Nature Reviews Cancer最新文献_第2页

Implementing practice-changing progress for managing cancer of unknown primary. 在原发不明的癌症管理中实施改变实践的进展。

IF 78.5 1区医学

Nature Reviews Cancer Pub Date : 2025-09-24 DOI: 10.1038/s41568-025-00877-w

F Anthony Greco

引用次数: 0

Discovering genetic interactions that cause melanoma in a non-model species. 发现非模式物种中导致黑色素瘤的基因相互作用。

IF 78.5 1区医学

Nature Reviews Cancer Pub Date : 2025-09-24 DOI: 10.1038/s41568-025-00884-x

Alessandro Lopez-Hernandez,Diego Ortega-Del Vecchyo

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Slaying the pre-TCR beast 杀死tcr之前的野兽。

IF 66.8 1区医学

Nature Reviews Cancer Pub Date : 2025-09-22 DOI: 10.1038/s41568-025-00880-1

Gabrielle Brewer

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The immune microenvironment of colorectal cancer. 结直肠癌的免疫微环境。

IF 78.5 1区医学

Nature Reviews Cancer Pub Date : 2025-09-22 DOI: 10.1038/s41568-025-00872-1

Kilian B Kennel,Florian R Greten

{"title":"The immune microenvironment of colorectal cancer.","authors":"Kilian B Kennel,Florian R Greten","doi":"10.1038/s41568-025-00872-1","DOIUrl":"https://doi.org/10.1038/s41568-025-00872-1","url":null,"abstract":"Colorectal cancer (CRC) progression depends on the close interaction of tumour cells and the tumour microenvironment (TME). Although the TME contributes to poor therapy responses and immune evasion, immune cells within the TME can be therapeutically leveraged, as exemplified by immune checkpoint blockade (ICB). Unfortunately, only a small subset of patients with CRC benefit from ICB therapy; those with immune-activated, microsatellite unstable CRC respond, whereas the predominant group of patients with CRC, those with microsatellite-stable tumours, do not. Although challenging, modulating the TME of CRC to convert these lowly immunogenic and immunosuppressed tumours into immune-activated tumours holds tremendous therapeutic potential. In this Review we provide an overview of the cellular and molecular components of immunity in the TME of CRCs at various stages of disease as well as the mechanisms of immunosuppression and immune evasion. We further describe how systemic and local therapies for CRC impact the tumour and systemic immune microenvironments, and how immunity could serve as a therapeutic and prognostic biomarker. Lastly, we highlight novel immunotherapeutic strategies and approaches that modulate the TME of CRCs to make them amenable to immunotherapy.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"40 1","pages":""},"PeriodicalIF":78.5,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145116797","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

Are GLP-1 receptor agonists a ‘magic bullet’ for cancer? GLP-1受体激动剂是治疗癌症的“魔弹”吗？

IF 78.5 1区医学

Nature Reviews Cancer Pub Date : 2025-09-10 DOI: 10.1038/s41568-025-00874-z

James R. Hebert, E. Angela Murphy, Mary C. Playdon, Liza Makowski, Anna R. Ibele, Ciaran M. Fairman, Lorne J. Hofseth

引用次数: 0

Mechanisms and treatment of cancer therapy-induced peripheral and central neurotoxicity 癌症治疗诱导的周围和中枢神经毒性的机制和治疗

IF 78.5 1区医学

Nature Reviews Cancer Pub Date : 2025-09-09 DOI: 10.1038/s41568-025-00863-2

Philipp Karschnia, Thomas A. Nelson, Jorg Dietrich

{"title":"Mechanisms and treatment of cancer therapy-induced peripheral and central neurotoxicity","authors":"Philipp Karschnia, Thomas A. Nelson, Jorg Dietrich","doi":"10.1038/s41568-025-00863-2","DOIUrl":"https://doi.org/10.1038/s41568-025-00863-2","url":null,"abstract":"<p>Neurotoxicity is a common and potentially severe adverse effect from conventional and novel cancer therapy. The mechanisms that underlie clinical symptoms of central and peripheral nervous system injury remain incompletely understood. For conventional cytotoxic chemotherapy or radiotherapy, direct toxicities to brain structures and neurovascular damage may result in myelin degradation and impaired neurogenesis, which eventually translates into delayed neurodegeneration accompanied by cognitive symptoms. Chemotherapy-induced peripheral neuropathy is one of the most prevalent adverse events of chemotherapy, seen specifically with platinum- and taxane-based regimens, vinca alkaloids, thalidomide and bortezomib, and is also emerging as a concerning feature of novel targeted therapies and immunotherapies. In patients treated with molecularly targeted compounds or immune-activating agents, on-target but off-tumour effects and systemic inflammation characterize a distinct clinical profile with predominantly acute neurological symptoms with a phenotype defined by the specific antigen target. The development of mechanistically driven treatment strategies for both central and peripheral nervous system injury from cancer therapies is a major unmet medical need. Clinical trials designed to test pharmacotherapeutic interventions (including anti-dementia drugs or cognitive stimulants) for cognitive symptoms after conventional chemotherapy have produced conflicting results. In the case of acute neurotoxic adverse events from immunotherapies, reversal of T cell expansion together with drugs targeting specific pro-inflammatory interleukins have shown beneficial effects in selected patients. Large clinical trials to test novel strategies and pharmacotherapeutic interventions for acute or delayed neurotoxicity are ongoing. Informed by data derived from clinical trials and preclinical models, promising treatment strategies are on the horizon.</p>","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"65 1","pages":""},"PeriodicalIF":78.5,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145017231","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

Aggregating premalignancy 聚合初癌

IF 66.8 1区医学

Nature Reviews Cancer Pub Date : 2025-09-08 DOI: 10.1038/s41568-025-00876-x

Daniela Senft

引用次数: 0

Unravelling the genetics and epigenetics of the ageing tumour microenvironment in cancer 揭示癌症中衰老肿瘤微环境的遗传学和表观遗传学

IF 66.8 1区医学

Nature Reviews Cancer Pub Date : 2025-09-08 DOI: 10.1038/s41568-025-00868-x

Hariharan Easwaran, Ashani T. Weeraratna

{"title":"Unravelling the genetics and epigenetics of the ageing tumour microenvironment in cancer","authors":"Hariharan Easwaran, Ashani T. Weeraratna","doi":"10.1038/s41568-025-00868-x","DOIUrl":"10.1038/s41568-025-00868-x","url":null,"abstract":"Somatic mutations in several genes, including key oncogenes and tumour suppressor genes, are present from early life and can accumulate as an individual ages, indicating that the potential for cancer is present and growing throughout life. However, the risk of developing cancer rises sharply after 50–60 years of age, suggesting that the ability of these mutations to undergo clonal expansion and drive cancer development is dependent on the progressive changes in the epigenome and microenvironment that occur during ageing. Epigenetic changes, including DNA methylation and histone modifications, can drive various hallmarks of ageing in precancerous cells, including induction of senescence, the senescence-associated secretory phenotype, genomic instability and reduction of nuclear integrity, metabolic and inflammatory stress responses, stem cell function and differentiation potential, and redox balance. This can also alter the normal immune and stromal cells in the tissue microenvironment, which cumulatively enhances the effects of cancer driver mutations, ultimately promoting cancer development and progression in aged individuals. Unravelling these mechanisms will provide novel preventive and therapeutic strategies to limit the burden and progression of cancer in aged individuals. In this Review, Easwaran and Weeraratna outline how ageing leads to epigenetic alterations in the tissue microenvironment, enhancing clonal expansion of mutations and ultimately increasing cancer risk.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"25 11","pages":"828-847"},"PeriodicalIF":66.8,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145017233","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

3D chromatin architecture as a predictor of somatic mutations in cancer genomes 三维染色质结构作为癌症基因组体细胞突变的预测因子

IF 78.5 1区医学

Nature Reviews Cancer Pub Date : 2025-09-01 DOI: 10.1038/s41568-025-00875-y

Karan Bansal, Aprotim Mazumder

引用次数: 0

The evolution of cancer and ageing: a history of constraint 癌症和衰老的演变：约束的历史

IF 66.8 1区医学

Nature Reviews Cancer Pub Date : 2025-08-26 DOI: 10.1038/s41568-025-00861-4

João Pedro de Magalhães

{"title":"The evolution of cancer and ageing: a history of constraint","authors":"João Pedro de Magalhães","doi":"10.1038/s41568-025-00861-4","DOIUrl":"10.1038/s41568-025-00861-4","url":null,"abstract":"Ageing and cancer are ubiquitous in animals. They are fundamental and generally intrinsic to multicellular life. Nonetheless, ageing and cancer rates vary widely across species and understanding their evolution and interaction is of great biological interest. Although cancer arises from uncontrolled cell proliferation, ageing involves cell loss and degeneration, making them seemingly opposite yet interconnected processes. Because cancer can affect young individuals, natural selection will favour the evolution of cancer resistance over processes that maintain health in later life. As such, I propose that species evolve longer lifespans under the constraints imposed by the need to reduce cancer risk. Mechanisms that suppress cancer, such as telomere shortening and cellular senescence, may inadvertently promote ageing by limiting cell proliferation and tissue regeneration. Selection for tumour suppression may also impact stem cell ageing and contribute to the limited ability of adult tissues to regenerate. Overall, although cancer resistance is essential for the evolution of longevity, tumour suppression mechanisms may also contribute to ageing-related tissue degeneration and functional decline. Studying the trade-offs between the evolution of tumour suppression processes and their impact later in life may provide important insights into ageing processes. In this Perspective, de Magalhães explores the evolutionary relationship between cancer and ageing, proposing that the need to minimize cancer risk early in life may contribute to tissue degeneration later on, representing a trade-off that constrains the evolution of longer lifespans.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"25 11","pages":"873-880"},"PeriodicalIF":66.8,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144899109","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