NATURE REVIEWS CANCER自然综述·癌症
NATURE REVIEWS CANCER(英文缩写 NAT REV CANCER),ISSN 1474-175X,eISSN 1474-1768,中文译名:自然综述·癌症 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 69.800 | Q1 |
| 2022 | 78.500 | Q1 |
| 2023 | 72.500 | Q1 |
| 2024 | 66.800 | Q1 |
| 2025 | 60.700 | Q1 |
NATURE REVIEWS CANCER 最新收录文献
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2. From blunt-force treatment to precision: 25 years of transformation in cancer research.
2. 从粗放治疗到精准医疗：癌症研究25年变革之路PMID:日期:2026-09-23该文献暂无摘要。
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3. Replication stress in cancer: origins, consequences and therapeutic opportunities.
3. 癌症中的复制应激：起源、后果与治疗机遇PMID:日期:2026-09-22Replication stress, defined as impaired DNA replication leading to genomic instability, is a central feature of tumour development and progression. In cancer cells, it arises from oncogene activation, transcription-replication conflicts, altered nucleotide metabolism and DNA secondary structures that hinder DNA synthesis. These pressures compromise accurate genome duplication and promote chromosomal instability and mutagenesis. Recent advances have clarified the molecular mechanisms that stabilize, remodel and restart stressed replication forks, and highlighted the essential role of the ataxia telangiectasia and Rad3-related protein (ATR)-checkpoint kinase 1 (CHK1) pathway in preventing excessive single-stranded DNA accumulation and catastrophic genome fragmentation. Although replication stress fuels tumour evolution and heterogeneity, it also creates dependencies on replication stress response pathways that can be therapeutically exploited. Inhibitors targeting ATR, CHK1 and WEE1 kinases, which override the G2 checkpoint, are in clinical development, whereas synthetic lethal strategies, including poly(ADP-ribose) polymerase (PARP) inhibition in BRCA1-deficient or BRCA2-deficient tumours and inhibition of the DNA helicase WRN in microsatellite-unstable cancers, illustrate how replication stress-associated vulnerabilities can be targeted. In this Review, we position replication stress as both a driver of cancer genome evolution and a tractable framework for precision oncology. We emphasize that replication stress in tumours is often chronic and sublethal, shaping genome evolution. We further highlight its integration with oncogenic and metabolic alterations and broader impact on tumour-microenvironment interactions, which create dynamic and context-dependent therapeutic vulnerabilities.
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4. Viral mimicry escape as a necessary feature of malignant transformation.
PMID:日期:2026-09-15Malignant transformation is driven by disruption of pathways regulating proliferation and cell fate, but these same disruptions can create a collateral vulnerability: loss of transcriptional and epigenetic control over transposable elements and other normally silenced genomic regions. Consequently, emerging cancer cells can accumulate transposable element-derived and other endogenous immunogenic nucleic acids capable of triggering antiviral responses, a process termed viral mimicry. Increasing evidence indicates that viral mimicry can eliminate precancerous cells and shape tumour evolution, positioning it as an intrinsic tumour-suppressive mechanism. Here we highlight how cancer-associated changes in DNA methylation, histone modifications, splicing and RNA processing can lead to the presence of immunogenic nucleic acids that can activate viral mimicry pathways. We outline how cancer cells suppress viral mimicry, including compensatory epigenetic repression, RNA editing, nucleic acid decay and dampening of interferon signalling to enable cancer cell growth. Finally, we highlight the evidence suggesting that escaping viral mimicry is a fundamental process for cancer initiation and progression, and suggest that viral mimicry escape is necessary for cancer transformation and a therapeutic target in combination with immunotherapies. By framing viral mimicry escape as a necessary part of cancer transformation, this Review provides a unifying conceptual model for its translational exploitation.
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5. Making breast cancer innovation deliver for every woman.
5. 让乳腺癌创新惠及每一位女性PMID:日期:2026-09-11该文献暂无摘要。
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6. A guide to understanding tumour evolution through the lens of population genetics.
6. 从群体遗传学视角理解肿瘤演变的指南PMID:日期:2026-09-09Every cancer carries the history of its own evolution, hidden in its genome. Modern DNA sequencing can catalogue millions of mutations and profile tumours across space and time, but sequencing alone struggles to answer the questions that matter most: when did key adaptations emerge, how strongly were they selected, why do some tumours relapse whereas others do not, and how will the cancer evolve next? The reason is fundamental: sequencing is a snapshot, whereas evolution is a dynamic process. Bridging this gap requires moving beyond descriptive cancer genomics towards quantitative evolutionary inference. In this Review, we argue that population genetics provides the mathematical framework needed to extract evolutionary dynamics from cancer genomes. We show how models of mutation, selection and drift transform allele frequencies from descriptive measurements into quantitative estimates of clonal fitness and evolutionary timings. We discuss how these principles extend to epigenetic inheritance, plasticity and ecological interactions within the tumour ecosystem, and examine the assumptions and limitations for their application to modern sequencing data. By reframing cancer genomes as quantitative records of evolutionary processes rather than catalogues of mutations, researchers have used population genetics to provide a foundation for understanding - and ultimately predicting - the trajectories of cancer evolution.
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7. Reflecting on 25 years of cancer research: transformative advances and unmet expectations.
PMID:日期:2026-09-08该文献暂无摘要。
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8. Neutrophils in cancer.
8. 癌症中的中性粒细胞PMID:日期:2026-09-07Neutrophils, long appreciated for their central role in host defences, have largely pro-tumorigenic effects in cancer owing to their sensitivity to signals in the tumour environment. Cancers regularly co-opt the functions of neutrophils to promote angiogenesis, immunosuppression, tumour growth and metastasis. However, depending on context, many of the same neutrophil-derived factors involved in these processes can mediate tumour cell killing. In this Review, we examine the functions of neutrophils and their impact on cancer, drawing parallels between their roles in cancer and non-cancer contexts, and highlighting their remarkable sensitivity to environmental cues. We call attention to promising strategies for targeting and manipulating neutrophils for the treatment of cancer.
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9. The next 25 years of cancer research: emerging perspectives and priorities.
PMID:日期:2026-09-07该文献暂无摘要。