详细内容（前10条）

1. ⭐ GSE309664 线粒体DNA耗竭神经元细胞的全局转录组变化揭示了阿尔茨海默病相关通路的变化

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer、Neuronal、pathway
• 📝 描述：Contributors : Blaise W Menta ; Emily Schueddig ; Amol Ranjan ; Yanming Li ; Heather M Wilkins ; Dong Pei ; Russell H SwerdlowSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBackground: Mitochondrial dysfunction, a prominent feature of Alzheimer’s disease (AD), could represent a cause or consequence of the disease. Objective: We determined the extent to which mitochondrial dysfunction due to mitochondrial DNA (mtDNA) depletion induces transcription changes that link to AD phenomena. Methods: We performed a transcriptomic survey of human neuronal SH SY5Y and NTERA 2/NT2 mtDNA-depleted (ρ0) and intact (ρ+) cell lines. Differentially expressed genes (DEGs) between SH-SY5Y or NT2 ρ0 and ρ+ cells were identified using edgeR, and we used the Equivalent Change Index (ECI) approach to quantify concordant DEG behavior across the cell lines. Gene set enrichment and over representation analysis (GSEA; ORA) were used to determine impact on the KEGG Alzheimer’s and other neurodegenerative disease pathways, ascertain pathway and term enrichment in the Reactome and Gene Ontology databases, and generate activation z-scores in the Ingenuity Pathway Analysis (IPA) database. Results: Relative to their ρ+ comparators, ρ0 lines differentially expressed >75% of their genes, and >20% more than doubled or halved expression. The KEGG Alzheimer’s pathway was significantly enriched, and ECI-identified genes ranked the Alzheimer’s, Parkinson’s, ALS, and Huntington’s KEGG pathways among the most enriched gene sets. There was broad enrichment of pathways and terms relating to AD phenomena, which reflected lipid, insulin signaling, inflammation/immune response, synapse, endosome/endocytosis, RNA, and proteostasis biology. Conclusion: In neuronal cell lines, mitochondrial dysfunction due to mtDNA depletion alters gene expression in ways that recapitulate or predictably promote AD molecular phenomena.
• 🔗 查看原文

2. ⭐ GSE308273 合成齐墩果烷三萜类化合物可抑制肿瘤生长并促进抗肿瘤免疫反应，且该作用独立于癌症KEAP1突变状态

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immune
• 📝 描述：Contributors : Christopher J Occhiuto ; Jessica A Moerland ; Karen T Liby ; Ana S LealSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusKEAP1 negatively regulates the cytoprotective factor NRF2 and is commonly inactivated in lung cancer cells. Loss of function KEAP1 mutations in cancer cells contribute to NRF2 activation and tumor immune evasion through immunosuppression and drug resistance. Counterintuitively, treatment with synthetic oleanane triterpenoids, potent NRF2 activa-tors, reduces preclinical tumor burden. This suggests the functional target of these drugs in cancer models is not the cancer cells but another tumor immune microenvironment (TIME) cell population. The anti-tumor potential of cells within the TIME, particularly macrophages, is potentiated by triterpenoid treatment in cancers with wild-type KEAP1 status. As KEAP1-mutant cancers show reduced tumor immune responses, triterpenoid-mediated immune stimulation may particularly benefit these cases, but this has not been investigated. To characterize the immunomodulatory effects of triterpenoids in KEAP1-mutant lung cancer, we studied tumor-educated bone marrow-derived macrophages (TE-BMDMs) and lung cancer models treated with the triterpenoids CDDO-Me or omaveloxolone. RNA-sequencing of TE-BMDMs cultured in KEAP1 KO compared to WT cancer-conditioned media had enhanced tumor-promoting phenotypes which reversed with CDDO-Me treatment. Similarly, subcutaneous KEAP1 KO tumors were larger and more immune-suppressed compared to WT tumors. Both CDDO-Me and omaveloxolone reduced tumor burden and improved immune cell phenotypes within the TIME, independent of KEAP1 mutational status.
• 🔗 查看原文

3. ⭐ GSE308945 组蛋白甲基转移酶 KMT2D 是去势抵抗性前列腺癌谱系可塑性和治疗反应的关键介质 [FOSL1 ChIP-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、ChIP-seq、histone
• 📝 描述：Contributors : Eneda Toska ; Wouter Karthaus ; Srushti Kittane ; Erik Ladewig ; Taibo Li ; Yangzhenyu GaoSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensCastration-resistant prostate cancer (CRPC) is largely dependent on the androgen receptor (AR) for growth and often exhibits hyperactive PI3K signaling, most frequently due to PTEN loss. Therapeutic pressure from anti-AR therapies can induce trans-differentiation toward an AR-independent phenotype. Recently, different subtypes of AR-independent CRPC have been redefined, with the stem cell-like (SCL) subtype emerging as one of the most prevalent. Elucidation of the epigenetic mechanisms controlling the maintenance of these distinct CRPC cell states could pave the way for effective combinatorial therapies for CRPC. In this study, we identified a key role for the histone methyltransferase KMT2D in establishing the chromatin competence necessary for the recruitment of AR and FOXA1 transcription factors (TFs) that are essential for the AR transcriptional output in AR-dependent CRPC cell lines, patient derived organoids, and patient samples. Unexpectedly, KMT2D maintained the identity of the AR-low CRPC-SCL subtype and controlled activity of AP-1 TFs such as FOSL1, which acts as a master regulator of this subtype. Single cell transcriptomics and chromatin assays underscored the role of KMT2D in sustaining a mixed lineage cell state via AP-1 and FOXA1. The combined suppression of PI3K/AKT and KMT2D reduced cell proliferation in prostate cancer cells and patient-derived organoids in both CRPC-AR and CRPC-SCL subtypes. Altogether, these results unveil KMT2D as a major mediator of the epigenetic landscape in subtype-specific CRPC, contributing to tumor growth and therapeutic response.
• 🔗 查看原文

4. ⭐ GSE296116 组蛋白甲基转移酶 KMT2D 是去势抵抗性前列腺癌谱系可塑性和治疗反应的关键介质 [MSKPCA3 Bulk RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq、histone
• 📝 描述：Contributors : Eneda Toska ; Wouter Karthaus ; Srushti Kittane ; Erik Ladewig ; Taibo LiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensCastration-resistant prostate cancer (CRPC) is largely dependent on the androgen receptor (AR) for growth and often exhibits hyperactive PI3K signaling, most frequently due to PTEN loss. Therapeutic pressure from anti-AR therapies can induce trans-differentiation toward an AR-independent phenotype. Recently, different subtypes of AR-independent CRPC have been redefined, with the stem cell-like (SCL) subtype emerging as one of the most prevalent. Elucidation of the epigenetic mechanisms controlling the maintenance of these distinct CRPC cell states could pave the way for effective combinatorial therapies for CRPC. In this study, we identified a key role for the histone methyltransferase KMT2D in establishing the chromatin competence necessary for the recruitment of AR and FOXA1 transcription factors (TFs) that are essential for the AR transcriptional output in AR-dependent CRPC cell lines, patient derived organoids, and patient samples. Unexpectedly, KMT2D maintained the identity of the AR-low CRPC-SCL subtype and controlled activity of AP-1 TFs such as FOSL1, which acts as a master regulator of this subtype. Single cell transcriptomics and chromatin assays underscored the role of KMT2D in sustaining a mixed lineage cell state via AP-1 and FOXA1. The combined suppression of PI3K/AKT and KMT2D reduced cell proliferation in prostate cancer cells and patient-derived organoids in both CRPC-AR and CRPC-SCL subtypes. Altogether, these results unveil KMT2D as a major mediator of the epigenetic landscape in subtype-specific CRPC, contributing to tumor growth and therapeutic response.
• 🔗 查看原文

5. ⭐ GSE296115 组蛋白甲基转移酶 KMT2D 是去势抵抗性前列腺癌谱系可塑性和治疗反应的关键介质 [LNCaP Bulk RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq、histone
• 📝 描述：Contributors : Eneda Toska ; Wouter Karthaus ; Srushti Kittane ; Erik Ladewig ; Taibo LiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensCastration-resistant prostate cancer (CRPC) is largely dependent on the androgen receptor (AR) for growth and often exhibits hyperactive PI3K signaling, most frequently due to PTEN loss. Therapeutic pressure from anti-AR therapies can induce trans-differentiation toward an AR-independent phenotype. Recently, different subtypes of AR-independent CRPC have been redefined, with the stem cell-like (SCL) subtype emerging as one of the most prevalent. Elucidation of the epigenetic mechanisms controlling the maintenance of these distinct CRPC cell states could pave the way for effective combinatorial therapies for CRPC. In this study, we identified a key role for the histone methyltransferase KMT2D in establishing the chromatin competence necessary for the recruitment of AR and FOXA1 transcription factors (TFs) that are essential for the AR transcriptional output in AR-dependent CRPC cell lines, patient derived organoids, and patient samples. Unexpectedly, KMT2D maintained the identity of the AR-low CRPC-SCL subtype and controlled activity of AP-1 TFs such as FOSL1, which acts as a master regulator of this subtype. Single cell transcriptomics and chromatin assays underscored the role of KMT2D in sustaining a mixed lineage cell state via AP-1 and FOXA1. The combined suppression of PI3K/AKT and KMT2D reduced cell proliferation in prostate cancer cells and patient-derived organoids in both CRPC-AR and CRPC-SCL subtypes. Altogether, these results unveil KMT2D as a major mediator of the epigenetic landscape in subtype-specific CRPC, contributing to tumor growth and therapeutic response.
• 🔗 查看原文

6. ⭐ GSE293211 组蛋白甲基转移酶 KMT2D 是去势抵抗性前列腺癌谱系可塑性和治疗反应的关键介质 [MSKPCA2 Bulk RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq、histone
• 📝 描述：Contributors : Eneda Toska ; Wouter Karthaus ; Srushti Kittane ; Erik Ladewig ; Taibo Li ; Wanlu ChenSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensCastration-resistant prostate cancer (CRPC) is largely dependent on the androgen receptor (AR) for growth and often exhibits hyperactive PI3K signaling, most frequently due to PTEN loss. Therapeutic pressure from anti-AR therapies can induce trans-differentiation toward an AR-independent phenotype. Recently, different subtypes of AR-independent CRPC have been redefined, with the stem cell-like (SCL) subtype emerging as one of the most prevalent. Elucidation of the epigenetic mechanisms controlling the maintenance of these distinct CRPC cell states could pave the way for effective combinatorial therapies for CRPC. In this study, we identified a key role for the histone methyltransferase KMT2D in establishing the chromatin competence necessary for the recruitment of AR and FOXA1 transcription factors (TFs) that are essential for the AR transcriptional output in AR-dependent CRPC cell lines, patient derived organoids, and patient samples. Unexpectedly, KMT2D maintained the identity of the AR-low CRPC-SCL subtype and controlled activity of AP-1 TFs such as FOSL1, which acts as a master regulator of this subtype. Single cell transcriptomics and chromatin assays underscored the role of KMT2D in sustaining a mixed lineage cell state via AP-1 and FOXA1. The combined suppression of PI3K/AKT and KMT2D reduced cell proliferation in prostate cancer cells and patient-derived organoids in both CRPC-AR and CRPC-SCL subtypes. Altogether, these results unveil KMT2D as a major mediator of the epigenetic landscape in subtype-specific CRPC, contributing to tumor growth and therapeutic response.
• 🔗 查看原文

7. ⭐ GSE293202 组蛋白甲基转移酶 KMT2D 是去势抵抗性前列腺癌谱系可塑性和治疗反应的关键介质 [H3K4me2 ChIP-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、ChIP-seq、histone
• 📝 描述：Contributors : Eneda Toska ; Wouter Karthaus ; Srushti Kittane ; Erik Ladewig ; Taibo LiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensCastration-resistant prostate cancer (CRPC) is largely dependent on the androgen receptor (AR) for growth and often exhibits hyperactive PI3K signaling, most frequently due to PTEN loss. Therapeutic pressure from anti-AR therapies can induce trans-differentiation toward an AR-independent phenotype. Recently, different subtypes of AR-independent CRPC have been redefined, with the stem cell-like (SCL) subtype emerging as one of the most prevalent. Elucidation of the epigenetic mechanisms controlling the maintenance of these distinct CRPC cell states could pave the way for effective combinatorial therapies for CRPC. In this study, we identified a key role for the histone methyltransferase KMT2D in establishing the chromatin competence necessary for the recruitment of AR and FOXA1 transcription factors (TFs) that are essential for the AR transcriptional output in AR-dependent CRPC cell lines, patient derived organoids, and patient samples. Unexpectedly, KMT2D maintained the identity of the AR-low CRPC-SCL subtype and controlled activity of AP-1 TFs such as FOSL1, which acts as a master regulator of this subtype. Single cell transcriptomics and chromatin assays underscored the role of KMT2D in sustaining a mixed lineage cell state via AP-1 and FOXA1. The combined suppression of PI3K/AKT and KMT2D reduced cell proliferation in prostate cancer cells and patient-derived organoids in both CRPC-AR and CRPC-SCL subtypes. Altogether, these results unveil KMT2D as a major mediator of the epigenetic landscape in subtype-specific CRPC, contributing to tumor growth and therapeutic response.
• 🔗 查看原文

8. ⭐ GSE293182 组蛋白甲基转移酶 KMT2D 是去势抵抗性前列腺癌谱系可塑性和治疗反应的关键介质 [PC3 Bulk RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq、histone
• 📝 描述：Contributors : Eneda Toska ; Wouter Karthaus ; Srushti Kittane ; Erik Ladewig ; Taibo Li ; Yangzhenyu GaoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensCastration-resistant prostate cancer (CRPC) is largely dependent on the androgen receptor (AR) for growth and often exhibits hyperactive PI3K signaling, most frequently due to PTEN loss. Therapeutic pressure from anti-AR therapies can induce trans-differentiation toward an AR-independent phenotype. Recently, different subtypes of AR-independent CRPC have been redefined, with the stem cell-like (SCL) subtype emerging as one of the most prevalent. Elucidation of the epigenetic mechanisms controlling the maintenance of these distinct CRPC cell states could pave the way for effective combinatorial therapies for CRPC. In this study, we identified a key role for the histone methyltransferase KMT2D in establishing the chromatin competence necessary for the recruitment of AR and FOXA1 transcription factors (TFs) that are essential for the AR transcriptional output in AR-dependent CRPC cell lines, patient derived organoids, and patient samples. Unexpectedly, KMT2D maintained the identity of the AR-low CRPC-SCL subtype and controlled activity of AP-1 TFs such as FOSL1, which acts as a master regulator of this subtype. Single cell transcriptomics and chromatin assays underscored the role of KMT2D in sustaining a mixed lineage cell state via AP-1 and FOXA1. The combined suppression of PI3K/AKT and KMT2D reduced cell proliferation in prostate cancer cells and patient-derived organoids in both CRPC-AR and CRPC-SCL subtypes. Altogether, these results unveil KMT2D as a major mediator of the epigenetic landscape in subtype-specific CRPC, contributing to tumor growth and therapeutic response.
• 🔗 查看原文

9. ⭐ GSE293140 组蛋白甲基转移酶 KMT2D 是去势抵抗性前列腺癌谱系可塑性和治疗反应的关键介质 [PC3 Bulk ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、ATAC-seq、histone
• 📝 描述：Contributors : Eneda Toska ; Wouter Karthaus ; Srushti Kittane ; Erik Ladewig ; Taibo Li ; Yangzhenyu GaoSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensCastration-resistant prostate cancer (CRPC) is largely dependent on the androgen receptor (AR) for growth and often exhibits hyperactive PI3K signaling, most frequently due to PTEN loss. Therapeutic pressure from anti-AR therapies can induce trans-differentiation toward an AR-independent phenotype. Recently, different subtypes of AR-independent CRPC have been redefined, with the stem cell-like (SCL) subtype emerging as one of the most prevalent. Elucidation of the epigenetic mechanisms controlling the maintenance of these distinct CRPC cell states could pave the way for effective combinatorial therapies for CRPC. In this study, we identified a key role for the histone methyltransferase KMT2D in establishing the chromatin competence necessary for the recruitment of AR and FOXA1 transcription factors (TFs) that are essential for the AR transcriptional output in AR-dependent CRPC cell lines, patient derived organoids, and patient samples. Unexpectedly, KMT2D maintained the identity of the AR-low CRPC-SCL subtype and controlled activity of AP-1 TFs such as FOSL1, which acts as a master regulator of this subtype. Single cell transcriptomics and chromatin assays underscored the role of KMT2D in sustaining a mixed lineage cell state via AP-1 and FOXA1. The combined suppression of PI3K/AKT and KMT2D reduced cell proliferation in prostate cancer cells and patient-derived organoids in both CRPC-AR and CRPC-SCL subtypes. Altogether, these results unveil KMT2D as a major mediator of the epigenetic landscape in subtype-specific CRPC, contributing to tumor growth and therapeutic response.
• 🔗 查看原文

10. ⭐ GSE293101 组蛋白甲基转移酶 KMT2D 是去势抵抗性前列腺癌谱系可塑性和治疗反应的关键介质 [KMT2D ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、ChIP-seq、histone
• 📝 描述：Contributors : Eneda Toska ; Wouter Karthaus ; Srushti Kittane ; Erik Ladewig ; Taibo LiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensCastration-resistant prostate cancer (CRPC) is largely dependent on the androgen receptor (AR) for growth and often exhibits hyperactive PI3K signaling, most frequently due to PTEN loss. Therapeutic pressure from anti-AR therapies can induce trans-differentiation toward an AR-independent phenotype. Recently, different subtypes of AR-independent CRPC have been redefined, with the stem cell-like (SCL) subtype emerging as one of the most prevalent. Elucidation of the epigenetic mechanisms controlling the maintenance of these distinct CRPC cell states could pave the way for effective combinatorial therapies for CRPC. In this study, we identified a key role for the histone methyltransferase KMT2D in establishing the chromatin competence necessary for the recruitment of AR and FOXA1 transcription factors (TFs) that are essential for the AR transcriptional output in AR-dependent CRPC cell lines, patient derived organoids, and patient samples. Unexpectedly, KMT2D maintained the identity of the AR-low CRPC-SCL subtype and controlled activity of AP-1 TFs such as FOSL1, which acts as a master regulator of this subtype. Single cell transcriptomics and chromatin assays underscored the role of KMT2D in sustaining a mixed lineage cell state via AP-1 and FOXA1. The combined suppression of PI3K/AKT and KMT2D reduced cell proliferation in prostate cancer cells and patient-derived organoids in both CRPC-AR and CRPC-SCL subtypes. Altogether, these results unveil KMT2D as a major mediator of the epigenetic landscape in subtype-specific CRPC, contributing to tumor growth and therapeutic response.
• 🔗 查看原文

💡 该来源还有 73 条内容，详见 文末

详细内容（全部4条）

1. 淋巴细胞计数及慢性淋巴细胞白血病风险。

• ✍️ 作者：未知作者
• 🏷️ 关键词：淋巴
• 📝 描述：Secret hovertext: 背景 绝对淋巴细胞（ALC）计数升高常被用作慢性淋巴细胞白血病（CLL）诊断检查的首要指标。CLL 的绝对风险与年龄、性别和 ALC 的关系尚未被描述。方法 我们使用了来自英国生物样本库的 475,399 名纵向随访研究参与者的诊断前 ALC 信息，中位随访 11.6 年，其中 854 名参与者被诊断为 CLL。基于性别、招募年龄和诊断前 ALC 的灵活参数生存模型，建立了 CLL 风险模型。结果与 ALC 低于 2 x109 细胞/升的研究参与者相比，ALC 细胞数为 3 至 4x109 细胞/升的患者，CLL 风险几乎高出 8 倍（心率 7.76,95%置信区间：6.24-9.65）。男性的 CLL 绝对风险是女性的两倍。对于 60 岁 ALC 为 5x109 细胞/L 的人群，男性估计 10 年 CLL 风险为 6.5%（95%置信区间：5.6%-7.5%），女性为 3.5%（3.0%-4
• 🔗 查看原文

2. HER2DX 基因组检测与 HER2 阳性乳腺癌生物学和病理特征的关联。

• ✍️ 作者：未知作者
• 🏷️ 关键词：基因组
• 📝 描述：Secret hovertext: 背景 HER2DX 是一种经过验证的基因组检测法，用于支持早期 HER2 阳性（HER2+）乳腺癌的治疗决策。它提供三个评分：复发风险、病理完全反应（pCR）的可能性和 ERBB2 mRNA 表达。本研究旨在评估 HER2DX 与组织病理特征之间的关联，并评估其与新辅助疗法后 pCR 的关系。方法 在西班牙常规护理期间（2022 年 1 月至 2025 年 6 月），根据现有 HER2DX 结果分析了新诊断的 I-III 期 HER2+乳腺癌患者。集中 HER2DX 检测对固定福马林、石蜡嵌入的肿瘤样本进行了。组织病理学分析包括肿瘤等级、激素受体（HR）状态、组织学亚型、Ki67 指数、HER2 免疫组化（IHC）评分、间质肿瘤浸润淋巴细胞（TILs）、三级淋巴结构（TLS）及空间免疫分布。进行了单变量和多变量逻辑回归分析，以识别新辅助曲妥珠单抗治疗后 pCR 相关的因素。结果 共分析 410
• 🔗 查看原文

3. 在携带 PIK3CA 突变的 HER2 阳性转移性乳腺肿瘤中，将 ipatasertib 加入双重抗 HER2 维持治疗：1b 期 SOLTI-1507 IPATHER 试验。

• ✍️ 作者：未知作者
• 🏷️ 关键词：肿瘤
• 📝 描述：Secret hovertext: 目的 评估伊帕托西布联合曲妥珠单抗和派妥祖单抗作为 HER2 阳性转移性乳腺癌患者在一线治疗后维持治疗的安全性和可行性，适用于携带 PIK3CA 突变的 HER2 阳性转移性乳腺癌患者。实验设计 本前瞻性、多中心、单臂、1b 期临床研究评估了 AKT 抑制剂伊帕托西单抗（ipatasertib）与曲妥珠单抗（trastuzumab）和派妥祖单抗（HP）联合使用，配合或不使用内分泌治疗作为维持疗法的安全性和初步疗效，适用于一线诱导化疗和 HP 后不可切除的局部晚期或转移性 PIK3CAmut、HER2 阳性乳腺癌患者。结果 共纳入 17 例患者， 中位随访时间为 27.7 个月。在剂量选择阶段，依帕托沙替布每日 400 毫克（21 天服用，7 天停药）与标准 HP 剂量被确立为推荐的第二阶段剂量（RP2D）。这一决定基于在初始 28 天周期内，前六名接受该剂量治疗的患者均未出现剂量限制性毒性，该为主要终点。7
• 🔗 查看原文

4. 肠道检查：约翰逊乳酸杆菌利用胆汁酸和活性氧来抑制高脂饮食引起的结直肠癌。

• ✍️ 作者：未知作者
• 🏷️ 关键词：肠道
• 📝 描述：Secret hovertext: 结直肠癌是全球最常见且致命的恶性肿瘤之一，其发病率与生活方式因素密切相关，包括高脂饮食（HFD）。流行病学研究将高脂肪饮食与结直肠癌风险增加相关，但个体易感性差异很大，潜在驱动因素仍不充分。近期进展使研究范式从仅关注饮食组成转向考虑宿主-微生物相互作用及微生物代谢物谱对高脂肪饮食驱动结直肠癌风险的个体差异贡献。在本期《癌症研究》杂志中，刘氏及其同事研究了约翰逊乳酸杆菌作为抑制高脂蛋白驱动肿瘤发生的保护性细菌。通过促进共轭胆酸转化为顺便卵质胆酸，强森氏长杆菌引发线粒体功能障碍，从而促进活性氧物种的产生，并诱导凋亡以抑制结直肠癌的发展。这些临床前发现为胆汁酸代谢、肠道微生物群与致癌机制的交汇提供了机制性见解，并为未来基于益生菌的癌症预防转化研究奠定了基础。参见 Liu 等人相关文章，第 4600 页。
• 🔗 查看原文

详细内容（全部1条）

1. 通过RNA表达了解肿瘤异质性

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor
• 📝 描述：RNA sequencing was used to evaluate tumor heterogeneity in breast cancer, revealing links to cell growth and immune activity but limited power in predicting treatment response…
• 🔗 查看原文

• GSE293089 组蛋白甲基转移酶 KMT2D 是去势抵抗性前列腺癌谱系可塑性和治疗反应的关键介质 [FOXA1 ChIP-seq]
• GSE293080 组蛋白甲基转移酶 KMT2D 是去势抵抗性前列腺癌谱系可塑性和治疗反应的关键介质 [AR ChIP-Seq]
• GSE293079 组蛋白甲基转移酶 KMT2D 是去势抵抗性前列腺癌谱系可塑性和治疗反应的关键介质 [MSKPCA3 Bulk ATAC-seq]
• GSE293067 组蛋白甲基转移酶 KMT2D 是去势抵抗性前列腺癌谱系可塑性和治疗反应的关键介质 [LNCAP Bulk ATAC-seq]
• GSE293060 组蛋白甲基转移酶 KMT2D 是去势抵抗性前列腺癌谱系可塑性和治疗反应的关键介质 [DU145 Bulk RNA-seq]
• GSE293025 组蛋白甲基转移酶 KMT2D 是去势抵抗性前列腺癌谱系可塑性和治疗反应的关键介质 [DU145 Bulk ATAC-seq]
• GSE290943 scRNAseq 分析了原发性黑色素瘤小鼠 BP (TyrCre-ERT2Tg/0 BrafLSL-V600E/+ Ptenlox/lox) 和 BPT (TyrCre-ERT2Tg/0 BrafLSL-V600E/+ Ptenlox/lox Tslp-/-) 肿瘤引流淋巴结 (tdLN) 中迁移性树突状细胞 (DC) 和 CD4+ T 细胞的分布情况。
• GSE311935 毛细胞白血病 (HCL) 患者癌细胞的单细胞转录组分析
• GSE311267 靶向 Syndecan-1 的治疗性抗体抑制巨胞饮作用并诱导胰腺癌的抗肿瘤免疫
• GSE298098 诱导型 CD147 上调增强持续性 SARS-CoV-2 感染，引发重症 COVID-19，且与 ACE2 无关 [空间转录组学]
• GSE230037 猪脂肪组织的单细胞转录组测序
• GSE309586 全转录本 m6A 甲基化影响不依赖帽结构的翻译起始 [RNA-seq]
• GSE307942 人类白细胞中CBL的体细胞缺陷会损害B细胞而非T细胞的发育和功能
• GSE288188 转录因子 NKX2-1 与 RUNX1 协同作用，保护 T 细胞急性淋巴细胞白血病细胞免受 DNA 损伤 [ChIP-seq]
• GSE288187 转录因子 NKX2-1 与 RUNX1 协同作用，保护 T 细胞急性淋巴细胞白血病细胞免受 DNA 损伤 [RNA-seq]
• GSE266626 TCF3::HLF 通过激活 MEF2C 协调增强子-启动子网络，促进白血病中未成熟 HSC 基因表达 [RNA-seq]
• GSE308946 组蛋白甲基转移酶 KMT2D 是去势抵抗性前列腺癌谱系可塑性和治疗反应的关键介质 [CUT&Run]
• GSE296270 组蛋白甲基转移酶KMT2D是去势抵抗性前列腺癌谱系可塑性和治疗反应的关键介质
• GSE291282 组蛋白甲基转移酶KMT2D是去势抵抗性前列腺癌谱系可塑性和治疗反应的关键介质
• GSE278892 MC903 处理小鼠皮肤引流淋巴结中迁移性 nLCncDC1 的 CITEseq
• GSE308702 ARMCX3 敲低的转录组分析揭示了乳腺癌细胞中 p53–IFIH1 轴和免疫通路的激活。
• GSE290391：小鼠造血层级结构的单细胞RNA测序、ULAC测序和RNA测序
• GSE311811 多重嵌合肿瘤模型揭示了群体内和群体间药物反应的自然表型变异 [scRNA-seq]
• GSE304316 构建广藿香胚状体的单细胞转录组图谱，揭示 PcNAC048 作为双重调控因子，协调侧根形态发生和广藿香醇生物合成。
• GSE303432 RELB 重编程耗竭的肿瘤浸润淋巴细胞以改善过继细胞疗法 [RNA-Seq]
• GSE274326 IKKa 通过阻止紧密连接稳定和集体细胞迁移来调节结直肠癌转移 [RNA-seq PDX]
• GSE274325 IKKa 通过阻止紧密连接稳定和集体细胞迁移来调节结直肠癌转移 [RNA-seq Tumoroid]
• GSE274321 IKKa 通过阻止紧密连接稳定和集体细胞迁移来调节结直肠癌转移 [scRNA-seq]
• GSE310670 TCF3::HLF 通过激活 MEF2C 协调增强子-启动子网络，促进白血病中未成熟 HSC 基因表达程序。
• GSE310669 TCF3::HLF 通过激活 MEF2C 协调增强子-启动子网络，从而促进白血病中未成熟 HSC 基因表达程序。
• GSE309588 全转录本 m6A 甲基化影响不依赖帽结构的翻译起始 [Ribo-seq]
• GSE296077 人类神经元分化过程中的代谢重编程揭示谷氨酰胺酶是脆性X综合征的关键决定因素
• GSE278790 PDX1 磷酸化介导胰岛β细胞中的氨基酸-mTORC1 信号传导 [RNA-seq]
• GSE278789 PDX1 磷酸化介导胰腺 β 细胞中的氨基酸-mTORC1 信号传导 [ChIP-seq]
• GSE266625 TCF3::HLF 通过激活 MEF2C 协调增强子-启动子网络，促进白血病中未成熟 HSC 基因表达 [HiChIP]
• GSE311806 膳食盐损害盐敏感性高血压患者的昼夜节律生理代谢适应
• GSE304330 RNA测序揭示了铜绿假单胞菌生长阶段特异性的整体转录体温调节差异
• GSE304229 RNA-seq 数据来自在 37°C 或 25°C 下培养至稳定期的 PAO1 和 ΔlasR 菌株。
• GSE304114 PAO1 在两种温度和两个生长阶段的 RNA-seq
• GSE295016 TREM2 表达水平对小胶质细胞状态、代谢能力和 TREM2 激动剂的功效至关重要。
• GSE291343 雄性肾上腺皮质类固醇生成谱系的单细胞RNA测序
• GSE284496 小鼠胚胎晚期和出生早期肾脏的单核 RNA 测序。
• GSE283722 SGLT2抑制剂恩格列净增强肌球蛋白R403Q突变肥厚型心肌病小鼠的代谢效率并改善左心室肥厚
• GSE282712 新生小鼠脑内先天性巨细胞病毒感染的单细胞分辨率分子特征
• GSE281413 早发型和中发型结直肠癌及其匹配的正常结肠组织
• GSE277899 对感染鸟分枝杆菌四周的野生型 HSC、MPP3、GMP 和巨噬细胞进行 CUT&RUN 测序
• GSE271074 TREM2表达水平对小胶质细胞状态、代谢能力和TREM2激动剂的疗效至关重要
• GSE311914：二硫腙处理小鼠潘氏细胞后，肠上皮细胞来源的细胞外囊泡的 miRNA 表达谱分析
• GSE290390 小鼠造血层级的全局mRNA谱分析（RNA-seq）
• GSE290388：Nat10缺失后小鼠造血干细胞的单细胞转录组分析
• GSE269664 用于靶向降解 MYC 和 KRAS 的异双功能蛋白模拟聚合物
• GSE311917 凋亡细胞清除触发前列腺退化过程中上皮细胞命运重编程 [ChIP-seq]
• GSE311846 非小细胞肺癌中线粒体双链RNA依赖性脂质重编程
• GSE311813 多重嵌合肿瘤模型揭示了群体内和群体间药物反应的自然表型变异[异种移植]
• GSE311810 多重嵌合肿瘤模型揭示了群体内和群体间药物反应的自然表型变异 [CRISPR 筛选]
• GSE311794 跨膜蛋白功能筛选鉴定出多萜醇焦磷酸磷酸酶 CAX-4 是粗糙脉孢菌中麦角甾醇生物合成和唑类耐药性的关键调控因子
• GSE311745 基于空间转录组学的IgA肾病内毛细血管内细胞增生
• GSE311711 牙龈成纤维细胞暴露于活化血小板的 RNA 测序
• GSE311707 硬度介导的旁分泌信号增强口腔鳞状细胞癌中上皮间质转化（EMT）的诱导
• GSE303442 RELB 重编程耗竭的肿瘤浸润淋巴细胞以改善过继细胞疗法[增殖]
• GSE303438 RELB 重编程耗竭的肿瘤浸润淋巴细胞以改善过继细胞疗法 [TCR-Seq]
• GSE302983 靶向前列腺癌中已存在的棒状细胞可增强雄激素剥夺疗法的效果
• GSE300781 C13 细菌群落对空肠弯曲菌感染敏感，这会影响靶向细菌和宿主基因的宿主来源 miRNA。
• GSE298097 诱导型 CD147 上调增强持续性 SARS-CoV-2 感染，引发重症 COVID-19，且与 ACE2 无关 [scRNA-seq]
• GSE284367 抑制整合应激反应通​​过 mTOR 通路促进原始卵泡活化
• GSE282999 棉花胚珠表皮早期纤维发育过程中染色质可及性的单细胞分析 [scATAC-seq]
• GSE274368 IKKa 通过抑制紧密连接稳定和细胞集体迁移来调节结直肠癌转移
• GSE273832 ROS激活NETs释放骨髓CD55+中性粒细胞，促进骨骼早期老化
• GSE271019 小鼠脑中的 RNA 修饰、可变剪接和环状 RNA 图谱：肌苷及其他 [RNA-seq]
• GSE262356 包裹哺乳动物细胞的小型非编码RNA促进先天免疫
• GSE252429 包裹哺乳动物细胞的小型非编码RNA促进先天免疫
• GSE246570 血红素加氧酶-1对肾脏中心碳代谢的控制
• GSE195999 解冻后骨髓间充质干细胞的单细胞测序