Cancer Cell最新文献_第10页

Let it be: Preserving tumor-draining lymph nodes in the era of immuno-oncology 顺其自然：在免疫肿瘤学时代保留肿瘤引流淋巴结

IF 50.3 1区医学

Cancer Cell Pub Date : 2024-06-10 DOI: 10.1016/j.ccell.2024.05.015

Robert Saddawi-Konefka, Shiruyeh Schokrpur, J. Silvio Gutkind

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Selective inhibition of tumor microvascular permeability by cavtratin blocks tumor progression in mice. 腔棘肽（cavtratin）对肿瘤微血管通透性的选择性抑制可阻止小鼠的肿瘤进展。

IF 50.3 1区医学

Cancer Cell Pub Date : 2024-06-10 Epub Date: 2024-05-30 DOI: 10.1016/j.ccell.2024.05.009

Jean-Philippe Gratton, Michelle I Lin, Jun Yu, Erik D Weiss, Zao Li Jiang, Todd A Fairchild, Yasuko Iwakiri, Roberto Groszmann, Kevin P Claffey, Yung-Chi Cheng, William C Sessa

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RNA vaccines for cancer: Principles to practice 治疗癌症的 RNA 疫苗：从原理到实践

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Cancer Cell Pub Date : 2024-06-06 DOI: 10.1016/j.ccell.2024.05.005

Pablo Guasp, Charlotte Reiche, Zachary Sethna, Vinod P. Balachandran

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Engineering cancer’s end: An interdisciplinary approach to confront the complexities of cancer 工程学终结癌症：应对癌症复杂性的跨学科方法

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Cancer Cell Pub Date : 2024-06-06 DOI: 10.1016/j.ccell.2024.05.017

Elsa R. Flores, W. Gregory Sawyer

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Engineering focusing on cancer 以癌症为重点的工程学

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Cancer Cell Pub Date : 2024-06-06 DOI: 10.1016/j.ccell.2024.04.013

Kayvan R. Keshari, Daniel A. Heller, Rostislav Boltyanskiy, Hedvig Hricak, Thomas Magaldi, Michael Overholtzer

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Identification of specific PP2A complexes involved in human cell transformation 鉴定参与人类细胞转化的特定 PP2A 复合物

IF 50.3 1区医学

Cancer Cell Pub Date : 2024-05-30 DOI: 10.1016/j.ccell.2024.05.010

Wen Chen, Richard Possemato, K. Thirza Campbell, Courtney A. Plattner, David C. Pallas, William C. Hahn

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Neural deception: Breast cancer co-opts neuronal mechanisms to evade the immune system 神经欺骗：乳腺癌利用神经元机制躲避免疫系统的攻击

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Cancer Cell Pub Date : 2024-05-30 DOI: 10.1016/j.ccell.2024.05.007

Nikolas Layer, Lukas Bunse, Varun Venkataramani

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Tumor cells impair immunological synapse formation via central nervous system-enriched metabolite 肿瘤细胞通过富含中枢神经系统的代谢物损害免疫突触的形成

IF 50.3 1区医学

Cancer Cell Pub Date : 2024-05-30 DOI: 10.1016/j.ccell.2024.05.006

Yihong Li, Min Huang, Minger Wang, Yi Wang, Peng Deng, Chunni Li, Jingying Huang, Hui Chen, Zhihao Wei, Qian Ouyang, Jinghua Zhao, Yiwen Lu, Shicheng Su

{"title":"Tumor cells impair immunological synapse formation via central nervous system-enriched metabolite","authors":"Yihong Li, Min Huang, Minger Wang, Yi Wang, Peng Deng, Chunni Li, Jingying Huang, Hui Chen, Zhihao Wei, Qian Ouyang, Jinghua Zhao, Yiwen Lu, Shicheng Su","doi":"10.1016/j.ccell.2024.05.006","DOIUrl":"https://doi.org/10.1016/j.ccell.2024.05.006","url":null,"abstract":"Tumors employ various strategies to evade immune surveillance. Central nervous system (CNS) has multiple features to restrain immune response. Whether tumors and CNS share similar programs of immunosuppression is elusive. Here, we analyze multi-omics data of tumors from HER2+ breast cancer patients receiving trastuzumab and anti-PD-L1 antibody and find that CNS-enriched N-acetyltransferase 8-like (NAT8L) and its metabolite N-acetylaspartate (NAA) are overexpressed in resistant tumors. In CNS, NAA is released during brain inflammation. NAT8L attenuates brain inflammation and impairs anti-tumor immunity by inhibiting cytotoxicity of natural killer (NK) cells and CD8+ T cells via NAA. NAA disrupts the formation of immunological synapse by promoting PCAF-induced acetylation of lamin A-K542, which inhibits the integration between lamin A and SUN2 and impairs polarization of lytic granules. We uncover that tumor cells mimic the anti-inflammatory mechanism of CNS to evade anti-tumor immunity and NAT8L is a potential target to enhance efficacy of anti-cancer agents.","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":null,"pages":null},"PeriodicalIF":50.3,"publicationDate":"2024-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141177884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Olfactory neuroblastoma mimics molecular heterogeneity and lineage trajectories of small-cell lung cancer 嗅神经母细胞瘤模拟小细胞肺癌的分子异质性和细胞系轨迹

IF 50.3 1区医学

Cancer Cell Pub Date : 2024-05-23 DOI: 10.1016/j.ccell.2024.05.003

John B. Finlay, Abbie S. Ireland, Sarah B. Hawgood, Tony Reyes, Tiffany Ko, Rachelle R. Olsen, Ralph Abi Hachem, David W. Jang, Diana Bell, Joseph M. Chan, Bradley J. Goldstein, Trudy G. Oliver

{"title":"Olfactory neuroblastoma mimics molecular heterogeneity and lineage trajectories of small-cell lung cancer","authors":"John B. Finlay, Abbie S. Ireland, Sarah B. Hawgood, Tony Reyes, Tiffany Ko, Rachelle R. Olsen, Ralph Abi Hachem, David W. Jang, Diana Bell, Joseph M. Chan, Bradley J. Goldstein, Trudy G. Oliver","doi":"10.1016/j.ccell.2024.05.003","DOIUrl":"https://doi.org/10.1016/j.ccell.2024.05.003","url":null,"abstract":"The olfactory epithelium undergoes neuronal regeneration from basal stem cells and is susceptible to olfactory neuroblastoma (ONB), a rare tumor of unclear origins. Employing alterations in Rb1/Trp53/Myc (RPM), we establish a genetically engineered mouse model of high-grade metastatic ONB exhibiting a NEUROD1+ immature neuronal phenotype. We demonstrate that globose basal cells (GBCs) are a permissive cell of origin for ONB and that ONBs exhibit cell fate heterogeneity that mimics normal GBC developmental trajectories. ASCL1 loss in RPM ONB leads to emergence of non-neuronal histopathologies, including a POU2F3+ microvillar-like state. Similar to small-cell lung cancer (SCLC), mouse and human ONBs exhibit mutually exclusive NEUROD1 and POU2F3-like states, an immune-cold tumor microenvironment, intratumoral cell fate heterogeneity comprising neuronal and non-neuronal lineages, and cell fate plasticity—evidenced by barcode-based lineage tracing and single-cell transcriptomics. Collectively, our findings highlight conserved similarities between ONB and neuroendocrine tumors with significant implications for ONB classification and treatment.","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":null,"pages":null},"PeriodicalIF":50.3,"publicationDate":"2024-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141085727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Molecular subtypes of neuroendocrine carcinomas: A cross-tissue classification framework based on five transcriptional regulators 神经内分泌癌的分子亚型：基于五种转录调节因子的跨组织分类框架

IF 50.3 1区医学

Cancer Cell Pub Date : 2024-05-23 DOI: 10.1016/j.ccell.2024.05.002

Zhanyu Wang, Chengming Liu, Sufei Zheng, Yuxin Yao, Sihui Wang, Xinfeng Wang, Enzhi Yin, Qingpeng Zeng, Chaoqi Zhang, Guochao Zhang, Wei Tang, Bo Zheng, Liyan Xue, Zhen Wang, Xiaoli Feng, Yan Wang, Jianming Ying, Qi Xue, Nan Sun, Jie He

{"title":"Molecular subtypes of neuroendocrine carcinomas: A cross-tissue classification framework based on five transcriptional regulators","authors":"Zhanyu Wang, Chengming Liu, Sufei Zheng, Yuxin Yao, Sihui Wang, Xinfeng Wang, Enzhi Yin, Qingpeng Zeng, Chaoqi Zhang, Guochao Zhang, Wei Tang, Bo Zheng, Liyan Xue, Zhen Wang, Xiaoli Feng, Yan Wang, Jianming Ying, Qi Xue, Nan Sun, Jie He","doi":"10.1016/j.ccell.2024.05.002","DOIUrl":"https://doi.org/10.1016/j.ccell.2024.05.002","url":null,"abstract":"Neuroendocrine carcinomas (NECs) are extremely lethal malignancies that can arise at almost any anatomic site. Characterization of NECs is hindered by their rarity and significant inter- and intra-tissue heterogeneity. Herein, through an integrative analysis of over 1,000 NECs originating from 31 various tissues, we reveal their tissue-independent convergence and further unveil molecular divergence driven by distinct transcriptional regulators. Pan-tissue NECs are therefore categorized into five intrinsic subtypes defined by ASCL1, NEUROD1, HNF4A, POU2F3, and YAP1. A comprehensive portrait of these subtypes is depicted, highlighting subtype-specific transcriptional programs, genomic alterations, evolution trajectories, therapeutic vulnerabilities, and clinicopathological presentations. Notably, the newly discovered HNF4A-dominated subtype-H exhibits a gastrointestinal-like signature, wild-type RB1, unique neuroendocrine differentiation, poor chemotherapeutic response, and prevalent large-cell morphology. The proposal of uniform classification paradigm illuminates transcriptional basis of NEC heterogeneity and bridges the gap across different lineages and cytomorphological variants, in which context-dependent prevalence of subtypes underlies their phenotypic disparities.","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":null,"pages":null},"PeriodicalIF":50.3,"publicationDate":"2024-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141085698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0