• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

相似文献

1
Clonal evolution in cancer.癌症中的克隆进化。
Nature. 2012 Jan 18;481(7381):306-13. doi: 10.1038/nature10762.
2
Comparison of Burnet's clonal selection theory with tumor cell-clone development.比较伯内特克隆选择理论与肿瘤细胞克隆发展。
Theranostics. 2018 May 23;8(12):3392-3399. doi: 10.7150/thno.24083. eCollection 2018.
3
Population genetics of cancer cell clones: possible implications of cancer stem cells.癌细胞克隆的群体遗传学:癌症干细胞的潜在影响。
Theor Biol Med Model. 2010 Nov 9;7:42. doi: 10.1186/1742-4682-7-42.
4
Dynamics of genomic clones in breast cancer patient xenografts at single-cell resolution.单细胞分辨率下乳腺癌患者异种移植物中基因组克隆的动态。
Nature. 2015 Feb 19;518(7539):422-6. doi: 10.1038/nature13952. Epub 2014 Nov 26.
5
Cancer - An Insurgency of Clones.癌症——克隆体的叛乱
Trends Cancer. 2017 Feb;3(2):73-75. doi: 10.1016/j.trecan.2016.11.010. Epub 2016 Dec 23.
6
Cancer heterogeneity--a multifaceted view.癌症异质性——多角度的观察。
EMBO Rep. 2013 Aug;14(8):686-95. doi: 10.1038/embor.2013.92. Epub 2013 Jul 12.
7
To portray clonal evolution in blood cancer, count your stem cells.要描绘血液癌症中的克隆进化,就请计算您的干细胞数量。
Blood. 2021 Apr 8;137(14):1862-1870. doi: 10.1182/blood.2020008407.
8
Non-cell-autonomous driving of tumour growth supports sub-clonal heterogeneity.非细胞自主驱动肿瘤生长支持亚克隆异质性。
Nature. 2014 Oct 2;514(7520):54-8. doi: 10.1038/nature13556. Epub 2014 Jul 30.
9
Clonal evolution models of tumor heterogeneity.肿瘤异质性的克隆进化模型
Am Soc Clin Oncol Educ Book. 2015:e662-5. doi: 10.14694/EdBook_AM.2015.35.e662.
10
Adapting clinical paradigms to the challenges of cancer clonal evolution.适应临床模式以应对癌症克隆进化的挑战。
Am J Pathol. 2013 Jun;182(6):1962-71. doi: 10.1016/j.ajpath.2013.02.026.

引用本文的文献

1
Taming cancer evolution surprises.驯服癌症演变的意外情况。
Nat Methods. 2025 Sep 10. doi: 10.1038/s41592-025-02802-3.
2
Fluctuating DNA methylation tracks cancer evolution at clinical scale.动态DNA甲基化在临床规模上追踪癌症演变。
Nature. 2025 Sep 10. doi: 10.1038/s41586-025-09374-4.
3
Unraveling cellular dynamic changes in tumor evolution induced by long-term low dose-rate radiation.揭示长期低剂量率辐射诱导的肿瘤演化中的细胞动态变化。
Br J Cancer. 2025 Sep 5. doi: 10.1038/s41416-025-03128-9.
4
A graph homomorphism approach for unraveling histories of metastatic cancers and viral outbreaks under evolutionary constraints.一种用于在进化约束下揭示转移性癌症和病毒爆发历史的图同态方法。
Nat Commun. 2025 Aug 28;16(1):8027. doi: 10.1038/s41467-025-63411-4.
5
Clonal diversity shapes the tumour microenvironment leading to distinct immunotherapy responses in metastatic urothelial carcinoma.克隆多样性塑造肿瘤微环境,导致转移性尿路上皮癌产生不同的免疫治疗反应。
Nat Commun. 2025 Aug 27;16(1):7995. doi: 10.1038/s41467-025-63309-1.
6
High-content confocal analysis of tumorigenesis, cancer stem cells, and drug response in 3D cholangiocarcinoma cultures.3D胆管癌培养物中肿瘤发生、癌症干细胞及药物反应的高内涵共聚焦分析
Sci Rep. 2025 Aug 26;15(1):31387. doi: 10.1038/s41598-025-16144-9.
7
Systems biology successes and areas for opportunity in prostate cancer.系统生物学在前列腺癌中的成功案例与机遇领域
Endocr Relat Cancer. 2025 Aug 20;32(8). doi: 10.1530/ERC-25-0067. Print 2025 Aug 1.
8
Clone copy number diversity is linked to survival in lung cancer.克隆拷贝数多样性与肺癌患者的生存率相关。
Nature. 2025 Aug 13. doi: 10.1038/s41586-025-09398-w.
9
Decoding the epigenetic-immune nexus in hepatocellular carcinoma: a Mendelian randomization study reveals BTN3A2, S100A12 and TRIM27 as white blood cell regulators.解码肝细胞癌中的表观遗传-免疫关联:一项孟德尔随机化研究揭示BTN3A2、S100A12和TRIM27作为白细胞调节因子。
BMC Cancer. 2025 Aug 8;25(1):1282. doi: 10.1186/s12885-025-14693-w.
10
The glucose sensor NSUN2-mC modification regulates tumor-immune glucose metabolism reprogramming to drive hepatocellular carcinoma evolution.葡萄糖传感器NSUN2-mC修饰调节肿瘤免疫葡萄糖代谢重编程以驱动肝细胞癌进展。
Int J Biol Sci. 2025 Jul 11;21(10):4529-4548. doi: 10.7150/ijbs.115610. eCollection 2025.

本文引用的文献

1
Cancer research meets evolutionary biology.癌症研究与进化生物学相遇。
Evol Appl. 2009 Feb;2(1):62-70. doi: 10.1111/j.1752-4571.2008.00063.x.
2
Overlooking evolution: a systematic analysis of cancer relapse and therapeutic resistance research.忽视进化:癌症复发和治疗抵抗研究的系统分析。
PLoS One. 2011;6(11):e26100. doi: 10.1371/journal.pone.0026100. Epub 2011 Nov 17.
3
Temporal dissection of tumorigenesis in primary cancers.原发性癌症中肿瘤发生的时程剖析。
Cancer Discov. 2011 Jul;1(2):137-43. doi: 10.1158/2159-8290.CD-11-0028. Epub 2011 Jun 29.
4
Cancer stem cells renew their impact.癌症干细胞会持续发挥其影响。
Nat Med. 2011 Sep 7;17(9):1046-8. doi: 10.1038/nm.2458.
5
Rapid growth of a hepatocellular carcinoma and the driving mutations revealed by cell-population genetic analysis of whole-genome data.全基因组数据的细胞群体遗传分析揭示了肝细胞癌的快速生长和驱动突变。
Proc Natl Acad Sci U S A. 2011 Jul 19;108(29):12042-7. doi: 10.1073/pnas.1108715108. Epub 2011 Jul 5.
6
Xenografts of highly resistant leukemia recapitulate the clonal composition of the leukemogenic compartment.高度耐药白血病的异种移植物再现了白血病形成区的克隆组成。
Blood. 2011 Aug 18;118(7):1854-64. doi: 10.1182/blood-2010-11-320309. Epub 2011 Jun 13.
7
BCL6 enables Ph+ acute lymphoblastic leukaemia cells to survive BCR-ABL1 kinase inhibition.BCL6 使 Ph+ 急性淋巴细胞白血病细胞能够在 BCR-ABL1 激酶抑制的情况下存活。
Nature. 2011 May 19;473(7347):384-8. doi: 10.1038/nature09883.
8
Human cancers express mutator phenotypes: origin, consequences and targeting.人类癌症表现出突变型表型:起源、后果和靶向治疗。
Nat Rev Cancer. 2011 Jun;11(6):450-7. doi: 10.1038/nrc3063. Epub 2011 May 19.
9
Solving the puzzle of metastasis: the evolution of cell migration in neoplasms.破解转移之谜:肿瘤细胞迁移的演变。
PLoS One. 2011 Apr 27;6(4):e17933. doi: 10.1371/journal.pone.0017933.
10
Deadly teamwork: neural cancer stem cells and the tumor microenvironment.致命的合作:神经癌细胞和肿瘤微环境。
Cell Stem Cell. 2011 May 6;8(5):482-5. doi: 10.1016/j.stem.2011.04.013.

癌症中的克隆进化。

Clonal evolution in cancer.

机构信息

Division of Molecular Pathology, The Institute of Cancer Research, Brookes Lawley Building, 15 Cotswold Road, Sutton, Surrey SM2 5NG, UK.

出版信息

Nature. 2012 Jan 18;481(7381):306-13. doi: 10.1038/nature10762.

DOI:10.1038/nature10762
PMID:22258609
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3367003/
Abstract

Cancers evolve by a reiterative process of clonal expansion, genetic diversification and clonal selection within the adaptive landscapes of tissue ecosystems. The dynamics are complex, with highly variable patterns of genetic diversity and resulting clonal architecture. Therapeutic intervention may destroy cancer clones and erode their habitats, but it can also inadvertently provide a potent selective pressure for the expansion of resistant variants. The inherently Darwinian character of cancer is the primary reason for this therapeutic failure, but it may also hold the key to more effective control.

摘要

癌症是通过在组织生态系统的适应景观内进行克隆扩张、遗传多样化和克隆选择的反复过程而进化的。其动态是复杂的,具有高度可变的遗传多样性模式和由此产生的克隆结构。治疗干预可能会破坏癌细胞克隆并侵蚀其栖息地,但也可能无意中为耐药变体的扩张提供强大的选择压力。癌症固有的达尔文特征是导致这种治疗失败的主要原因,但它也可能是更有效控制癌症的关键。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c9c/3367003/175e84d74887/nihms377748f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c9c/3367003/48130791c235/nihms377748f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c9c/3367003/b9ae1600e442/nihms377748f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c9c/3367003/e03c125a6bac/nihms377748f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c9c/3367003/a800babc9bbb/nihms377748f4a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c9c/3367003/175e84d74887/nihms377748f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c9c/3367003/48130791c235/nihms377748f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c9c/3367003/b9ae1600e442/nihms377748f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c9c/3367003/e03c125a6bac/nihms377748f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c9c/3367003/a800babc9bbb/nihms377748f4a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c9c/3367003/175e84d74887/nihms377748f5.jpg