面重塑 STAT 信号通路 [IL21 Trikine 的 RNA 测序]
• GSE309905 PTEN 调节迷走神经-胰岛素信号传导以优化自主神经输出，从而决定外周炎症和代谢稳态
• GSE307560 Dis3l2 介导的 RNA 监视和细胞外囊泡包装可防止异常细胞 RNA 激活先天免疫 [miRNA-Seq]
• GSE307559 Dis3l2 介导的 RNA 监视和细胞外囊泡包装可防止异常细胞 RNA 激活先天免疫 [TGIRT-seq]
• GSE307558 Dis3l2 介导的 RNA 监视和细胞外囊泡包装可防止异常细胞 RNA 激活先天免疫 [THP TGIRT-seq]
• GSE303256 下丘脑室旁细胞类型的空间和投影转录组图谱
• GSE303082 下丘脑室旁细胞类型的空间和投影转录组图谱 (DroNc-Seq)
• GSE303081 下丘脑室旁细胞类型的空间和投影转录组图谱（Smart-Seq2）
• GSE303080 下丘脑室旁核细胞类型的空间和投影转录组图谱（Drop-Seq）
• GSE291190 基于转录组学的特发性肺纤维化药物再利用筛选
• GSE274297 NADS 基因敲除小鼠骨骼肌的综合转录组分析。
• GSE313882 通过酵母代谢工程阐明南非醉茄中醉茄内酯生物合成相关的基因簇
• GSE277188 解码脂肪细胞分化和去分化中的 YAP/TAZ–PPARγ 调控轴 [ChIP-seq]
• GSE252503 解码 YAP/TAZ–PPARγ 调控轴在脂肪细胞分化和去分化中的作用 [ATAC-Seq]
• GSE248364 解码 YAP/TAZ–PPARγ 调控轴在脂肪细胞分化和去分化中的作用 [RNA-Seq]
• GSE313585 Lcariin 通过促进 TFEB 依赖性线粒体清除和代谢重编程来改善运动引起的疲劳
• GSE313312 通过捕获和修复纳米药物恢复小胶质细胞溶酶体稳态治疗阿尔茨海默病
• GSE313250 糖皮质激素-Fas轴控制转移播散过程中的免疫逃逸 [CUT&Run_4T1-Dex]
• GSE313249 糖皮质激素-Fas轴控制转移播散过程中的免疫逃逸 [RNAseq_4T1-tdTomato]
• GSE313245 糖皮质激素-Fas轴控制转移播散过程中的免疫逃逸 [scRNAseq_4T1-GFPThy11]
• GSE313243 糖皮质激素-Fas 轴控制转移播种期间的免疫逃避 [scRNAseq_4T1-tdTomato-cTAT-zsGreen]。
• GSE313241 糖皮质激素-Fas轴控制转移播散过程中的免疫逃逸 [RNAseq_4T1-GFP]
• GSE313045 通过CBP/p300抑制实现默克尔细胞癌的药理学逆转
• GSE308512 ALFQ佐剂HIV-1包膜蛋白疫苗可在非人灵长类动物中诱导持久的功能性抗体和细胞反应
• GSE296528 神经发生过程中PHF8对丝氨酸生物合成的表观遗传调控
• GSE284762 艾滋病毒感染者肠道屏障受损的恢复能力
• GSE284761 HIV感染者肠道屏障受损对破坏的恢复能力[回肠]
• GSE284755 HIV感染者肠道屏障受损对破坏的恢复能力[结肠]

• 一个让患者和公众参与基础癌症研究的新框架。
• N6-Methyladenosine：作为癌症中枢调控因子的 RNA 修饰。
• 感知歧视和社会人口学对乳腺癌症状负担中种族差异的潜在作用。
• 高级泌尿系统癌症共识会议（AUC3）2025：关于肾细胞癌和尿路癌管理的专家共识
• 介入肿瘤学：临床医生关于消融和栓塞在实体肿瘤中作用的入门指南
• 晚期泌尿癌症的共识与争议：2025 年高级泌尿系统癌症共识会议（AUC3）的见解
• 2008-2017 年非洲、亚洲、拉丁美洲和加勒比地区儿童癌症存活率（SURVCAN-3）：一项基于人口的基准研究，涵盖 16,821 名儿童。
• 三维癌症成像中的实际权衡
• 弥合癌症鸿沟：美国公平的政策与结构性解决方案