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1. ⭐ GSE253035 肿瘤细胞 JAGGED-1 促进淋巴结转移并预测淋巴结阳性乳腺癌患者的复发 [MDA231-P_MDA231-LN]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、lymph、regex:lymph(o|atic)?
• 📝 描述：Contributors : Gordon Benjamin ; Swaminathan Bhairavi ; Vadakath Rahul ; Teneqexhi Pamela ; Youn Seock Won ; Alvarez-Lopez Isabel ; Rezola Marta ; Xu Ziqiao ; Chen Zhengjia ; Er Ekrem Emrah ; Naiche LA ; Caffarel María Muñoz ; Kitajewski JanSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensPurpose: Lymph node invasion is a hallmark of breast cancer disease progression, but current treatment strategies lack guidance from lymph node biomarkers. We investigated JAGGED1 (JAG1) as a promoter of lymph node metastasis and a prognostic biomarker in metastatic lymph node specimens. Experimental Design: We used mouse models to assess the role of JAG1 expression in human and mouse breast cancer cells on lymphovascular invasion, lymph node metastatic potential, transcriptional profiles, and tumor interactions with lymphatic endothelium. We examined breast and lymph node samples from 284 breast cancer patients to determine the correlative and prognostic value of tumoral JAG1 expression in the lymph node. Results: In matched human breast tumor and lymph node samples, tumor cells that invaded lymph nodes showed higher JAG1 expression than their associated primary tumors (P value < 0.0001). In multiple models, breast cancer cells with high JAG1 expression showed increased lymphovascular invasion, lymph node metastasis, lymph node metastatic outgrowth, and migration through lymphatic endothelium. Transcriptomic analysis indicated that tumoral JAG1 regulates both juxtacrine and paracrine signaling pathways that induce inflammatory and pro-metastatic genes in lymphatic endothelium. When examining patients with identical surgical treatments, patients with lymph node JAG1 H-scorelow showed increased 5-year recurrence free survival rates than patients with lymph node JAG1 H-scorehi (87% vs 70%, P=0.016). Conclusions: JAG1 expression promotes lymphovascular invasion and lymph node metastasis in murine models. In patients, high expression of JAG1 in tumor cells in lymph node metastases predicts reduced recurrence free survival.
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2. ⭐ GSE252953 肿瘤细胞 JAGGED-1 促进淋巴结转移并预测淋巴结阳性乳腺癌患者的复发 [hdLEC_JAG1_TLA]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、lymph、regex:lymph(o|atic)?
• 📝 描述：Contributors : Gordon Benjamin ; Swaminathan Bhairavi ; Vadakath Rahul ; Teneqexhi Pamela ; Youn Seock Won ; Alvarez-Lopez Isabel ; Rezola Marta ; Xu Ziqiao ; Chen Zhengjia ; Er Ekrem Emrah ; Naiche LA ; Caffarel María Muñoz ; Kitajewski JanSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensPurpose: Lymph node invasion is a hallmark of breast cancer disease progression, but current treatment strategies lack guidance from lymph node biomarkers. We investigated JAGGED1 (JAG1) as a promoter of lymph node metastasis and a prognostic biomarker in metastatic lymph node specimens. Experimental Design: We used mouse models to assess the role of JAG1 expression in human and mouse breast cancer cells on lymphovascular invasion, lymph node metastatic potential, transcriptional profiles, and tumor interactions with lymphatic endothelium. We examined breast and lymph node samples from 284 breast cancer patients to determine the correlative and prognostic value of tumoral JAG1 expression in the lymph node. Results: In matched human breast tumor and lymph node samples, tumor cells that invaded lymph nodes showed higher JAG1 expression than their associated primary tumors (P value < 0.0001). In multiple models, breast cancer cells with high JAG1 expression showed increased lymphovascular invasion, lymph node metastasis, lymph node metastatic outgrowth, and migration through lymphatic endothelium. Transcriptomic analysis indicated that tumoral JAG1 regulates both juxtacrine and paracrine signaling pathways that induce inflammatory and pro-metastatic genes in lymphatic endothelium. When examining patients with identical surgical treatments, patients with lymph node JAG1 H-scorelow showed increased 5-year recurrence free survival rates than patients with lymph node JAG1 H-scorehi (87% vs 70%, P=0.016). Conclusions: JAG1 expression promotes lymphovascular invasion and lymph node metastasis in murine models. In patients, high expression of JAG1 in tumor cells in lymph node metastases predicts reduced recurrence free survival.
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3. ⭐ GSE252952 肿瘤细胞 JAGGED-1 促进淋巴结转移并预测淋巴结阳性乳腺癌患者的复发 [MDA231LN_JAG1_KO1cnt_KO1rescue]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、lymph、regex:lymph(o|atic)?
• 📝 描述：Contributors : Gordon Benjamin ; Swaminathan Bhairavi ; Vadakath Rahul ; Teneqexhi Pamela ; Youn Seock Won ; Alvarez-Lopez Isabel ; Rezola Marta ; Xu Ziqiao ; Chen Zhengjia ; Er Ekrem Emrah ; Naiche LA ; Caffarel María Muñoz ; Kitajewski JanSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensPurpose: Lymph node invasion is a hallmark of breast cancer disease progression, but current treatment strategies lack guidance from lymph node biomarkers. We investigated JAGGED1 (JAG1) as a promoter of lymph node metastasis and a prognostic biomarker in metastatic lymph node specimens. Experimental Design: We used mouse models to assess the role of JAG1 expression in human and mouse breast cancer cells on lymphovascular invasion, lymph node metastatic potential, transcriptional profiles, and tumor interactions with lymphatic endothelium. We examined breast and lymph node samples from 284 breast cancer patients to determine the correlative and prognostic value of tumoral JAG1 expression in the lymph node. Results: In matched human breast tumor and lymph node samples, tumor cells that invaded lymph nodes showed higher JAG1 expression than their associated primary tumors (P value < 0.0001). In multiple models, breast cancer cells with high JAG1 expression showed increased lymphovascular invasion, lymph node metastasis, lymph node metastatic outgrowth, and migration through lymphatic endothelium. Transcriptomic analysis indicated that tumoral JAG1 regulates both juxtacrine and paracrine signaling pathways that induce inflammatory and pro-metastatic genes in lymphatic endothelium. When examining patients with identical surgical treatments, patients with lymph node JAG1 H-scorelow showed increased 5-year recurrence free survival rates than patients with lymph node JAG1 H-scorehi (87% vs 70%, P=0.016). Conclusions: JAG1 expression promotes lymphovascular invasion and lymph node metastasis in murine models. In patients, high expression of JAG1 in tumor cells in lymph node metastases predicts reduced recurrence free survival.
• 🔗 查看原文

4. ⭐ GSE252950 肿瘤细胞 JAGGED-1 促进淋巴结转移并预测淋巴结阳性乳腺癌患者的复发 [MDA231LN_JAG1_KO1_KO2]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、lymph、regex:lymph(o|atic)?
• 📝 描述：Contributors : Gordon Benjamin ; Swaminathan Bhairavi ; Vadakath Rahul ; Teneqexhi Pamela ; Youn Seock Won ; Alvarez-Lopez Isabel ; Rezola Marta ; Xu Ziqiao ; Chen Zhengjia ; Er Ekrem Emrah ; Naiche LA ; Caffarel María Muñoz ; Kitajewski JanSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensPurpose: Lymph node invasion is a hallmark of breast cancer disease progression, but current treatment strategies lack guidance from lymph node biomarkers. We investigated JAGGED1 (JAG1) as a promoter of lymph node metastasis and a prognostic biomarker in metastatic lymph node specimens. Experimental Design: We used mouse models to assess the role of JAG1 expression in human and mouse breast cancer cells on lymphovascular invasion, lymph node metastatic potential, transcriptional profiles, and tumor interactions with lymphatic endothelium. We examined breast and lymph node samples from 284 breast cancer patients to determine the correlative and prognostic value of tumoral JAG1 expression in the lymph node. Results: In matched human breast tumor and lymph node samples, tumor cells that invaded lymph nodes showed higher JAG1 expression than their associated primary tumors (P value < 0.0001). In multiple models, breast cancer cells with high JAG1 expression showed increased lymphovascular invasion, lymph node metastasis, lymph node metastatic outgrowth, and migration through lymphatic endothelium. Transcriptomic analysis indicated that tumoral JAG1 regulates both juxtacrine and paracrine signaling pathways that induce inflammatory and pro-metastatic genes in lymphatic endothelium. When examining patients with identical surgical treatments, patients with lymph node JAG1 H-scorelow showed increased 5-year recurrence free survival rates than patients with lymph node JAG1 H-scorehi (87% vs 70%, P=0.016). Conclusions: JAG1 expression promotes lymphovascular invasion and lymph node metastasis in murine models. In patients, high expression of JAG1 in tumor cells in lymph node metastases predicts reduced recurrence free survival.
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5. ⭐ GSE341379 组蛋白3赖氨酸甲基化的不同状态是肿瘤免疫监视的基础

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune、methylation、histone
• 📝 描述：Contributors : Amy Gladstein ; David FeldserSeries Type : Expression profiling by high throughput sequencing ; Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusMutations in histone 3 at or near lysine 36 (H3K36) have dominantly acting oncogenic effects in multiple tumor types by limiting H3K36-directed methyltransferases. Paradoxically, we find that expression of the H3K36M oncohistone unexpectedly inhibits tumor formation in KRAS-driven lung adenocarcinoma by inducing a potent immune-mediated tumor clearance. Mechanistically, oncohistone expression derepresses endogenous retroviral element transcription, results in the accumulation of double-stranded RNA (dsRNA), and activates an innate antiviral-like immune response that eradicates tumor growth. Surprisingly, while inactivation of the H3K36 di-methyltransferase NSD2 replicated all effects of oncohistone expression, inactivation of the H3K36 tri-methyltransferase SETD2 abolished element derepression and all associated downstream anti-cancer effects that are induced by oncohistone expression. These observations restructure our understanding of the roles of H3K36 methylation, the consequences of its deregulation in cancer, and shape our expectations for therapeutic interventions targeting H3K36 methyltransferases.
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6. ⭐ GSE309010 研究揭示了大麻素通过 ARID1A 驱动染色质-脂质稳态轴的表观遗传重塑，从而揭示了癌症的代谢脆弱性。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、metabolic、epigenetic
• 📝 描述：Contributor : David LLobet- NavasSeries Type : Expression profiling by high throughput sequencing ; Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensA substantial body of evidence supports a tumor suppressor role for the chromatin remodeler ARID1A, whose inactivating mutations and loss of function are common across human cancers. These alterations have spurred extensive efforts to uncover vulnerabilities associated with ARID1A deficiency. However, emerging studies suggest that ARID1A may also exert context-dependent tumor-promoting functions, opening new therapeutic avenues in ARID1A-proficient tumors. In endometrial cancer (EC), ARID1A mutations typically arise late during tumor progression and are dispensable for tumor initiation, providing a relevant context to interrogate its noncanonical homeostatic roles. Here, through integrated multiomics analyses, cellular bioenergetics and in vivo studies using EC patient-derived xenografts and genetically engineered mouse models, we demonstrate that functional ARID1A is required for acquired resistance to nutrient deprivation induced by antiangiogenic (starvation) therapy. Mechanistically, ARID1A orchestrates an epigenetically regulated chromatin-lipid homeostatic program involving lipid metabolism and mitochondrial fatty acid oxidation. Unexpectedly, we find that Δ9- tetrahydrocannabinol (THC), a phytocannabinoid and orthosteric CB1/CB2 agonist, exerts its antitumor activity by repressing ARID1A, thereby dismantling this chromatin- lipid metabolic axis and restoring sensitivity to starvation therapy. These findings position ARID1A as a central node linking chromatin remodeling to metabolic plasticity, and identify THC as a pharmacologic disruptor of this epigenetic metabolic program with therapeutic potential in ARID1A-proficient tumors.
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7. ⭐ GSE304907 RHOAY42C 驱动的弥漫性胃癌细胞谱系可塑性和免疫重塑 [scRNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、scRNA
• 📝 描述：Contributors : Kyung-Pil Ko ; Sangmin Kim ; Jinho Jang ; Yoojeong Seo ; Gengyi Zou ; Jie Zhang ; Sohee Jun ; Brittany Morrow ; Ryan Park ; Yuan-Hung Lo ; Jaffer A. Ajani ; Michael A. Curran ; Hyunki Kim ; Jae-Il ParkSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusDiffuse gastric adenocarcinoma (DGA) is an aggressive gastric cancer subtype with a poor prognosis. RHOAY42C is a recurrent mutation in DGA, yet its independent oncogenic role remains unclear. We used genetically engineered gastric organoid models to demonstrate that RHOAY42C, along with KrasG12D activation and Trp53 loss (RKP), is sufficient to drive DGA without loss of E-cadherin. Integrated single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (Xenium In Situ) revealed that RKP tumors exhibit mucinous histopathology and a unique lineage trajectory originating from Aqp5+ cells and differentiating into Muc1/Muc4+ cells via YAP1 signaling. RKP tumors establish a highly immunosuppressive tumor microenvironment in which AREG-mediated activation of EGFR promotes T cell exhaustion. Unlike E-cadherin loss-induced DGA, RKP tumors display strong susceptibility to PD-1 blockade. These findings redefine the oncogenic role of RHOAY42C, highlighting its sufficiency for DGA development and identifying PD-1 inhibition as a promising therapeutic strategy for patients with DGA harboring this mutation.
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8. ⭐ GSE329415 利用 Xenium 对两例注射了 B16F10 的 PRF1-/- 小鼠和一例健康对照小鼠的骨组织进行空间转录组学分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Elbanna Yassmin A ; Huse MorganSeries Type : OtherOrganism : Mus musculusSpatial transcriptomic profiling was performed on bone tissue from perforin-deficient (Prf1⁻/⁻) mice following bone injection and from Prf1⁻/⁻ uninjected control bone tissue using the 10x Genomics Xenium platform. The study aimed to characterize spatially resolved gene expression changes associated with tumor or cell injection in the absence of perforin-mediated cytotoxic immunity.
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9. GSE334980 慢性抗体介导排斥反应的转录组学

• ✍️ 作者：未知作者
• 🏷️ 关键词：antibody、transcriptomics
• 📝 描述：Series Type : Expression profiling by high throughput sequencing ; OtherOrganism : Homo sapiensThis SuperSeries is composed of the SubSeries listed below.
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10. GSE328673 墨西哥丽脂鲤幼体地表鱼和帕琼洞穴鱼的比较单细胞RNA测序脑图谱

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell
• 📝 描述：Contributors : Kathryn Gallman ; Edward S Ricemeyer ; Aakriti Rastogi ; X Maggs ; Emilio Mendez ; Erik R Duboué ; Nicolas Rohner ; Harini Iyer ; Wesley C Warren ; Alex C KeeneSeries Type : Expression profiling by high throughput sequencingOrganism : Astyanax mexicanusTranscriptional changes underlie not only adaptations of animals to novel or changing environments, but also to human disease phenotypes, such as insomnia. Linking specific transcriptional variations to observable traits can reveal the genetic basis of adaptive trait evolution and disease. To link genetic variation to phenotypic differences, we constructed the first single nucleus RNA sequencing (snRNA seq) brain atlas in a uniquely suited model system, the Mexican tetra Astyanax mexicanus. We made comparisons between surface and cavefish A. mexicanus morphs, which despite having dramatically different life histories, physiologies, and morphologies, can nevertheless interbreed. Here we show a suite of genetic changes that underlie specific differences in phenotypes, including synaptic and neural rewiring, as well as circadian dysregulation between surface and cave-dwelling morphs that may underlie human sleep disorders. Our comprehensive snRNA seq brain atlas revealed widespread divergence in the abundance and molecular signatures of neurons and glia between surface and cavefish and establishes a platform for uncovering the genetic underpinnings of cavefish disease phenotypes.
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1. CRISPR技术使前列腺癌更容易受到免疫疗法的攻击。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、regex:immuno(logy|therapy|suppression)
• 📝 描述：Scientists used CRISPR to make prostate cancer cells easier for the immune system to detect and destroy. The experimental treatment dramatically improved the effects of immunotherapy in mice and may offer hope for other hard-to-treat tumors.
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2. 纳米孔RNA测序绘制酵母线粒体tRNA修饰图谱

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：RNA sequencing mapped chemical modifications across yeast mitochondrial tRNAs, providing new insight into RNA maturation and mechanisms that may influence human…
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3. 八小时内进食可能有助于保持老年人大脑的敏锐度。

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging
• 📝 描述：Eating within a shorter daily window may help protect certain thinking skills as people age. In a small six-month trial, older women who limited eating to about 8 to 9 hours a day performed better on planning and problem-solving tests than those who ate over 12 hours. Both groups lost similar amounts of weight, hinting that when people eat could matter in addition to how much they eat.
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4. 为什么同样的DNA损伤会导致一些人患癌，而另一些人则不会？

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：A controlled mouse study has provided direct evidence that inherited genetics can steer how cancer begins and evolves after DNA damage. The discovery could eventually help doctors better predict cancer risk and tailor screening and treatments to each patient.
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5. 一个隐藏的阿尔茨海默病临界点可能决定谁会患上痴呆症。

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：Scientists have identified a possible tipping point that helps determine whether Alzheimer’s-related brain changes lead to dementia. The key may lie in how the brain’s immune cells respond to plaques and tau, offering a promising new target for treatments designed to extend cognitive resilience.
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• GSE293592 母体免疫激活延迟皮层兴奋性神经元的DNA甲基化和生理成熟
• GSE341599 CTCFL(BORIS) 通过放松 CTCF 介导的三维基因组结构，参与卵巢癌的转录程序。
• GSE305003 RHOAY42C 驱动的弥漫性胃癌细胞谱系可塑性和免疫重塑 [CUT&Run]
• GSE304811 RHOAY42C驱动的弥漫性胃癌细胞谱系可塑性和免疫重塑
• GSE341225 空间分析揭示了IDH突变型胶质瘤的演变组织结构
• GSE303754 通过 H3K79me2 修饰在 SW1990 胰腺癌细胞中鉴定 DOT1L 调控的靶基因
• GSE240763 一线信迪利单抗联合 P-GEMOX 化疗治疗晚期结外自然杀伤/T 细胞淋巴瘤（SPIRIT）：一项单臂、多中心 II 期试验
• GSE304534 激活 RARβ 以克服 t(4;14) 人类骨髓瘤的免疫调节药物耐药性 [ChIP-seq]
• GSE341485 异质性表观遗传变异在阿片类药物成瘾中汇聚于剪接失调
• GSE341318 用于对人 HepaRG 细胞中化学诱导的组蛋白去乙酰化酶抑制进行分类的转录组学生物标志物
• GSE339382 恶性疟原​​虫环境诱导性转化的分子机制 [AP2-HS ChIP-seq]
• GSE298061 异染色质和 AP2-HS 是人类疟原虫环境诱导性转化的基础 [RNA-seq]
• GSE298024 异染色质和 AP2-HS 是人类疟原虫环境诱导性转化的基础 [H3K9me3 ChIP-seq]
• GSE283350 利用体外模型对 2 细胞胚胎中的增强子进行功能解析 [RNA-seq]
• GSE283348 利用体外模型对 2 细胞胚胎中的增强子进行功能解析 [scRNA-seq]
• GSE283347 利用体外模型对 2 细胞胚胎中的增强子进行功能解析 [ChIP-seq]
• GSE283346 利用体外模型对 2 细胞胚胎中的增强子进行功能解析 [ATAC-seq]
• GSE268108 TAD边界的染色质可及性分类揭示了新的染色质绝缘子（Hi-C 1）
• GSE268028 TAD边界的染色质可及性分类揭示了新的染色质绝缘子（Hi-C 2）
• GSE333619：老年高容量和低容量跑步大鼠比目鱼肌在基线和自愿跑步后的RNA测序分析
• GSE333221 肠道脂肪酶抑制通过重塑肝脏脂质组，使饮食诱导的肥胖与 MASH 解耦联。
• GSE319338 不同的转录和功能模块介导胶质母细胞瘤对靶向治疗的耐药性
• GSE281562 独特的表观基因组特征可识别具有生物学意义的 MDS 亚型并预测对阿扎胞苷的反应 [RNA-Seq]
• GSE341199 肝细胞RIPK1支架功能通过抑制内质网应激驱动的细胞凋亡和炎症反应来保护肝脏免受酒精性损伤
• GSE341133 NREP 缺陷重塑肝脏-脂肪脂质代谢和脂肪组织的炎症微环境
• GSE339400 子宫内膜异位症疼痛：与炎症相关的基因可区分有症状和无症状疾病
• GSE339275 肽靶向脂质纳米颗粒协调IFN-γ和顺铂的相互作用，从而消除卵巢癌
• GSE330079 对照组 (NT) 和 Spp1 基因敲除小鼠样本的批量 RNA 测序
• GSE303903 DOT1L抑制对SW1990胰腺癌细胞基因表达的影响
• GSE303416 AoHal4b 与 AoAdv-1 相互作用，调控寡孢节丛枝菌的菌丝融合、线虫捕食能力和次级代谢
• GSE239580 广东小耳猪（GS）和约克夏猪（YK）不同年龄（9日龄和80日龄）皮下脂肪的转录组测序
• GSE341501 OGT通过协调mTORC1活性来调控肠道上皮稳态和修复
• GSE326173 核受体 Nur77 主要通过调节 AP-1 转录因子及其靶基因的表达来缓解巨噬细胞的炎症反应 [ChIP-seq]
• GSE326041 核受体 Nur77 主要通过调节 AP-1 转录因子及其靶基因的表达来缓解巨噬细胞的炎症反应 [ATAC-seq]
• GSE325918 核受体 Nur77 主要通过调节 AP-1 转录因子及其靶基因的表达来缓解巨噬细胞的炎症反应 [RNA-seq]
• GSE304474 激活 RARβ 以克服 t(4;14) 人类骨髓瘤的免疫调节药物耐药性
• GSE304473 激活 RARβ 以克服 t(4;14) 人类骨髓瘤的免疫调节药物耐药性
• GSE274016 核受体 Nur77 主要通过顺式和反式调控 AP-1 靶基因来缓解巨噬细胞的炎症反应 [RNA-Seq]
• GSE273993 核受体 Nur77 主要通过顺式和反式调控 AP-1 靶基因来缓解巨噬细胞的炎症反应 [ChIP-Seq]
• GSE273991 核受体 Nur77 主要通过顺式和反式调控 AP-1 靶基因来缓解巨噬细胞的炎症反应 [ATAC-Seq]