详细内容（前10条）

1. ⭐ GSE267166 CSF1R 抑制剂联合化疗可诱导三阴性乳腺癌的全身抗肿瘤免疫反应，并通过缓解驻留记忆 T 细胞功能障碍使肿瘤对 PD-1 抑制剂疗法更加敏感 [淋巴结]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immune、lymph、T cell、regex:lymph(o|atic)?
• 📝 描述：Contributors : Hope S Rugo ; Amanda Poissonnier ; Eivind V Egeland ; Wesley Horton ; Tiziana Cotechini ; Brian Ruffell ; Cecil Gomes ; Shamilene Sivagnanam ; Nicky Belen ; Dhaarini Murugan ; Nell Kirchberger ; Courtney Betts ; Motomi Mori ; Shivaani Kummar ; K Blackwell ; E Mayer ; Shelley E Hwang ; Lisa M CoussensSeries Type : OtherOrganism : Mus musculusTriple-negative breast cancer (TNBC) is a heterogeneous and aggressive disease where limited therapeutic options are available. A significant correlation exists between presence of intratumoral macrophages, tumor progression, and poor outcomes in TNBC. Preclinical in vivo studies revealed that inhibition of myelomonocytic colony stimulating factor 1 (CSF1) or its receptor (CSF1R), plus cytotoxic therapy decreases primary tumor growth kinetics and pulmonary metastases by CD8+ T cell-dependent mechanisms. To evaluate safety and tolerability of this immune-based therapeutic strategy, we conducted a phase Ib/II clinical trial evaluating Pexidartinib (PLX3397), a small molecule CSF1R inhibitor plus Eribulin chemotherapy in patients with heavily pretreated metastatic TNBC. Correlate analyses from baseline revealed increased leukocyte activation biomarkers, increased presence of CD8+ and CD4+ T central memory cells, and increased PD-1 expression on CD4+ T cells in patients experiencing a partial response or stable disease, together providing evidence of enhanced anti-tumor immunity. We hypothesized that addition of either PD-1 and PD-L1-blockade following CSF1R inhibition and chemotherapy would lead to a further enhanced anti-tumor T cell response. To test this, we evaluated tumor-bearing MMTV-PyMT transgenic mice comparing addition of PD-1- or PD-L1-blockade to Pexidartinib/Paclitaxel therapy. This revealed tumor regression in ~60% of transgenic mice with combined PD-1, but not PD-L1-blockade. Analysis of mammary tumors from mice treated with the PD-1 combination revealed activation and expansion of short-lived effector and memory T cells, and unique clonally-expanded T cells not observed with the PD-L1-blockade combination. These clinical and preclinical findings together provide rationale for addition of CSF1/CSF1R inhibitors to chemotherapy and PD-1-blocakde to further improve outcomes for patients with BC.
• 🔗 查看原文

2. ⭐ GSE267169 CSF1R 抑制剂联合化疗可诱导三阴性乳腺癌的全身抗肿瘤免疫反应，并通过缓解驻留记忆 T 细胞功能障碍使肿瘤对 PD-1 抑制剂疗法更加敏感 [nanostring]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immune、T cell
• 📝 描述：Contributors : Hope S Rugo ; Amanda Poissonnier ; Eivind V Egeland ; Wesley Horton ; Tiziana Cotechini ; Brian Ruffell ; Cecil Gomes ; Shamilene Sivagnanam ; Nicky Belen ; Dhaarini Murugan ; Nell Kirchberger ; Courtney Betts ; Motomi Mori ; Shivaani Kummar ; K Blackwell ; E Mayer ; Shelley Hwang ; Lisa CoussensSeries Type : Expression profiling by arrayOrganism : Mus musculusTriple-negative breast cancer (TNBC) is a heterogeneous and aggressive disease where limited therapeutic options are available. A significant correlation exists between presence of intratumoral macrophages, tumor progression, and poor outcomes in TNBC. Preclinical in vivo studies revealed that inhibition of myelomonocytic colony stimulating factor 1 (CSF1) or its receptor (CSF1R), plus cytotoxic therapy decreases primary tumor growth kinetics and pulmonary metastases by CD8+ T cell-dependent mechanisms. To evaluate safety and tolerability of this immune-based therapeutic strategy, we conducted a phase Ib/II clinical trial evaluating Pexidartinib (PLX3397), a small molecule CSF1R inhibitor plus Eribulin chemotherapy in patients with heavily pretreated metastatic TNBC. Correlate analyses from baseline revealed increased leukocyte activation biomarkers, increased presence of CD8+ and CD4+ T central memory cells, and increased PD-1 expression on CD4+ T cells in patients experiencing a partial response or stable disease, together providing evidence of enhanced anti-tumor immunity. We hypothesized that addition of either PD-1 and PD-L1-blockade following CSF1R inhibition and chemotherapy would lead to a further enhanced anti-tumor T cell response. To test this, we evaluated tumor-bearing MMTV-PyMT transgenic mice comparing addition of PD-1- or PD-L1-blockade to Pexidartinib/Paclitaxel therapy. This revealed tumor regression in ~60% of transgenic mice with combined PD-1, but not PD-L1-blockade. Analysis of mammary tumors from mice treated with the PD-1 combination revealed activation and expansion of short-lived effector and memory T cells, and unique clonally-expanded T cells not observed with the PD-L1-blockade combination. These clinical and preclinical findings together provide rationale for addition of CSF1/CSF1R inhibitors to chemotherapy and PD-1-blocakde to further improve outcomes for patients with BC.
• 🔗 查看原文

3. ⭐ GSE267168 CSF1R 抑制剂联合化疗可诱导三阴性乳腺癌的全身抗肿瘤免疫反应，并通过缓解驻留记忆 T 细胞功能障碍使肿瘤对 PD-1 抑制剂疗法更加敏感 [luminex]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immune、T cell
• 📝 描述：Contributors : Hope S Rugo ; Amanda Poissonnier ; Eivind V Egeland ; Wesley Horton ; Tiziana Cotechini ; Brian Ruffell ; Cecil Gomes ; Shamilene Sivagnanam ; Nicky Belen ; Dhaarini Murugan ; Nell Kirchberger ; Courtney Betts ; Motomi Mori ; Shivaani Kummar ; K Blackwell ; E Mayer ; Shelley Hwang ; Lisa CoussensSeries Type : Protein profiling by protein arrayOrganism : Homo sapiensTriple-negative breast cancer (TNBC) is a heterogeneous and aggressive disease where limited therapeutic options are available. A significant correlation exists between presence of intratumoral macrophages, tumor progression, and poor outcomes in TNBC. Preclinical in vivo studies revealed that inhibition of myelomonocytic colony stimulating factor 1 (CSF1) or its receptor (CSF1R), plus cytotoxic therapy decreases primary tumor growth kinetics and pulmonary metastases by CD8+ T cell-dependent mechanisms. To evaluate safety and tolerability of this immune-based therapeutic strategy, we conducted a phase Ib/II clinical trial evaluating Pexidartinib (PLX3397), a small molecule CSF1R inhibitor plus Eribulin chemotherapy in patients with heavily pretreated metastatic TNBC. Correlate analyses from baseline revealed increased leukocyte activation biomarkers, increased presence of CD8+ and CD4+ T central memory cells, and increased PD-1 expression on CD4+ T cells in patients experiencing a partial response or stable disease, together providing evidence of enhanced anti-tumor immunity. We hypothesized that addition of either PD-1 and PD-L1-blockade following CSF1R inhibition and chemotherapy would lead to a further enhanced anti-tumor T cell response. To test this, we evaluated tumor-bearing MMTV-PyMT transgenic mice comparing addition of PD-1- or PD-L1-blockade to Pexidartinib/Paclitaxel therapy. This revealed tumor regression in ~60% of transgenic mice with combined PD-1, but not PD-L1-blockade. Analysis of mammary tumors from mice treated with the PD-1 combination revealed activation and expansion of short-lived effector and memory T cells, and unique clonally-expanded T cells not observed with the PD-L1-blockade combination. These clinical and preclinical findings together provide rationale for addition of CSF1/CSF1R inhibitors to chemotherapy and PD-1-blocakde to further improve outcomes for patients with BC.
• 🔗 查看原文

4. ⭐ GSE267167 CSF1R 抑制剂联合化疗可诱导三阴性乳腺癌的全身抗肿瘤免疫反应，并通过缓解驻留记忆 T 细胞功能障碍使肿瘤对 PD-1 抑制剂疗法更加敏感 [肿瘤]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immune、T cell
• 📝 描述：Contributors : Hope S Rugo ; Amanda Poissonnier ; Eivind V Egeland ; Wesley Horton ; Tiziana Cotechini ; Brian Ruffell ; Cecil Gomes ; Shamilene Sivagnanam ; Nicky Belen ; Dhaarini Murugan ; Nell Kirchberger ; Courtney Betts ; Motomi Mori ; Shivaani Kummar ; K Blackwell ; E Mayer ; Shelley E Hwang ; Lisa M CoussensSeries Type : OtherOrganism : Mus musculusTriple-negative breast cancer (TNBC) is a heterogeneous and aggressive disease where limited therapeutic options are available. A significant correlation exists between presence of intratumoral macrophages, tumor progression, and poor outcomes in TNBC. Preclinical in vivo studies revealed that inhibition of myelomonocytic colony stimulating factor 1 (CSF1) or its receptor (CSF1R), plus cytotoxic therapy decreases primary tumor growth kinetics and pulmonary metastases by CD8+ T cell-dependent mechanisms. To evaluate safety and tolerability of this immune-based therapeutic strategy, we conducted a phase Ib/II clinical trial evaluating Pexidartinib (PLX3397), a small molecule CSF1R inhibitor plus Eribulin chemotherapy in patients with heavily pretreated metastatic TNBC. Correlate analyses from baseline revealed increased leukocyte activation biomarkers, increased presence of CD8+ and CD4+ T central memory cells, and increased PD-1 expression on CD4+ T cells in patients experiencing a partial response or stable disease, together providing evidence of enhanced anti-tumor immunity. We hypothesized that addition of either PD-1 and PD-L1-blockade following CSF1R inhibition and chemotherapy would lead to a further enhanced anti-tumor T cell response. To test this, we evaluated tumor-bearing MMTV-PyMT transgenic mice comparing addition of PD-1- or PD-L1-blockade to Pexidartinib/Paclitaxel therapy. This revealed tumor regression in ~60% of transgenic mice with combined PD-1, but not PD-L1-blockade. Analysis of mammary tumors from mice treated with the PD-1 combination revealed activation and expansion of short-lived effector and memory T cells, and unique clonally-expanded T cells not observed with the PD-L1-blockade combination. These clinical and preclinical findings together provide rationale for addition of CSF1/CSF1R inhibitors to chemotherapy and PD-1-blocakde to further improve outcomes for patients with BC.
• 🔗 查看原文

5. ⭐ GSE267165 CSF1R 抑制剂联合化疗可诱导三阴性乳腺癌的全身抗肿瘤免疫反应，并通过缓解驻留记忆 T 细胞功能障碍使肿瘤对 PD-1 抑制剂疗法更加敏感 [肺]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immune、T cell
• 📝 描述：Contributors : Hope S Rugo ; Amanda Poissonnier ; Eivind V Egeland ; Wesley Horton ; Tiziana Cotechini ; Brian Ruffell ; Cecil Gomes ; Shamilene Sivagnanam ; Nicky Belen ; Dhaarini Murugan ; Nell Kirchberger ; Courtney Betts ; Motomi Mori ; Shivaani Kummar ; K Blackwell ; E Mayer ; Shelley E Hwang ; Lisa M CoussensSeries Type : OtherOrganism : Mus musculusTriple-negative breast cancer (TNBC) is a heterogeneous and aggressive disease where limited therapeutic options are available. A significant correlation exists between presence of intratumoral macrophages, tumor progression, and poor outcomes in TNBC. Preclinical in vivo studies revealed that inhibition of myelomonocytic colony stimulating factor 1 (CSF1) or its receptor (CSF1R), plus cytotoxic therapy decreases primary tumor growth kinetics and pulmonary metastases by CD8+ T cell-dependent mechanisms. To evaluate safety and tolerability of this immune-based therapeutic strategy, we conducted a phase Ib/II clinical trial evaluating Pexidartinib (PLX3397), a small molecule CSF1R inhibitor plus Eribulin chemotherapy in patients with heavily pretreated metastatic TNBC. Correlate analyses from baseline revealed increased leukocyte activation biomarkers, increased presence of CD8+ and CD4+ T central memory cells, and increased PD-1 expression on CD4+ T cells in patients experiencing a partial response or stable disease, together providing evidence of enhanced anti-tumor immunity. We hypothesized that addition of either PD-1 and PD-L1-blockade following CSF1R inhibition and chemotherapy would lead to a further enhanced anti-tumor T cell response. To test this, we evaluated tumor-bearing MMTV-PyMT transgenic mice comparing addition of PD-1- or PD-L1-blockade to Pexidartinib/Paclitaxel therapy. This revealed tumor regression in ~60% of transgenic mice with combined PD-1, but not PD-L1-blockade. Analysis of mammary tumors from mice treated with the PD-1 combination revealed activation and expansion of short-lived effector and memory T cells, and unique clonally-expanded T cells not observed with the PD-L1-blockade combination. These clinical and preclinical findings together provide rationale for addition of CSF1/CSF1R inhibitors to chemotherapy and PD-1-blocakde to further improve outcomes for patients with BC.
• 🔗 查看原文

6. ⭐ GSE267164 CSF1R 抑制剂联合化疗可诱导三阴性乳腺癌的全身抗肿瘤免疫反应，并通过缓解驻留记忆 T 细胞功能障碍使肿瘤对 PD-1 抑制剂疗法更加敏感 [血液]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immune、T cell
• 📝 描述：Contributors : Hope S Rugo ; Amanda Poissonnier ; Eivind V Egeland ; Wesley Horton ; Tiziana Cotechini ; Brian Ruffell ; Cecil Gomes ; Shamilene Sivagnanam ; Nicky Belen ; Dhaarini Murugan ; Nell Kirchberger ; Courtney Betts ; Motomi Mori ; Shivaani Kummar ; K Blackwell ; E Mayer ; Shelley E Hwang ; Lisa M CoussensSeries Type : OtherOrganism : Mus musculusTriple-negative breast cancer (TNBC) is a heterogeneous and aggressive disease where limited therapeutic options are available. A significant correlation exists between presence of intratumoral macrophages, tumor progression, and poor outcomes in TNBC. Preclinical in vivo studies revealed that inhibition of myelomonocytic colony stimulating factor 1 (CSF1) or its receptor (CSF1R), plus cytotoxic therapy decreases primary tumor growth kinetics and pulmonary metastases by CD8+ T cell-dependent mechanisms. To evaluate safety and tolerability of this immune-based therapeutic strategy, we conducted a phase Ib/II clinical trial evaluating Pexidartinib (PLX3397), a small molecule CSF1R inhibitor plus Eribulin chemotherapy in patients with heavily pretreated metastatic TNBC. Correlate analyses from baseline revealed increased leukocyte activation biomarkers, increased presence of CD8+ and CD4+ T central memory cells, and increased PD-1 expression on CD4+ T cells in patients experiencing a partial response or stable disease, together providing evidence of enhanced anti-tumor immunity. We hypothesized that addition of either PD-1 and PD-L1-blockade following CSF1R inhibition and chemotherapy would lead to a further enhanced anti-tumor T cell response. To test this, we evaluated tumor-bearing MMTV-PyMT transgenic mice comparing addition of PD-1- or PD-L1-blockade to Pexidartinib/Paclitaxel therapy. This revealed tumor regression in ~60% of transgenic mice with combined PD-1, but not PD-L1-blockade. Analysis of mammary tumors from mice treated with the PD-1 combination revealed activation and expansion of short-lived effector and memory T cells, and unique clonally-expanded T cells not observed with the PD-L1-blockade combination. These clinical and preclinical findings together provide rationale for addition of CSF1/CSF1R inhibitors to chemotherapy and PD-1-blocakde to further improve outcomes for patients with BC.
• 🔗 查看原文

7. ⭐ GSE294715 The membrane-associated ubiquitin ligase MARCHF8 promotes cancer immune evasion by degrading MHC class I proteins

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、MHC
• 📝 描述：Contributors : Mohamed I. Khalil ; Jie Wang ; Canchai Yang ; Lexi Vu ; Smriti Chadha ; Harrison Nabors ; Daniel Vocelle ; Danielle May ; Kyle Roux ; Matthew Bernard ; Qing-Sheng Mi ; Dohun PyeonSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe current immunotherapy is effective, but many cancer patients do not respond. The loss of major histocompatibility complex class I (MHC-I) molecules has been proposed as a mechanism by which cancer cells evade tumor-specific T cells in Immune Checkpoint Inhibitor (ICI)-refractory patients. Nevertheless, how cancer cells downregulate MHC-I is poorly understood. We report here that membrane-associated RING-CH-type finger 8 (MARCHF8), upregulated by human papillomavirus (HPV), ubiquitinates and degrades MHC-I proteins in HPV-positive head and neck cancer (HPV+ HNC). MARCHF8 knockdown restores MHC-I levels on HPV+ HNC cells. We further reveal that Marchf8 knockout significantly suppresses tumor growth and increases the infiltration of natural killer (NK) and T cells in the tumor microenvironment (TME). Furthermore, Marchf8 knockout markedly increases the cytotoxic NK cells and CD8+ T cells and their crosstalk with macrophages and enhances the tumor cell-killing activity of CD8+ T cells. CD8+ T cell depletion in mice abrogates Marchf8 knockout-driven tumor suppression and NK and T cell infiltration. Interestingly, Marchf8 knockout, in combination with anti-PD-1 treatment, synergistically suppresses tumor growth in mice bearing ICI-refractory tumors. Taken together, our finding suggests that MARCHF8 could be a promising target for novel immunotherapy for HPV+ HNC patients.
• 🔗 查看原文

8. ⭐ GSE244561 AtDEK2, a dual histone mark reader regulates plant immunity [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、RNA-seq、histone
• 📝 描述：Contributors : Hanna Alhoraibi ; Santiago Alejandro-Martinez ; David Latrasse ; Papita Mandal ; Léa Faivre ; Deborah Manza ; Xiaoning HE ; Aala A Abulfaraj ; Siba Alharbi ; Kiruthiga Mariappan ; Olga Artyukh ; Fatimah Abdulhakim ; Fatimah Aljedaani ; Stefan David ; Marilia Almeida-Trapp ; Jean Bigeard ; Delphine Pflieger ; Wolfgang Fischle ; Stefan Arold ; Jean Colcombet ; Daniel Schubert ; Moussa Benhamed ; Ikram Blilou ; Heribert Hirt ; Naganand RayapuramSeries Type : Expression profiling by high throughput sequencingOrganism : Arabidopsis thalianaArabidopsis DEK2, a nuclear protein involved in multiple chromatin-related processes, was found to be phosphorylated in response to flg22 treatment suggesting a role in plant immunity to bacterial pathogens. dek2 loss of function mutants were susceptible to bacterial as well as fungal pathogens. Transcriptome data of the dek2-1 mutant shows that AtDEK2 is a transcriptional repressor of defense related genes, hormone synthesis & signaling genes. ChIP-Seq analysis indicates that DEK2 binds to motifs of several families of transcription factors (TFs) and to class I TCP binding motif regions with the highest affinity. We determined that DEK2 is recruited to specific regions on the chromatin by transcription factors. Our data suggests that DEK2 is a reader of the dual histone mark, H3K4me3K27me3. Finally, based on our data we postulate a hypothetical working model for the function of DEK2 as a transcriptional repressor and targets regions with H3K4me3K27me3 marks.
• 🔗 查看原文

9. ⭐ GSE310424 全转录组图谱揭示铂类抗癌药物的 RNA 依赖性机制 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq、transcriptome
• 📝 描述：Contributors : Sreejith Nair ; Arun Krishnaraj ; Richi ThakralSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensClinically used small molecules has been predicted to off-target to RNAs. However, the extend of this interaction is small molecule cancer therapeutics has not been characterized. Here, we screened for anticancer smalll molecules for their RNA interactions and uncovered widespread RNA off-targeting. Cisplatin was found to be one among the RNA binders. We used it as a model agent to identify the specific transcripts it interact with. To accomplish this, we developed Plat-RNAseq, a click-chemistry-mediated transcriptome-wide assay. Our results revealed that cisplatin binding was enriched at guanine-rich regions capable of forming RNA G-quadruplexes (rG4s) .We found that the recruitment of cisplatin to rG4s partially contributed to its cytotoxicity, revealing a noncanonical mechanism of action for this widely used chemotherapeutic agent. RNA seq was performed to catalogue all non-ribosomal RNAs present in A2780 cells.
• 🔗 查看原文

10. ⭐ GSE310419 全转录组图谱揭示铂类抗癌药物的 RNA 依赖性机制 [Plat-RNAseq cPDS]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNAseq、transcriptome
• 📝 描述：Contributors : Sreejith Nair ; Weiyi Guo ; Richi ThakralSeries Type : OtherOrganism : Homo sapiensClinically used small molecules has been predicted to off-target to RNAs. However, the extend of this interaction is small molecule cancer therapeutics has not been characterized. Here, we screened for anticancer smalll molecules for their RNA interactions and uncovered widespread RNA off-targeting. Cisplatin was found to be one among the RNA binders. We used it as a model agent to identify the specific transcripts it interact with. We developed Plat-RNAseq, a click-chemistry-mediated transcriptome-wide assay to map transcriptome-wide interaction of cisplatin. Our results revealed that cisplatin binding was enriched at guanine-rich regions capable of forming RNA G-quadruplexes (rG4s). We use an rG4 ligand, carboxy-Pyridostatin (cPDS), to block access of platin-drug to rG4. This experiment test whether cPDS blocked platinum drug accumulation on cellular RNAs.
• 🔗 查看原文

💡 该来源还有 60 条内容，详见 文末

详细内容（全部6条）

1. ⭐ 新的单细胞转录组时钟揭示了 COVID-19 和 HIV 中 T 细胞的内在和系统性衰老

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、T cell、single-cell
• 📝 描述：Using RNA sequencing at single-cell resolution, researchers developed Tictock to distinguish intrinsic and systemic T cell aging, revealing accelerated immune aging in COVID-19 and…
• 🔗 查看原文

2. ⭐ 科学家改造细菌，使其从内部吞噬癌细胞肿瘤。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、bacteria、regex:bacter(ia|ial|ium)
• 📝 描述：Researchers are engineering bacteria to invade tumors and consume them from the inside. Because tumor cores lack oxygen, they’re the perfect breeding ground for these microbes. The team added a genetic tweak that helps the bacteria survive longer near oxygen-exposed edges — but only once enough of them are present to trigger the change. It’s a carefully programmed biological attack that could one day offer a new way to destroy cancer.
• 🔗 查看原文

3. 简单的血液检测可以在记忆丧失前数年预测阿尔茨海默病。

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：Scientists have created a blood test that can estimate when Alzheimer’s symptoms are likely to begin. By measuring a protein called p-tau217, the model predicts symptom onset within roughly three to four years. The protein mirrors the silent buildup of amyloid and tau in the brain long before memory loss appears. This advance could speed up preventive drug trials and eventually guide personalized care.
• 🔗 查看原文

4. 科学家研发出一种通用鼻喷疫苗，可预防新冠病毒、流感和肺炎。

• ✍️ 作者：未知作者
• 🏷️ 关键词：vaccine
• 📝 描述：Scientists at Stanford Medicine have unveiled a bold new kind of “universal” vaccine that could one day protect against everything from COVID-19 and the flu to bacterial pneumonia and even common allergens. Instead of targeting a specific virus or bacterium, the nasal spray vaccine supercharges the lungs’ own immune defenses, keeping them on high alert for months. In mice, it slashed viral levels, prevented severe illness, and even blocked allergic reactions.
• 🔗 查看原文

5. 美国一项大型研究发现，核电站附近癌症死亡率较高。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：A sweeping nationwide study has found that U.S. counties located closer to operating nuclear power plants have higher cancer death rates than those farther away. Researchers analyzed data from every nuclear facility and all U.S. counties between 2000 and 2018, adjusting for income, education, smoking, obesity, environmental conditions, and access to health care. Even after accounting for those factors, cancer mortality was higher in communities nearer to nuclear plants, particularly among older adults.
• 🔗 查看原文

6. 科学家逆转了小鼠的肌肉衰老，并发现了一个令人惊讶的现象。

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging
• 📝 描述：A UCLA study in mice reveals that aging muscle stem cells accumulate a protein that slows repair but boosts survival. This protein, NDRG1, acts like a brake, preventing cells from activating quickly after injury. When researchers blocked it in older mice, muscle healing sped up dramatically — but stem cells became less resilient over time. The work suggests aging may reflect a survival trade-off rather than straightforward decline.
• 🔗 查看原文

• GSE310416 全转录组图谱揭示铂类抗癌药物的 RNA 依赖性机制 [Plat-RNAseq A549]
• GSE309934 全转录组图谱揭示铂类抗癌药物的 RNA 依赖性机制 [ChIP-seq]
• GSE309812 全转录组图谱揭示铂类抗癌药物的 RNA 依赖性机制 [Plat-RNAseq A2780]
• GSE314812 克隆演化分歧和肿瘤微环境重塑塑造胃癌腹膜转移
• GSE320007 溶瘤病毒疗法和铂类化疗协同作用，通过靶向激活化疗持续存在的旁观者 CD8+ T 细胞来增强抗肿瘤免疫力 [scRNA-seq]
• GSE300820 羊绒生长过程中次级毛囊干细胞的全基因组组蛋白修饰 [ChIP-Seq]
• GSE320254 靶向 RNase H2：一种提高三阴性乳腺癌复制压力、DNA 损伤和抗肿瘤免疫的双重机制策略
• GSE310425 全转录组图谱揭示铂类抗癌药物的 RNA 依赖性机制
• GSE310421 全转录组图谱揭示铂类抗癌药物的 RNA 依赖性机制 [CUT&TAG]
• GSE310413 全转录组图谱揭示铂类抗癌药物的 RNA 依赖性机制 [RIP-seq]
• GSE290685 对从小鼠脾脏中分离的 PDX（患者来源的异种移植）肿瘤进行单细胞 RNA 测序分析，这些肿瘤分别用空载 CAR、抗 CD72 H24 nanoCAR 或抗 CD72 NbD4.13 nanoCAR 治疗。
• GSE290380 RNA-seq 分析：布里奥斯他汀治疗后人 SC1 淋巴瘤细胞系的变化
• GSE310931 C9orf72 六核苷酸重复 RNA 通过全基因组混合 G-四链体驱动转录失调 [RNA-Seq]
• GSE310928 C9orf72 六核苷酸重复 RNA 通过全基因组混合 G-四链体驱动转录失调 [ChIP-Seq]
• GSE310926 C9orf72 六核苷酸重复 RNA 通过全基因组混合 G-四链体驱动转录失调 [ATAC-Seq]
• GSE310849 老年大鼠骨骼肌反复废用性萎缩（RNA-seq / 转录组）
• GSE310344 成人骨骼肌反复废用性萎缩（RNA-seq / 转录组）
• GSE300821 羊绒生长过程中次级毛囊干细胞的转录组分析 [RNA-Seq]
• GSE290340 dsRNA 病毒的病毒转录调节因子通过操纵宿主共转录因子 DHX9 来拮抗先天免疫反应 [RNA-Seq]
• GSE290339 dsRNA 病毒的病毒转录调节因子通过操纵宿主共转录因子 DHX9 来拮抗先天免疫反应 [ChIP-Seq]
• GSE290327 RNA-seq 分析晚期尿路上皮癌对顺铂和吉西他滨化疗的反应：外部验证队列
• GSE288223 整合轨迹推断和自解释预测模型，以单细胞分辨率探索乳腺癌细胞状态转变
• GSE271982 组蛋白乙酰化依赖的BRD2聚集指导转录动力学
• GSE320213 揭示 linc00645：一种 Wnt 调控的 lncRNA 通过 linc00645/miR-452-5p/波形蛋白轴驱动三阴性乳腺癌的上皮-间质转化
• GSE309448 印度医院中氟康唑耐药性热带念珠菌的多因素唑类耐药性、广泛出现和克隆传播
• GSE299614 CBP-IDRs 调控乙酰化和基因表达 [RNA-Seq]
• GSE296518 Prevotella intermedia culture supernatant impairs alveolar macrophage function and promotes Mycobacterium avium persistence
• GSE281802 The metabolic signature of inflammatory skin-imprinted eosinophils accounts for the chronicity of Leishmania mexicana infections [Day50]
• GSE281715 The metabolic signature of inflammatory skin-imprinted eosinophils accounts for the chronicity of Leishmania mexicana infections [Day14]
• GSE280638 Polycomb Repressive Complex 1 Primes Non-Growing Oocytes for Growth and Early Embryogenesis [RNA-Seq]
• GSE274186 Maternal antibodies orchestrate the establishment of salivary and oral mucosal immunity
• GSE268266 CBP-IDRs regulate acetylation and gene expression [ChIP-Seq]
• GSE240512 Profiling of MCM2 and phosphorylated MCM2 in MLL3/4 double mutant and control ESCs [ChIP-seq]
• GSE213213 Human pluripotent stem cell–derived A10 dopaminergic neurons specifically integrate into host circuits and relieve depression [scRNA-seq]
• GSE315332 滋养层干细胞定向分化为牛胎盘发育的有用体外模型 [RNA-Seq]
• GSE314723 滋养层干细胞定向分化为牛胎盘发育的有用体外模型 [scRNA-seq]
• GSE309225 LMO2-LDB1-TAL1复合物调控AML中的转录网络[ChIP-Seq]
• GSE292624 分离的人类脑类器官在微电极阵列上发育形成神经元网络
• GSE267255 利用单细胞多组学对人类 cDC2 稳态成熟程序进行多维度表征
• GSE267253 通过单细胞RNA测序鉴定人类cDC2稳态成熟程序
• GSE262835 新鲜血小板分离术人血小板和冻干血小板（血栓小体）的 RNA 测序
• GSE115819 IL2Ra依赖性B细胞受体及其致癌模拟物的反馈控制
• GSE320238 致命性结核分枝杆菌播散发生在淋巴细胞缺失的情况下，且与先天免疫反应无关
• GSE314843 雄性小鼠条件性 Phf2 敲除腓肠肌骨骼肌转录组分析
• GSE293503 年轻野生型和Klotho KO雄性小鼠肾脏和脑组织样本的单核RNA测序
• GSE292885 转录组学特征揭示了衰老、慢性疾病和返老还童的普遍和特异性机制
• 来自 ITP 研究的暴露于各种化合物的 UM-HET3 小鼠肝脏样本的 GSE292884 RNA 测序
• GSE292843 野生型和Klotho基因敲除雄性小鼠肾脏和骨骼肌样本的RNA测序
• GSE290665 雄性小鼠条件性 Phf2 敲除腓肠肌骨骼肌转录组分析
• GSE290611：雄性小鼠条件性Phf2敲除小鼠腓肠肌和比目鱼肌的转录组分析
• GSE239775 通过基因评分量化全身炎症揭示急性失代偿期肝硬化的相关特征
• GSE320035 RNA-seq 分析秀丽隐杆线虫液体诱导休眠（LISA）
• GSE319827 驯化二粒小麦（Triticum turgidum subsp. dicoccum）对小麦颖枯病菌（Zymosptoria tritici）和禾柄锈菌（Puccinia graminis）单一感染与混合感染反应的转录组分析
• GSE319822 RNA-seq 分析小鼠脊髓挫伤后经丁香素治疗
• GSE310939 C9orf72 六核苷酸重复 RNA 通过全基因组混合 G-四链体驱动转录失调 [ChIRP-seq]
• GSE310934 C9orf72 六核苷酸重复 RNA 通过全基因组混合 G-四链体驱动转录失调 [DRIP-seq]
• GSE310932 C9orf72 六核苷酸重复 RNA 通过全基因组混合 G-四链体驱动转录失调 [MeDIP-Seq]
• GSE310930 C9orf72 六核苷酸重复 RNA 通过全基因组混合 G-四链体驱动转录失调 [RAP]
• GSE310004 来自双链RNA病毒的病毒转录调节因子通过操纵宿主共转录因子DHX9来拮抗先天免疫反应
• GSE275136 ERV衍生RNA-DNA杂交体上调C4b诱导自闭症小胶质细胞突触修剪[ChIP-seq]