• 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

癌症与神经退行性疾病:进退维谷。

Cancer and neurodegeneration: between the devil and the deep blue sea.

机构信息

Department of Molecular Neuroscience, UCL Institute of Neurology, London, United Kingdom.

出版信息

PLoS Genet. 2010 Dec 23;6(12):e1001257. doi: 10.1371/journal.pgen.1001257.

DOI:10.1371/journal.pgen.1001257
PMID:21203498
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3009676/
Abstract

Cancer and neurodegeneration are often thought of as disease mechanisms at opposite ends of a spectrum; one due to enhanced resistance to cell death and the other due to premature cell death. There is now accumulating evidence to link these two disparate processes. An increasing number of genetic studies add weight to epidemiological evidence suggesting that sufferers of a neurodegenerative disorder have a reduced incidence for most cancers, but an increased risk for other cancers. Many of the genes associated with either cancer and/or neurodegeneration play a central role in cell cycle control, DNA repair, and kinase signalling. However, the links between these two families of diseases remain to be proven. In this review, we discuss recent and sometimes as yet incomplete genetic discoveries that highlight the overlap of molecular pathways implicated in cancer and neurodegeneration.

摘要

癌症和神经退行性疾病通常被认为是处于两个极端的疾病机制;一个是由于增强的抗细胞死亡能力,另一个是由于过早的细胞死亡。现在有越来越多的证据将这两个截然不同的过程联系起来。越来越多的遗传研究增加了流行病学证据的权重,表明神经退行性疾病患者的大多数癌症发病率降低,但其他癌症的发病率增加。许多与癌症和/或神经退行性疾病相关的基因在细胞周期控制、DNA 修复和激酶信号转导中发挥核心作用。然而,这两种疾病之间的联系仍有待证实。在这篇综述中,我们讨论了最近的遗传发现,有时甚至是尚未完成的遗传发现,这些发现强调了癌症和神经退行性疾病中涉及的分子途径的重叠。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4002/3009676/11aa543bc1a9/pgen.1001257.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4002/3009676/11aa543bc1a9/pgen.1001257.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4002/3009676/11aa543bc1a9/pgen.1001257.g001.jpg

相似文献

1
Cancer and neurodegeneration: between the devil and the deep blue sea.癌症与神经退行性疾病:进退维谷。
PLoS Genet. 2010 Dec 23;6(12):e1001257. doi: 10.1371/journal.pgen.1001257.
2
Genetic determinants at the interface of cancer and neurodegenerative disease.癌症与神经退行性疾病交界处的遗传决定因素。
Oncogene. 2010 Jun 17;29(24):3453-64. doi: 10.1038/onc.2010.127. Epub 2010 Apr 26.
3
RNA-binding proteins as molecular links between cancer and neurodegeneration.RNA结合蛋白作为癌症与神经退行性变之间的分子纽带。
Biogerontology. 2014 Dec;15(6):587-610. doi: 10.1007/s10522-014-9531-2. Epub 2014 Sep 18.
4
At the Crossroads Between Neurodegeneration and Cancer: A Review of Overlapping Biology and Its Implications.神经退行性疾病与癌症的交叉点:重叠生物学及其影响的综述
Curr Aging Sci. 2018;11(2):77-89. doi: 10.2174/1874609811666180223154436.
5
Dysfunction of the ubiquitin-proteasome system in multiple disease conditions: therapeutic approaches.多种疾病状态下泛素-蛋白酶体系统功能障碍:治疗方法
Bioessays. 2008 Nov;30(11-12):1172-84. doi: 10.1002/bies.20852.
6
MicroRNAs and deregulated gene expression networks in neurodegeneration.微小 RNA 与神经退行性变中的基因表达网络失调。
Brain Res. 2010 Jun 18;1338:48-57. doi: 10.1016/j.brainres.2010.03.106. Epub 2010 Apr 7.
7
Regulation of the Nrf2 antioxidant pathway by microRNAs: New players in micromanaging redox homeostasis.miRNAs 调控 Nrf2 抗氧化通路:氧化还原平衡调控中的新角色
Free Radic Biol Med. 2013 Sep;64:4-11. doi: 10.1016/j.freeradbiomed.2013.07.025. Epub 2013 Jul 21.
8
DNA repair deficiencies and neurodegeneration.DNA 修复缺陷与神经退行性变。
DNA Repair (Amst). 2024 Jun;138:103679. doi: 10.1016/j.dnarep.2024.103679. Epub 2024 Apr 16.
9
Inflammation and DNA damage: Probing pathways to cancer and neurodegeneration.炎症与DNA损伤:探索通往癌症和神经退行性疾病的途径。
Drug Discov Today Technol. 2017 Nov;25:37-43. doi: 10.1016/j.ddtec.2017.11.001. Epub 2017 Nov 22.
10
p53 at the crossroads between cancer and neurodegeneration.p53 在癌症和神经退行性变之间的十字路口。
Free Radic Biol Med. 2012 May 1;52(9):1727-33. doi: 10.1016/j.freeradbiomed.2012.02.034. Epub 2012 Mar 3.

引用本文的文献

1
Mitophagy's impacts on cancer and neurodegenerative diseases: implications for future therapies.线粒体自噬对癌症和神经退行性疾病的影响:对未来治疗的启示
J Hematol Oncol. 2025 Aug 1;18(1):78. doi: 10.1186/s13045-025-01727-w.
2
Different Mechanisms in Doxorubicin-Induced Neurotoxicity: Impact of BRCA Mutations.多柔比星诱导神经毒性的不同机制:BRCA突变的影响
Int J Mol Sci. 2025 May 15;26(10):4736. doi: 10.3390/ijms26104736.
3
CHIP and aging: a key regulator of proteostasis and cellular senescence.CHIP与衰老:蛋白质稳态和细胞衰老的关键调节因子。

本文引用的文献

1
LRRK2 G2019S mutations are associated with an increased cancer risk in Parkinson disease.LRRK2 G2019S 突变与帕金森病患者的癌症风险增加相关。
Mov Disord. 2010 Nov 15;25(15):2536-41. doi: 10.1002/mds.23314.
2
Mitophagy and Parkinson's disease: the PINK1-parkin link.线粒体自噬与帕金森病:PINK1-帕金蛋白联系
Biochim Biophys Acta. 2011 Apr;1813(4):623-33. doi: 10.1016/j.bbamcr.2010.08.007. Epub 2010 Aug 21.
3
Genome-wide association studies: the key to unlocking neurodegeneration?全基因组关联研究:解锁神经退行性变的关键?
Biogerontology. 2025 May 5;26(3):104. doi: 10.1007/s10522-025-10247-6.
4
A population based study to analyse amyotrophic lateral sclerosis as a multi-step process.一项基于人群的研究,旨在分析肌萎缩侧索硬化症作为一个多步骤过程。
Sci Rep. 2025 Apr 1;15(1):11189. doi: 10.1038/s41598-025-89616-7.
5
α-synuclein expression in glioblastoma restores tumor suppressor function and rescues temozolomide drug resistance.胶质母细胞瘤中α-突触核蛋白的表达可恢复肿瘤抑制功能并挽救替莫唑胺耐药性。
Cell Death Dis. 2025 Mar 19;16(1):188. doi: 10.1038/s41419-025-07509-z.
6
and CAG triplet repeat sizes: exploring their role in the disease risk and cancer comorbidity in Parkinson's disease.以及CAG三联体重复序列长度:探讨它们在帕金森病的疾病风险和癌症合并症中的作用。
Brain Commun. 2025 Feb 6;7(1):fcaf060. doi: 10.1093/braincomms/fcaf060. eCollection 2025.
7
The cingulum: a central hotspot for the battle against chronic intractable pain?扣带束:对抗慢性顽固性疼痛的核心热点区域?
Brain Commun. 2024 Oct 16;6(5):fcae368. doi: 10.1093/braincomms/fcae368. eCollection 2024.
8
F-FDG PET/CT as a molecular biomarker in the diagnosis of amyotrophic lateral sclerosis associated with prostate cancer and progressive supranuclear palsy: A case report.F-FDG PET/CT作为诊断前列腺癌合并肌萎缩侧索硬化症及进行性核上性麻痹的分子生物标志物:一例报告
Front Nucl Med. 2023 Apr 17;3:1137875. doi: 10.3389/fnume.2023.1137875. eCollection 2023.
9
Insights into Dysregulated Neurological Biomarkers in Cancer.癌症中神经生物标志物失调的见解
Cancers (Basel). 2024 Jul 27;16(15):2680. doi: 10.3390/cancers16152680.
10
In-vivo neuronal dysfunction by Aβ and tau overlaps with brain-wide inflammatory mechanisms in Alzheimer's disease.β淀粉样蛋白(Aβ)和tau蛋白导致的体内神经元功能障碍与阿尔茨海默病中全脑炎症机制重叠。
Front Aging Neurosci. 2024 Jun 19;16:1383163. doi: 10.3389/fnagi.2024.1383163. eCollection 2024.
Nat Neurosci. 2010 Jul;13(7):789-94. doi: 10.1038/nn.2584.
4
Neurotoxic mechanisms of DNA damage: focus on transcriptional inhibition.DNA损伤的神经毒性机制:聚焦转录抑制
J Neurochem. 2010 Sep;114(6):1537-49. doi: 10.1111/j.1471-4159.2010.06859.x. Epub 2010 Aug 19.
5
Methylation regulates alpha-synuclein expression and is decreased in Parkinson's disease patients' brains.甲基化调节α-突触核蛋白的表达,并且在帕金森病患者的大脑中减少。
J Neurosci. 2010 May 5;30(18):6355-9. doi: 10.1523/JNEUROSCI.6119-09.2010.
6
Genetic determinants at the interface of cancer and neurodegenerative disease.癌症与神经退行性疾病交界处的遗传决定因素。
Oncogene. 2010 Jun 17;29(24):3453-64. doi: 10.1038/onc.2010.127. Epub 2010 Apr 26.
7
The familial Parkinson disease gene PARK2 is a multisite tumor suppressor on chromosome 6q25.2-27 that regulates cyclin E.家族性帕金森病基因PARK2是位于6号染色体q25.2 - 27区域的多位点肿瘤抑制基因,它调控细胞周期蛋白E。
Cell Cycle. 2010 Apr 15;9(8):1451-2. doi: 10.4161/cc.9.8.11583.
8
Targeting mitochondrial dysfunction in neurodegenerative disease: Part II.靶向神经退行性疾病中的线粒体功能障碍:第二部分。
Expert Opin Ther Targets. 2010 May;14(5):497-511. doi: 10.1517/14728221003730434.
9
Parkinson's disease and cancer: the unexplored connection.帕金森病与癌症:尚未被探索的联系。
J Natl Cancer Inst. 2010 Mar 17;102(6):371-4. doi: 10.1093/jnci/djq081. Epub 2010 Mar 9.
10
Targeted therapies in cancer.癌症的靶向治疗。
BioDrugs. 2010 Apr 1;24(2):77-88. doi: 10.2165/11530830-000000000-00000.