详细内容（前10条）

1. ⭐ GSE288758 EGFR突变型非小细胞肺癌中与靶向治疗耐药性相关的肿瘤微环境空间动态

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、tumor microenvironment、resistance、spatial
• 📝 描述：Contributors : Satoshi Nakamaura ; Daisuke Shibahara ; Kentaro Tanaka ; Yasuyuki Kishikawa ; Mikiko Hashisako ; Keita Nakatomi ; Noriaki Nakagaki ; Mikihiro Kohno ; Koichi Azuma ; Ritsu Ibusuki ; Kohei Otsubo ; Yasuto Yoneshima ; Eiji Iwama ; Yoshinao Oda ; Isamu OkamotoSeries Type : OtherOrganism : Homo sapiensEpidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) provide therapeutic benefit in EGFR mutation–positive non–small cell lung cancer, but some individuals develop early resistance. We performed spatial transcriptomics analysis of pre- and posttreatment tumor samples from the same patients to explore the underlying mechanisms of such early resistance. The proportion and activation of fibroblasts increased in association with the development of early resistance, whereas a distinct tumor cell cluster showed activation of tumor necrosis factor–α signaling via the NF-B pathway even before treatment. Also in the early resistance sample, specific tumor cell clusters interacted with immune and stromal cells. Immature tertiary lymphoid structures (TLSs) were enriched in the early resistance sample, whereas mature TLSs were observed in the long-term response sample. These findings implicate tumor heterogeneity and an inflammatory tumor microenvironment in early EGFR-TKI resistance, providing insight into potential therapeutic strategies to improve treatment outcomes.
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2. ⭐ GSE282302 胰腺癌原位多模态表征揭示肿瘤细胞特性是周围微环境的决定性因素 [空间转录组学]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Anna Lyubetskaya ; Brian Rabe ; Andrew J Kavran ; Yulong Bai ; Andrew Fisher ; Hannah Pliner ; Alba Font-Tello ; Anne Lewin ; Ruifeng Hu ; Alexandre P Alloy ; Yelena Cheng ; Chao Dai ; Yunfan Fan ; Constance Brett ; Todd Brett ; Lauren Giampapa ; Sören R Stahlschmidt ; Fayaz Seifuddin ; Steven Vasquez Grinnell ; Daniel Carrera ; Carlos Rios ; Tom Lila ; Pradeep Kar ; Abhishek Shukla ; Rachael Bashford-Rogers ; Lara Heij ; Mike Mason ; Ryan Golhar ; Isaac Neuhaus ; Enas A Shah ; Jimena T Tinoco ; Benjamin J Chen ; Shivan Sivakumar ; Konstantinos J Mavrakis ; Eugene DrokhlyanskySeries Type : OtherOrganism : Homo sapiensPancreatic Ductal Adenocarcinoma (PDAC) is heterogeneous with low tumor purity, prominent microenvironment and complex architecture, which preclude identification of shared tumor intrinsic biology within and across patients. We overcame these challenges by applying spatial omics approaches – providing necessary resolution and context – to primary untreated PDAC tumors from 39 patients capturing 340K low-bulk and 530K single-cell spatial transcriptomes. We observe a spectrum of classical-to-basal tumor subtypes present within all patients. We identify a distinct population of proliferative tumor cells enriched for the DNA synthesis-condensation-mitosis transcriptional network suggesting this subset disproportionately contribute to tumor growth. Furthermore, we characterize the microenvironment surrounding each tumor subtype and observe that basal identity is contextually defined by collagen, hypoxic adaptation and fibroblast neighbors expressing activated stroma and interferon stimulated gene therapy resistance signatures. Lastly, leveraging orthogonal patient, cell and mouse data, we determine which aspects of PDAC biology are recapitulated in bulk datasets and reductionist models.
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3. ⭐ GSE311909 一个可靶向的发育程序共同调控血管生成和免疫逃逸 [空间转录组学]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Markus Schober ; Iman Osman ; Robert Stagnitta ; Pietro Berico ; Eva HernandoSeries Type : OtherOrganism : Homo sapiensUltraviolet (UV)-induced DNA mutations produce genetic drivers of cutaneous melanoma initiation and numerous neoantigens that can trigger anti-tumor immune responses in the host. Consequently, melanoma cells must rapidly evolve to evade immune detection by simultaneously modulating cell-autonomous epigenetic mechanisms and tumor-microenvironment interactions. Angiogenesis has been implicated in this process; although an increase of vasculature facilitates the immune response in normal tissue, solid tumors manage to somehow enhance blood flow while preventing immune cell infiltration. By comparing the expression of transcription factors (TFs) across early-stage melanoma, naevi, and other cancer types, we found the homeodomain-containing TF HOXD13 drives a melanoblast-like developmental program, which is upregulated in melanoma and strongly correlated with angiogenesis and immune cell exclusion. Using transcriptomics, 3D chromatin profiling, and in vivo models, we demonstrate that HOXD13 upregulation promotes tumor growth in vivo by concomitantly enhancing angiogenesis and suppressing T-cell infiltration. HOXD13 orchestrates 3D chromatin contacts between distal enhancers and promoters, simultaneously activating VEGFA, SEMA3A, and CD73. VEGFA and SEMA3A remodel the tumor vasculature and CD73 elevates extracellular levels of adenosine, a vasodilator and immune suppressor that binds adenosine receptors (AdR) on endothelial and T cells. In line with these findings, HOXD13-induced growth advantage in vivo was significantly reversed by the concomitant administration of VEGFR and AdR inhibitors. By revealing a dual pro-angiogenic and immunosuppressive HOXD13-CD73/VEGF gene regulatory axis, we identify a subset of patients who might benefit from combinations of AdR and VEGFR inhibitors which are currently being tested in clinical trials.
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4. ⭐ GSE301973 奥希替尼治疗前EGFR突变型非小细胞肺癌的空间转录组学

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Ritsu Ibusuki ; Eiji Iwama ; Atsushi Shimauchi ; Hiromu Kawano ; Satoshi Nakamura ; Yui MiyazakiSeries Type : OtherOrganism : Homo sapiensEGFR-mutant non-small cell lung cancer (NSCLC) is commonly treated with EGFR tyrosine kinase inhibitors (TKIs) such as osimertinib. However, the development of resistance remains a major clinical challenge, with various resistance mechanisms having been identified. Emerging evidence suggests that the tumor microenvironment (TME) may contribute to this resistance. In this study, we analyzed the TME of pre-treatment tumor samples from EGFR-mutant NSCLC patients using the Visium HD spatial transcriptomics platform to explore its potential role in the development of resistance.
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5. ⭐ GSE301280 空间转录组学揭示寻常痤疮中脂质代谢功能障碍和毛囊皮脂腺分化异常

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Joseph S Durgin ; Sunny Y WongSeries Type : OtherOrganism : Homo sapiensAcne vulgaris is a common skin condition involving complex interactions among lipid-secreting sebaceous glands, keratinocytes, immune cells, and microbiota. While retinoids are effective for treating acne, disease pathogenesis remains poorly understood. In particular, it remains unclear how different subtypes of acne, including inflammatory (pustular) and non-inflammatory (comedonal) lesions, vary in gene expression, signaling, and sebaceous gland involvement. Here, we performed spatial transcriptomics on healthy, non-lesional, comedonal, and pustular acne skin using a custom panel targeting sebaceous differentiation, lipid metabolism, and retinoid signaling pathways. We also designed a specialized segmentation pipeline to improve transcript assignment in the spatially complex sebaceous gland. Our analyses identified a PPARG+ transitional basal cell state in sebocytes and revealed that comedonal skin upregulates sebogenesis genes, whereas pustular skin downregulates sebogenesis. Both lesion types exhibit increased AP-1 transcription factors and elevated FABP5, a chaperone that blunts retinoic acid receptor signaling. Finally, we demonstrate that an AP-1 inhibitor, T-5224, strongly downregulates FABP5 in human keratinocytes and reduces pustule formation in a mouse model of high fat diet-induced folliculitis. Altogether, these findings indicate that altered lipogenesis, retinoid signaling, and keratinocyte differentiation are key features of acne, and nominate AP-1 and FABP5 as potential novel therapeutic targets.
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6. ⭐ GSE289619 IFITM3-MET 相互作用通过 AKT 通路激活驱动 EGFR 突变型非小细胞肺癌中的奥希替尼耐药 II

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、resistance、pathway
• 📝 描述：Contributors : Ritsu Ibusuki ; Eiji Iwama ; Atsushi Shimauchi ; Hiromu Kawano ; Shun Mizusaki ; Satoshi Nakamura ; Isamu OkamotoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensDespite an initial favorable response of EGFR mutant non–small cell lung cancer (NSCLC) to osimertinib, an EGFR tyrosine kinase inhibitor (TKI), resistance inevitably develops. We here performed transcriptomics analysis of pretreatment specimens and identified IFITM3 as a gene specifically upregulated in tumors that develop early resistance to osimertinib. Immunohistochemistry confirmed patients with IFITM3-positive tumors experienced a shorter progression-free survival. Spatial transcriptomics and other analyses further revealed that IFITM3 expression was increased in response to cytokines derived from the tumor microenvironment (TME) during osimertinib treatment. IFITM3 was found to promote the development of osimertinib resistance through interaction with MET and activation of the AKT pathway. Furthermore, combined treatment with a MET inhibitor suppressed the development of osimertinib resistance in a mouse model. Our findings thus reveal that upregulation of IFITM3 represents a previously unrecognized mechanism of osimertinib resistance, and they suggest that targeting the IFITM3-MET axis may improve treatment outcomes.
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7. ⭐ GSE289383 IFITM3-MET 相互作用通过 AKT 通路激活驱动 EGFR 突变型非小细胞肺癌的奥希替尼耐药性

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、resistance、pathway
• 📝 描述：Contributors : Ritsu Ibusuki ; Eiji Iwama ; Atsushi Shimauchi ; Hiromu Kawano ; Shun Mizusaki ; Satoshi Nakamura ; Isamu OkamotoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensDespite an initial favorable response of EGFR mutant non–small cell lung cancer (NSCLC) to osimertinib, an EGFR tyrosine kinase inhibitor (TKI), resistance inevitably develops. We here performed transcriptomics analysis of pretreatment specimens and identified IFITM3 as a gene specifically upregulated in tumors that develop early resistance to osimertinib. Immunohistochemistry confirmed patients with IFITM3-positive tumors experienced a shorter progression-free survival. Spatial transcriptomics and other analyses further revealed that IFITM3 expression was increased in response to cytokines derived from the tumor microenvironment (TME) during osimertinib treatment. IFITM3 was found to promote the development of osimertinib resistance through interaction with MET and activation of the AKT pathway. Furthermore, combined treatment with a MET inhibitor suppressed the development of osimertinib resistance in a mouse model. Our findings thus reveal that upregulation of IFITM3 represents a previously unrecognized mechanism of osimertinib resistance, and they suggest that targeting the IFITM3-MET axis may improve treatment outcomes.
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8. ⭐ GSE310388 胰腺癌原位多模态表征揭示肿瘤细胞特性是周围微环境的决定性因素。[RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、RNA-seq
• 📝 描述：Contributors : Anna Lyubetskaya ; Brian Rabe ; Andrew Kavran ; Yulong Bai ; Andrew Fisher ; Alba Font-Tello ; Anne Lewin ; Hannah Pliner ; Yunfan Fan ; Lauren Giampapa ; Yelena Cheng ; Chao Dai ; Ruifeng Hu ; Tom Lila ; Alexandre P Alloy ; Mike Mason ; Constance Brett ; Todd Brett ; Fayaz Seifuddin ; Steven Vasquez Grinnell ; Soren R Stahlschmidt ; Yilin Zhao ; Ryan Golhar ; Isaac Neuhaus ; Daniel Carrera ; Carlos Rios ; Pradeep Kar ; Abhishek Shukla ; Rachael Bashford-Rogers ; Matthew J Meyer ; Enas Abu Shah ; Lara Heij ; Shivan Sivakumar ; Jimena Trillo Tinoco ; Benjamin J Chen ; Konstantinos J Mavrakis ; Eugene DrokhlyanskySeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensPancreatic ductal adenocarcinoma is heterogeneous, with low tumor purity, a prominent microenvironment, and complex architecture, which preclude the identification of shared tumor-intrinsic and stromal biology within and across patients. We overcame these challenges by achieving necessary resolution and context through the application of complimentary genomics, pathology and machine learning approaches to characterize primary untreated tumors from 39 patients. We capture 340K spatial low-bulk and 530K spatial single-cell transcriptomes and observe a spectrum of classical-to-basal tumor subtypes present within all patients. We find each subtype has distinct regulators, stromal neighborhoods, microenvironment, extracellular matrix and histology corresponding to multiple immunosuppressive and therapy resistance mechanisms. We define key tumor heterogeneity features including the presence of mixed KRAS mutations and tertiary lymphoid structures; identifying biomarkers that distinguish the latter from lymph nodes. Lastly, leveraging patient, cell and mouse data, we determine which aspects of tumor biology are recapitulated in bulk datasets and reductionist models.
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9. ⭐ GSE280735 PRDM16介导的代谢重编程驱动急性髓系白血病产生阿糖胞苷耐药性

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、metabolic、resistance
• 📝 描述：Contributors : Junji Ikeda ; Hiroyoshi KunimotoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAcute myeloid leukemia (AML) patients with high PRDM16 expression frequently experience induction failure and have a poor prognosis. However, the molecular mechanisms underlying these clinical features are elusive. We found that murine AML cells transformed by MLL::AF9 fusion and oncogenic short-isoform Prdm16 overexpression (hereafter, MF9/sPrdm16) exhibited resistance to cytarabine (AraC), but not to anthracycline, both in vitro and in vivo. Intriguingly, MF9/sPrdm16 cells displayed a gene expression signature of high oxidative phosphorylation (OxPHOS) and increased mitochondrial respiration. The inhibition of mitochondrial respiration with metformin or tigecycline abrogated AraC resistance in MF9/sPrdm16 cells via an energetic shift toward low OxPHOS status. Furthermore, sPrdm16 upregulated c-Myc and the glutamine transporter Slc1a5, activating TCA cycle and glutaminolysis. Of note, both OxPHOS and MYC-target gene signatures were significantly enriched in AML patient samples with high PRDM16 expression. Together, we showed that PRDM16 overexpression activates mitochondrial respiration through metabolic reprogramming via c-MYC-SLC1A5-Glutaminolysis axis, thereby conferring AraC resistance on AML cells. These results suggest that targeting mitochondrial respiration might be a novel treatment strategy to overcome chemoresistance in AML patients with high PRDM16 expression.
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10. ⭐ GSE279905 空间分割对肿瘤免疫反应影响的综合评价：以胶质母细胞瘤质子微束放射治疗为例。

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune、spatial
• 📝 描述：Contributors : Lorea Iturri ; Miriam Riquelme-Perez ; Pierre-Emannuel Bonté ; Sarah Potiron ; Christel Goudot ; Marjorie Juchaux ; Elise Brisebard ; Cristèle Gilbert ; Julie Espenon ; Ramón Ortiz ; Annalisa Patriarca ; Ludovic de Marzi ; Sebastián Amigorena ; Yolanda PrezadoSeries Type : Expression profiling by high throughput sequencingOrganism : Rattus norvegicusTreating radioresistant tumors like glioblastoma multiforme (GBM) remains a challenge exacerbated by their immunosuppressive nature. Radiation therapy has an immunomodulatory (immunosuppressive or immunostimulatory) role. The nature of the effects would depend on the total dose, dose per fraction, dose delivery method and treatment length. It is well-known that conventional fractionation schemes (2 Gy per fraction during several weeks) are mainly immunosuppressive and that hypofractionation tips the balance towards immune stimulation. However, the use of hypofractionation is restricted in bulky tumours, i.e. gliomas, due to the high risk of toxicity. Therefore, finding new strategies leading to more favourable immune responses while reducing normal tissue toxicities could be a game-changer. This is the case of proton minibeam radiation therapy (pMBRT). However, its immunomodulatory effects are not fully understood. To explore this, we conducted an in-depth characterization of the immune response to a curative dose of pMBRT in a preclinical orthotopic rat model of glioblastoma. Our findings revealed a close association between pMBRT and the immune response. pMBRT increased lymphocyte density in tumors more effectively than conventional proton therapy. Single-cell transcriptomics identified several immune cell types and unique transcriptional changes in tumor immune cells post-pMBRT, including increased antibody production, chemotactic cytokine expression, and interferon responses. These results underscore the critical role of adaptive immunity, specifically T cells, in pMBRT’s mechanism. The potential of pMBRT to trigger an anti-tumor immune response in a single radiotherapy session with minimal damage to healthy tissue makes it a promising candidate for future clinical trials and radio-immunotherapy combinations.
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1. ⭐ 利用巨噬细胞介导的抗体依赖性细胞吞噬作用进行癌症免疫治疗的事实与希望。

• ✍️ 作者：未知作者
• 🏷️ 关键词：癌症、免疫、巨噬细胞、抗体
• 📝 描述：Secret hovertext: 临床中使用的单克隆抗体（mAbs）可通过其 Fc 结构域作用免疫系统，诱导诸如抗体依赖性细胞毒性（ADCC）和抗体依赖性细胞吞噬作用（ADCP）等效应机制。虽然自然杀手（NK）细胞历来被认为是 ADCC 的主要介质，但新兴证据表明肿瘤相关巨噬细胞（TAM），尤其是单核细胞衍生的亚群，在 ADCP 中起着核心作用。这些巨噬细胞在肿瘤微环境中丰富，表达高水平的活化 Fc 伽马受体（FcγRs），并保持强健的吞噬能力。然而，TAMs 的异质性以及对不同肿瘤类型 FcγR 表达模式的有限了解限制了 ADCP 的治疗利用。本综述批判性地考察了巨噬细胞介导的 ADCP 对肿瘤靶向和免疫调控单抗抗体活性的贡献。我们讨论了 FcγR 多态性、同型工程和抗体效应器功能如何影响治疗效果，特别关注常用的肿瘤靶向和免疫调节抗体。还探讨了抑制性受体如 FcγRIIb、CD47 和 PD-1 在调节 ADCP 中的作用。针对肿瘤抗原的多特异性抗体与
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2. ⭐ 抗体介导的分泌蛋白 SCUBE3 通过抑制致癌信号传导并诱导抗肿瘤免疫来抑制癌症进展

• ✍️ 作者：未知作者
• 🏷️ 关键词：肿瘤、癌症、免疫、抗体
• 📝 描述：Secret hovertext: 针对同时促进肿瘤生长和进展、诱导治疗耐药性和抑制抗肿瘤免疫的因素的方法，明显优于仅针对其中一种肿瘤促进过程的治疗。通过全面的功能丧失基因组筛查，我们确认 SCUBE3 是支持生存和治疗耐药性的关键因素，同时也调节免疫抑制性肿瘤微环境。分泌性 SCUBE3 通过与关键致癌细胞表面受体蛋白（包括 EGFR、突变 CALR 和 TGFβRI/II）的相互作用支持致癌活性。这些相互作用激活了转录因子 FOXR2 和 c-Myc，通过增强 DNA 损伤修复，促进癌细胞增殖和治疗耐药性。此外，SCUBE3-FOXR2 轴通过促进 DNMT1 表观遗传抑制复合物招募至转录调控 IRF1，从而抑制 MHC-I 和 MHC-II 基因的表达，创造了免疫抑制性肿瘤微环境。一种首创的针对 SCUBE3 的中和抗体，利用先进的抗体发现平台开发，并通过重链中特定突变工程化，增强特异性和疗效，在包括乳腺癌和卵巢癌患者
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3. 癌症中的铁凋亡：代谢、机制及治疗前景。

• ✍️ 作者：未知作者
• 🏷️ 关键词：癌症、代谢
• 📝 描述：Secret hovertext: 铁剥落是一种细胞死亡的形式，区别于细胞凋亡、坏死和自噬。这是一种新型的程序性细胞死亡（PCD），由铁的积累和过氧化触发，与细胞内铁代谢疾病相关。自 2012 年命名以来，铁剥蚀因其在人类疾病中的作用而受到越来越多的关注，尤其是在肿瘤形成、进展和治疗方面。大量研究表明，铁消亡在杀死肿瘤细胞、抑制肿瘤增殖和转移以及逆转治疗耐药性方面起着关键作用。因此，针对肿瘤细胞中铁剥落症的靶向诱导被视为一种新型抗肿瘤治疗策略。
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4. 抗体正电子发射断层扫描在癌症影像中的临床转化。

• ✍️ 作者：未知作者
• 🏷️ 关键词：癌症、抗体
• 📝 描述：Secret hovertext: 肝细胞癌（HCC）缺乏精确且非侵入性的诊断工具。为此，开发了一种新的正电子发射断层扫描（PET）放射示踪剂[68Ga]Ga-XH-06。它利用抗体片段靶向高度特异性的生物标志物草甘-3（GPC3），成功观察肝细胞癌患者的 GPC3 表达，可能满足重要的未满足需求。
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5. 将受损线粒体从癌细胞转移到癌相关成纤维细胞，促进 EGFR 突变肺癌中酪氨酸激酶抑制剂耐受性

• ✍️ 作者：未知作者
• 🏷️ 关键词：线粒体、激酶
• 📝 描述：Secret hovertext: 耐药持久体（DTP）细胞驱动 EGFR 突变肺腺癌的治疗耐药性。利用单细胞 RNA 测序，我们鉴定出一个临床显著的 RGS5+MYL9+癌相关成纤维细胞（CAF）群体，该群体与 EGFR 酪氨酸激酶抑制剂（TKI）耐药性和预后较差相关。这些 CAFs 通过 CCL11 信号被招募到 DTP 生态位，并通过 TKI 产生的线粒体活性氧（ROS）诱导的 Miro1/RhoA 激活形成隧穿纳米管。值得注意的是，RGS5+MYL9+ CAFs 通过接受肿瘤来源的受损线粒体，作为“代谢汇”，从而促进 DTP 存活。使用法苏地尔（一种 Rho 激酶抑制剂）治疗，有效阻断线粒体转移，并在体内恢复了对 EGFR-TKI 奥西默替尼的敏感性。本研究共同揭示了可靶向的基质-肿瘤串扰，这些相互作用维持 DTP 群体，提出了克服 EGFR-TKI 耐药性的联合疗法。
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6. 癌症转录组解卷积指南。

• ✍️ 作者：未知作者
• 🏷️ 关键词：癌症、转录组
• 📝 描述：Secret hovertext: 癌组织是肿瘤、基质和免疫细胞的异质混合体，每个组成部分包含多种不同的细胞类型和/或状态。绘制这种异质性图谱并理解每种细胞类型对肿瘤转录组的独特贡献对于推动癌症生物学的发展至关重要，然而肿瘤组织的高通量表达谱仅代表来自所有细胞来源的综合信号。对这些混合信号的计算解卷积已成为剖析细胞组成和细胞类型特异表达模式的有力方法。本文为癌症研究人员提供一份全面的转录组去卷积指南，专门针对癌症研究人员，提出了一个系统框架，帮助选择和应用去卷积方法，同时考虑肿瘤组织的独特复杂性、数据可用性和方法假设。我们详细介绍了43种解卷积方法，并概述了不同方法在癌症研究中各自的独特应用：从理解肿瘤免疫监测到识别癌症亚型、发现预后生物标志物以及表征空间肿瘤结构。通过分析这些方法的能力与局限性，我们突显了新兴趋势和未来方向，特别是在肿瘤细胞可塑性和动态细胞状态方面的研究。
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7. 2025年癌症研究进展的反思。

• ✍️ 作者：未知作者
• 🏷️ 关键词：癌症
• 📝 描述：Secret hovertext:
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8. GFER 是胰腺腺癌中氧化还原稳态破坏和免疫反应再激活的靶点

• ✍️ 作者：未知作者
• 🏷️ 关键词：免疫
• 📝 描述：Secret hovertext: 胰管腺癌（PDAC）的代谢失调和免疫抑制性肿瘤微环境均导致该致命疾病的治疗迟缓。因此，我们旨在鉴定并表征一种通过破坏癌细胞氧化还原稳态和提高 PDAC 免疫原性来引发抗癌反应的靶点。首先，通过使用带有自定义 sgRNA 文库的 CRISPR-Cas9 筛选系统，鉴定了 PDAC 中的线粒体代谢依赖性。功能验证分析显示 GFER 是一种线粒体依赖 FAD 的磺碱氧化酶，是肿瘤生长的重要调控因子。体外和体内方法学表明，GFER 耗竭扰乱了氧化还原稳态，并刺激肿瘤免疫原性，包括对免疫检查点阻断的敏感化。在患者衍生的 PDAC 异种移植模型中，GFER 耗竭诱导的生长抑制反应是由改变的氧化平衡介导，该反应释放受损的线粒体 DNA 进入肿瘤细胞质，从而激活 cGAS-STING 通路并表达 I 型干扰素。这一效应在一个小鼠免疫正常的合成 PDAC 模型中得以重现，其中 GFER 耗竭抑制肿瘤生长，促进
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9. 多组学谱分析为小细胞肺癌的异质性、微环境特征及生物标志物景观提供了见解。

• ✍️ 作者：未知作者
• 🏷️ 关键词：微生物
• 📝 描述：Secret hovertext: 背景 需要更深入理解小细胞肺癌（SCLC）中针对免疫治疗的治疗敏感性差异。方法 我们通过对 159 名未治疗患者的肿瘤组织样本进行整合分子表征，利用遗传、表观遗传、转录和蛋白质组分析，对多种生物学相关标志物（包括转录亚型定义蛋白）进行免疫组化学染色，以及多重免疫荧光空间免疫分析，探索了 SCLC 的异质性。结果 多组学分析证实神经内分泌和非神经内分泌亚型之间存在高度异质性。甲基组学分析确定了四个甲基组簇，可能增强亚型预测、预后及亚型演化的纵向监测。免疫组化分析显示非神经内分泌亚型中 MHC-I 表达较高，这些亚型在化疗中加入免疫治疗具有最大潜在益处;与神经内分泌亚型及免疫性冷性肿瘤微环境相关的高 DLL3 表达。多重免疫荧光显示 MHC-I 与高 MHC-I 表达 SCLC 肿瘤微环境中免疫细胞的空间排列和表型特征相关，为 MHC-I 作为免疫治疗反应潜在生物标志物提供了机制依据。结论 这一多模态剖析分析进一步揭示了
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10. 老年癌症患者老年评估与管理的成本效用：从证据到实施。

• ✍️ 作者：未知作者
• 🏷️ 关键词：癌症
• 📝 描述：Secret hovertext:
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💡 该来源还有 1 条内容，详见 文末

• GSE303995 人类胶质母细胞瘤和脑膜瘤中特异性肿瘤内微生物组特征：肠-脑微生物轴的证据
• GSE271116 单细胞转录组学揭示了帕金森病人类中脑样器官模型中的分子脆弱性 [scRNA-Seq]
• GSE271115 单细胞转录组学揭示了帕金森病人类中脑样类器官模型中的分子脆弱性 [RNA-Seq]
• GSE311908 一个可靶向的发育程序共同调控血管生成和免疫逃逸 [RNA-Seq]
• GSE311907 一个可靶向的发育程序共同调节血管生成和免疫逃逸 [Hi-C]
• GSE311906 一个可靶向的发育程序共同调控血管生成和免疫逃逸 [ChIP-seq、ATACseq 和 CUT&Tag]
• GSE287963 癌症相关成纤维细胞衍生的CCL5促进神经内分泌前列腺癌的顺铂耐药性
• GSE283755 药物治疗对子宫内膜异位症患者恶性转化为透明细胞癌的影响：基于下一代测序（NGS）的基因表达比较研究
• GSE310353 胰腺癌原位多模态表征揭示肿瘤细胞特性是周围微环境的决定性因素
• GSE310352 胰腺癌原位多模态表征揭示肿瘤细胞特性是周围微环境的决定性因素 [Nanostring CosMx]
• GSE307850 巨噬细胞调节ILC2上PD-1和CTLA-4的表达及其在肿瘤微环境中的反应性
• GSE281045 Ctcf f/f 和 Ctcf Δ/Δ CALM-AF10 AML 细胞中 H3K4kme3、H3K27ac 和 H3K27me3 的全基因组定位 [Tgm2 RNA-seq]
• GSE281044 Ctcf f/f 和 Ctcf Δ/Δ CALM-AF10 AML 细胞中 H3K4kme3、H3K27ac 和 H3K27me3 的全基因组定位 [CTCF RNA-seq]
• GSE281043 Ctcf f/f 和 Ctcf Δ/Δ CALM-AF10 AML 细胞中 H3K4kme3、H3K27ac 和 H3K27me3 的全基因组定位 [ChIP-seq]
• GSE305400 研究发现，STING 诱导的血脑屏障开放与放射疗法联合应用可增强抗胶质瘤免疫和治疗活性，该活性可通过 [18F]-FLT PET 监测。
• GSE311895 线粒体硬度相关转移通过代谢重编程促进肿瘤进展
• GSE271118 单细胞转录组学揭示了帕金森病人类中脑样器官模型中的分子脆弱性 [MERFISH]
• GSE183843 FBXO11 的缺失通过 LONP1 失调在急性髓系白血病中建立干细胞程序 [RNA-seq]
• GSE312352 IL-22 诱导溃疡性结肠炎结肠上皮细胞发生潘氏细胞化生，通过 REG3A 促进伤口愈合 [小鼠 RNA-seq]
• GSE312136 高分辨率体内结合数据显示，TBP 在有或没有 TFIID 的情况下均可在 TATA 启动子处启动转录 [RNA-seq]
• GSE311910 一个可靶向的发育程序共同调控血管生成和免疫逃逸 [scRNAseq]
• GSE307724 肥大细胞类胰蛋白酶诱导乳腺癌细胞核重塑并抑制其生长
• GSE306834 EC359 通过抑制 LIFR 信号通路增强曲美替尼在 Ras/Raf 驱动的卵巢癌中的疗效
• GSE306270 低氮胁迫下乌苏里杨转录组响应分析
• GSE305912 绒毛蛋白样蛋白通过下调MYC抑制鼻咽癌增殖
• GSE299157 D419N突变对EuMyc小鼠淋巴瘤细胞中STAT6转录因子活性的影响
• GSE295068 蒽环类药物通过表观遗传调控ALDH1的表达，导致急性髓系白血病（AML）产生适应性氧化反应和耐药性
• GSE290907 ZDHHC12 棕榈酰化 HDAC8 并促进与高饱和脂肪酸饮食相关的肝细胞癌的发生发展
• GSE227658 利用转录组断层扫描技术对亨廷顿病模型小鼠 R6/2 出生后 5 周的正常同窝对照小鼠全脑进行基因表达谱分析
• GSE227657 利用转录组断层扫描技术对亨廷顿病模型小鼠 R6/2 出生后 5 周的全脑进行基因表达谱分析
• GSE312051 秀丽隐杆线虫转录组和表型上位性分析揭示了 daf-2/InsR 在 L1 期阻滞和恢复过程中 daf-16/FoxO 依赖性和非依赖性效应
• GSE311502 3’UTR衍生的小RNA调节霍乱毒素编码丝状噬菌体CTXϕ的生命周期[RNA-Seq]
• GSE303819 母体血液转录组反映了胎儿生长变化，并且是牛出生体重的准确预测指标。
• GSE298445 SOX10 通过 IRF1-ITGA3/EphA2-FAK 通路调控黑色素瘤转移。
• GSE295359 大规模单细胞分析揭示了与同种异体造血干细胞移植后急性移植物抗宿主病相关的新型生物标志物
• GSE294627 利用人类多能干细胞衍生的心肌细胞和3D心脏微组织模拟心肌生理生长
• GSE287043 结节病中独特的结核分枝杆菌特异性血液免疫特征：对临床诊断的意义
• GSE279320 口服葡聚糖硫酸钠治疗后，野生型和 VISTA-KO 小鼠结肠 CD45+ 细胞的单细胞 RNA 测序数据。
• GSE278119 研究发现，克隆扩增的效应 CD4+ 细胞毒性 T 淋巴细胞与免疫检查点抑制剂治疗后严重的神经系统不良事件相关。
• GSE271486 构建可转移的NGS算法模型以预测EBV相关鼻咽癌和高危突变
• GSE291676 TSniffer：RNA 编辑位点的无偏从头识别和 RNA-seq 数据中编辑活性的定量分析 [重新分析]
• GSE291675 TSniffer：对 RNA 编辑位点进行无偏倚的从头识别，并量化 RNA-seq 数据中的编辑活性
• GSE312368 一个可靶向的发育程序共同调节血管生成和免疫逃逸。
• GSE312339 豚鼠胎儿和母体肝脏转录组的比较 RNA-seq 分析揭示了广泛的转录差异。
• GSE312031 染色质拓扑结构和 H3K27me3 重分布的时空重塑是 Hutchinson-Gilford 早衰症血管病理的基础 [Hi-C]
• GSE311894 硒介导的RUNX2过表达及其转录组改变对卡欣贝克病软骨细胞损伤的影响
• GSE311574 胰腺癌上皮间质细胞可塑性的治疗靶向治疗
• GSE302100 尿嘧啶-DNA糖苷酶缺乏与肿瘤细胞内在炎症信号传导受抑制和对外源性干扰素的敏感性改变有关
• GSE292740 CPXM2 排列的胶原蛋白对 PaTu 8988t 细胞基因表达和细胞内信号通路的影响。
• GSE292738 临床肿瘤旁组织和胰腺导管腺癌样本中不同的基因表达
• GSE290161 利用 CITE-seq 对流感相关肺曲霉病肺部进行免疫谱分析
• GSE287134 蛋氨酸限制通过表观遗传抑制TGF-β/Smad3/Hoxc8/P-TEFb轴缓解肾纤维化
• GSE283201 对年轻（3 个月大）和年老（22 个月大）野生型小鼠在对照和乙醇喂养条件下的海马和肝脏 RNA-seq 数据进行比较基因表达谱分析。

• FLIPI24：新诊断滤泡性淋巴瘤的现代预后模型和临床试验丰富工具。