Nature Reviews Cancer最新文献_第3页

Rules of partitioning 划分规则

IF 66.8 1区医学

Nature Reviews Cancer Pub Date : 2025-08-08 DOI: 10.1038/s41568-025-00866-z

Anna Dart

引用次数: 0

Same same but different 相同但不同

IF 66.8 1区医学

Nature Reviews Cancer Pub Date : 2025-08-07 DOI: 10.1038/s41568-025-00862-3

Daniela Senft

引用次数: 0

Stromal senescence contributes to age-related increases in cancer 基质衰老会导致癌症与年龄相关的增加。

IF 66.8 1区医学

Nature Reviews Cancer Pub Date : 2025-08-04 DOI: 10.1038/s41568-025-00840-9

Jiayu Ye, Anupama Melam, Sheila A. Stewart

{"title":"Stromal senescence contributes to age-related increases in cancer","authors":"Jiayu Ye, Anupama Melam, Sheila A. Stewart","doi":"10.1038/s41568-025-00840-9","DOIUrl":"10.1038/s41568-025-00840-9","url":null,"abstract":"Ageing is a process characterized by a wide array of cellular and systemic changes that together increase the risk of developing cancer. While cell-autonomous mutations within incipient tumour cells are important, age-related changes in the microenvironment are critical partners in the transformation process and response to therapy. However, aspects of ageing that are important and the degree to which they contribute to cancer remain obscure. One of the factors that impacts ageing is increased cellular senescence but it is important to note that ageing and cellular senescence are not synonymous. We highlight open questions, including if senescent cells have phenotypically distinct impacts in aged versus young tissue, or if it is the cell type that dictates the impact of senescence on tissue homeostasis and disease. Finally, it is probable that our current definition of cellular senescence encompasses more than one mechanistically distinct cellular state; thus, we highlight phenotypic differences that have been noted across cell types and tissues of origin. This Review focuses on the role that senescent stromal cells have in cancer, with a particular emphasis on fibroblasts given the amount of work that has focused on them. Ageing influences cancer risk through cellular and environmental changes, including the induction of cellular senescence. In this Review, Ye, Melam and Stewart highlight the role of senescent stromal cells in cancer and the therapeutic implications of this.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"25 10","pages":"781-800"},"PeriodicalIF":66.8,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144777931","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

Advancing engineering design strategies for targeted cancer nanomedicine 推进靶向癌症纳米药物的工程设计策略

IF 66.8 1区医学

Nature Reviews Cancer Pub Date : 2025-08-01 DOI: 10.1038/s41568-025-00847-2

Victoria F. Gomerdinger, Namita Nabar, Paula T. Hammond

{"title":"Advancing engineering design strategies for targeted cancer nanomedicine","authors":"Victoria F. Gomerdinger, Namita Nabar, Paula T. Hammond","doi":"10.1038/s41568-025-00847-2","DOIUrl":"10.1038/s41568-025-00847-2","url":null,"abstract":"Engineered nanoparticles have greatly expanded cancer treatment by encapsulating and delivering therapeutic and diagnostic agents, otherwise limited by poor pharmacokinetics and toxicity, to target tumour cells. Leveraging our increased understanding of the tumour microenvironment, nanomedicine has expanded to additionally target key tissues and cells implicated in tumorigenesis, such as immune and stromal cells, to improve potency and further mitigate off-target toxicities. To design nanocarriers that overcome the body’s physiological barriers to access tumours, the field has explored broader routes of administration and nanoparticle design principles, beyond the enhanced permeation and retention effect. This Review explores the advantages of non-covalent surface modifications of nanoparticles, along with other surface modifications, to modulate nanoparticle trafficking from the injection site, into tumour and lymphoid tissues, to the target cell, and ultimately its subcellular fate. Using electrostatic or other non-covalent techniques, nanoparticle surfaces can be decorated with native and synthetic macromolecules that confer highly precise cell and tissue trafficking. Rational design can additionally minimize detection and clearance by the immune system and prolong half-life — key to maximizing efficacy of therapeutic cargos. Finally, we outline how cancer nanomedicine continues to evolve by incorporating learnings from novel screening technologies, computational approaches and patient-level data to design efficacious targeted therapies. Nanoparticle surfaces can be engineered for targeted delivery of cancer therapies. In this Review, Gomerdinger, Nabar and Hammond outline the role of surface chemistry at all levels of nanoparticle trafficking, from administration route, to tissue accumulation, cellular targeting and ultimately subcellular localization. They emphasize the utility of non-covalent surface modifications for improving stealth and targeting abilities of nanoparticles for cancer.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"25 9","pages":"657-683"},"PeriodicalIF":66.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144756374","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

No strain, no formate gains 没有应变，没有甲酸增益

IF 66.8 1区医学

Nature Reviews Cancer Pub Date : 2025-07-31 DOI: 10.1038/s41568-025-00860-5

Gabrielle Brewer

引用次数: 0

Metabolic adaptations of brain metastasis 脑转移的代谢适应

IF 66.8 1区医学

Nature Reviews Cancer Pub Date : 2025-07-24 DOI: 10.1038/s41568-025-00848-1

Pravat Kumar Parida, Srinivas Malladi

{"title":"Metabolic adaptations of brain metastasis","authors":"Pravat Kumar Parida, Srinivas Malladi","doi":"10.1038/s41568-025-00848-1","DOIUrl":"10.1038/s41568-025-00848-1","url":null,"abstract":"Brain metastases remain a major clinical challenge, characterized by high mortality rates and often limited therapeutic options. The cellular and molecular processes that drive brain metastases are highly intricate, underscored by dynamic metabolic adaptations that enable tumour cells to thrive in the unique microenvironment of the brain. Emerging clinical and preclinical evidence reveals that these metabolic adaptations are not uniform but vary based on the tumour’s tissue of origin, oncogenomic landscape and capacity to endure nutrient stress. Notably, proliferative and dormant metastatic cells within the brain exhibit distinct metabolic profiles, highlighting the complexity of targeting these cells. Key metabolic pathways, including glucose, fatty acid and amino acid metabolism, are co-opted not only to sustain cancer cell survival and growth but also to modulate interactions with resident brain cells, reshaping their function to support metastasis. Importantly, this metabolic heterogeneity underscores the inadequacy of a one-size-fits-all therapeutic approach. Here, we review the adaptive metabolic reprogramming that facilitates brain metastases and discuss emerging strategies to tailor interventions aimed at preventing and treating overt brain metastases. In this Review, Parida and Malladi summarize the metabolic adaptations of tumour cells upon dissemination to the brain, outline the metabolic crosstalk between cancer and brain-resident cells and discuss potential strategies to target these adaptations to improve outcomes for patients with brain metastasis.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"25 9","pages":"723-739"},"PeriodicalIF":66.8,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144693973","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

Replication timings affect the frequency of chromosomal translocation 复制时间影响染色体易位的频率

IF 78.5 1区医学

Nature Reviews Cancer Pub Date : 2025-07-23 DOI: 10.1038/s41568-025-00856-1

Promeet Halder, Mrinal Srivastava

引用次数: 0

Environmental endocrine disruptors: rethinking the origins of early-onset ER+ breast cancer 环境内分泌干扰物：重新思考早发性ER+乳腺癌的起源

IF 78.5 1区医学

Nature Reviews Cancer Pub Date : 2025-07-22 DOI: 10.1038/s41568-025-00854-3

Meadow Parrish, Charlotte Kuperwasser

引用次数: 0

Cas12a mice enable the rapid generation of highly complex tumour genotypes Cas12a小鼠能够快速产生高度复杂的肿瘤基因型