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1. ⭐ GSE337809 CYP3A4介导的代谢变异性驱动非小细胞肺癌靶向治疗的耐药性和全身毒性

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、metabolic、resistance
• 📝 描述：Contributors : Pragya Kumar ; Julia Pelesko ; Malgorzata T Weh ; Menkara C Henry ; Bina Desai ; Ramu Kakumanu ; Min Liu ; Natalia Siqueira ; Robert Vander Velde ; Viktoriya Marusyk ; Jyllica Aurelio ; Eric B Haura ; Jhanelle Gray ; Bruna Pellini ; David G Basanta ; Andriy MarusykSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTargeted therapies, including small molecule inhibitors of mutant ALK, EGFR, and RAS in lung cancers, can produce strong and durable clinical responses, yet a subset of tumors fail to respond, and even strong responders eventually relapse. Further, although targeted therapies are typically well tolerated, a subset of patients displays dose-limiting adverse effects. Therapy resistance is generally considered to be a tumor-intrinsic phenomenon, mediated by cell-intrinsic or microenvironmental mechanisms. We found that hyperactivation of CYP3A4, a P450 family enzyme, can lead to tumor-extrinsic resistance by altering pharmacokinetics and reducing systemic and tumor drug exposure, whereas reduced CYP3A4 activity is expected to increase systemic toxicities. Retrospective analysis of clinical cohorts suggests that variability in CYP3A4 activity might be a major contributor to variability in clinical outcomes. To understand the consequences of altered drug metabolism, we developed a mathematical model linking variability in CYP3A4 activity with temporal variability in systemic drug concentrations. These in silico studies indicate that the impact of altered CYP3A4 activity can be mitigated by altering drug dosing and intervals. Further, we demonstrate that tumor sensitivity can be restored by pharmacological inhibition of CYP3A4. These findings establish systemic metabolic variability as a clinically actionable driver of both resistance and toxicity and provide a framework for personalized dosing to improve safety and efficacy of targeted therapy. The Bulk RNA sequencing data is from mouse livers, either untreated or treated with candidate drug JIB-04 to assess the change in gene expression landscape.
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2. GSE302041 单细胞转录组学揭示LRFC特化动态

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell、transcriptomics
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Arabidopsis thalianaA conserved GA–ROS–GASA1 regulatory module specifies and commits plant lateral root founder cells by orchestrating nuclear migration, asymmetric division, and ROS homeostasis.
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3. GSE337077 治疗敏感型和治疗耐药型乳腺癌细胞系样本的 RNA-seq 分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq
• 📝 描述：Contributor : Jun XuSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBulk RNA sequencing was performed on human breast cancer cell-line samples to compare transcriptomic profiles between treatment-sensitive and treatment-resistant conditions.
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4. GSE336903 对照组和治疗组乳腺癌细胞系样本的 RNA-seq 分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq
• 📝 描述：Contributor : Jun XuSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBulk RNA sequencing was performed on human breast cancer cell-line samples to compare transcriptomic profiles between control and treatment conditions.
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5. GSE336902：LRIG1 和 EGFR L747A 操作的乳腺癌细胞系样本的 RNA-seq 分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq
• 📝 描述：Contributor : Jun XuSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBulk RNA sequencing was performed on human breast cancer cell-line samples to compare transcriptomic profiles among control, LRIG1-minus, LRIG1, and LRIG1 plus EGFR L747A conditions.
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6. GSE336901 对治疗敏感和治疗耐药乳腺癌病例的 FFPE 样本进行 RNA-seq 分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq
• 📝 描述：Contributor : Jun XuSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBulk RNA sequencing was performed on formalin-fixed paraffin-embedded (FFPE) tumor samples to compare transcriptomic profiles between treatment-sensitive and treatment-resistant breast cancer cases.
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7. GSE291140 AMPK抑制多种细胞死亡通路以维持肿瘤相关巨噬细胞比例并促进肿瘤进展

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、macrophage
• 📝 描述：Contributors : Ruixuan Wang ; Di Liu ; Huan Wang ; Li TangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTumor-associated macrophages (TAMs) are a major immune cell population in the tumor microenvironment (TME). This part depends on their capacity to resist cell death by adapting to the harsh tumor microenvironment, characterized by nutrient deprivation and the accumulation of metabolic waste, through metabolic reprogramming. This enables TAMs to not only utilize excess metabolites and metabolic waste in the tumor microenvironment as energy sources, but also to cope with metabolic stress by upregulating cysteine uptake and activating hypoxia-inducible factors, thereby maintaining their survival and function. However, the core genes that suppress TAM death in response to the metabolic dynamics of the tumor microenvironment during tumor progression remain unknown. In this study, we used proteomics analysis combined with experimental validation found that the degree of TAM apoptosis decreased while the level of AMPK activation increased during tumor progression. Notably, myeloid-specific knockout of AMPK significantly inhibits tumor growth, reduces TAM proportion in the tumor, and weakens its pro-tumor phenotype. Bulk RNA sequencing data analysis further revealed that specific knockout of AMPK in TAMs triggers multiple forms of cell death, including apoptosis, ferroptosis, and necroptosis. Further experimental validation confirmed that AMPK knockout not only induces apoptosis and ferroptosis in TAMs but may also trigger disulfidptosis. Mechanistic research suggested that AMPK might regulate cysteine uptake and the pentose phosphate pathway to inhibit ferroptosis and disulfidptosis in TAMs. In conclusion, this study identifies AMPK as a key regulator that responds to the metabolic dynamics of the TME and inhibits various forms of cell death in TAMs, providing new theoretical insights for TAM-targeted metabolic therapies.
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8. GSE330762 歌舞伎综合征 I 型成纤维细胞多组学数据集：来自原代皮肤成纤维细胞的批量 RNA-seq 谱

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq
• 📝 描述：Contributors : Emile Danvin ; Paolo Salerno ; Eleonora Di Venere ; Gabriella Squeo ; Dario Righelli ; Giuseppe MerlaSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensKabuki syndrome type 1 (KS1) is a rare congenital disorder caused by heterozygous loss-of-function mutations in KMT2D – an H3K4 histone methyltransferase. While KMT2D function during early development is increasingly understood, the transcriptional and chromatin accessibility consequences of its loss in differentiated somatic tissues remain poorly characterized. We present a multi-omic dataset from primary dermal fibroblasts of seven individuals with KS type I and nine unaffected donors. The dataset comprises bulk RNA-seq from sixteen donors (nineteen libraries across two sequencing batches, including three donors sequenced in both batches to assess technical replicability) and ATAC-seq from ten donors (six KS, four controls). All libraries were processed through standardized nf-core pipelines, with differential analyses performed using DESeq2 with RUVSeq batch correction. This resource is intended to facilitate research on Kabuki syndrome type 1 and by expanding the available models for studying the group of mendelian disorders known as chromatinopathies.
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9. GSE330760 歌舞伎综合征 I 型成纤维细胞多组学数据集：来自原代皮肤成纤维细胞的 ATAC-seq 谱

• ✍️ 作者：未知作者
• 🏷️ 关键词：ATAC-seq
• 📝 描述：Contributors : Emile Danvin ; Paolo Salerno ; Eleonora Di Venere ; Gabriella Squeo ; Dario Righelli ; Giuseppe MerlaSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensKabuki syndrome type 1 (KS1) is a rare congenital disorder caused by heterozygous loss-of-function mutations in KMT2D – an H3K4 histone methyltransferase. While KMT2D function during early development is increasingly understood, the transcriptional and chromatin accessibility consequences of its loss in differentiated somatic tissues remain poorly characterized. We present a multi-omic dataset from primary dermal fibroblasts of seven individuals with KS type I and nine unaffected donors. The dataset comprises bulk RNA-seq from sixteen donors (nineteen libraries across two sequencing batches, including three donors sequenced in both batches to assess technical replicability) and ATAC-seq from ten donors (six KS, four controls). All libraries were processed through standardized nf-core pipelines, with differential analyses performed using DESeq2 with RUVSeq batch correction. This resource is intended to facilitate research on Kabuki syndrome type 1 and by expanding the available models for studying the group of mendelian disorders known as chromatinopathies.
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10. GSE328395 高内在有氧能力在老年大鼠脑中塑造独特的表观遗传特征

• ✍️ 作者：未知作者
• 🏷️ 关键词：epigenetic
• 📝 描述：Contributors : Lei Zhou ; Radak ZsoltSeries Type : Methylation profiling by high throughput sequencingOrganism : Rattus norvegicusAging is accompanied by progressive decline in brain function, and aerobic fitness is thought to influence brain health. To examine whether intrinsic exercise capacity is associated with a distinct brain molecular phenotype in aging, we profiled hippocampal DNA methylation by reduced representation bisulfite sequencing (RRBS) in aged selectively bred rats with high or low intrinsic aerobic capacity.
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1. 阿尔茨海默病中的tau蛋白在记忆中扮演着令人惊讶的秘密角色

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：Researchers found that tau is essential for turning new experiences into lasting memories by helping organize the brain’s memory-storing cells. The mouse study also revealed how abnormal tau may contribute to Alzheimer’s by disrupting both the formation of new memories and the recall of existing ones.
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• GSE315916 大蹄蝠（Rhinolophus ferrumequinum）冬眠和活跃状态下脾脏组织的转录组数据集
• GSE337536 地西他滨诱导罕见黑色素瘤模型中先天免疫基因表达
• GSE337028 小非编码 RNA MicC 是肠外致病性大肠杆菌应激抵抗力和毒力的关键调控因子
• GSE288227 脱氧胆酸通过 GLP-1/iNKT 细胞串扰和 PPARα 激活抑制肝脂肪变性（批量 RNA 测序）