• 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

区域性表皮对紫外线致癌敏感性的差异反映了表皮祖细胞的增殖活性。

Regional Variation in Epidermal Susceptibility to UV-Induced Carcinogenesis Reflects Proliferative Activity of Epidermal Progenitors.

机构信息

The University of Queensland Diamantina Institute, The University of Queensland, Brisbane, QLD 4102, Australia.

UQ Centre for Clinical Research, The University of Queensland, Brisbane, QLD 4029, Australia.

出版信息

Cell Rep. 2020 Jun 2;31(9):107702. doi: 10.1016/j.celrep.2020.107702.

DOI:10.1016/j.celrep.2020.107702
PMID:32492418
Abstract

To better understand the influence of ultraviolet (UV) irradiation on the initial steps of skin carcinogenesis, we examine patches of labeled keratinocytes as a proxy for clones in the interfollicular epidermis (IFE) and measure their size variation upon UVB irradiation. Multicolor lineage tracing reveals that in chronically irradiated skin, patches near hair follicles (HFs) increase in size, whereas those far from follicles do not change. This is explained by proliferation of basal epidermal cells within 60 μm of HF openings. Upon interruption of UVB, patch size near HFs regresses significantly. These anatomical differences in proliferative behavior have significant consequences for the cell of origin of basal cell carcinomas (BCCs). Indeed, a UV-inducible murine BCC model shows that BCC patches are more frequent, larger, and more invasive near HFs. These findings have major implications for the prevention of field cancerization in the epidermis.

摘要

为了更好地理解紫外线(UV)辐射对皮肤癌发生初始步骤的影响,我们以标记角质形成细胞斑作为毛囊间表皮(IFE)中克隆的替代物进行检查,并测量它们在 UVB 照射下的大小变化。多色谱系追踪显示,在慢性辐射的皮肤中,靠近毛囊(HFs)的斑块会增大,而远离毛囊的斑块则不会改变。这是由于 HF 开口附近的基底表皮细胞增殖所致。中断 UVB 后,HF 附近斑块的大小显著缩小。这种增殖行为的解剖学差异对基底细胞癌(BCC)的起源细胞有重大影响。事实上,一种 UV 诱导的小鼠 BCC 模型表明,BCC 斑块在靠近 HFs 时更频繁、更大且更具侵袭性。这些发现对预防表皮的区域性癌变具有重大意义。

相似文献

1
Regional Variation in Epidermal Susceptibility to UV-Induced Carcinogenesis Reflects Proliferative Activity of Epidermal Progenitors.区域性表皮对紫外线致癌敏感性的差异反映了表皮祖细胞的增殖活性。
Cell Rep. 2020 Jun 2;31(9):107702. doi: 10.1016/j.celrep.2020.107702.
2
Hair follicle disruption facilitates pathogenesis to UVB-induced cutaneous inflammation and basal cell carcinoma development in Ptch(+/-) mice.毛囊破坏促进Ptch(+/-)小鼠中紫外线B诱导的皮肤炎症发病机制及基底细胞癌的发展。
Am J Pathol. 2014 May;184(5):1529-40. doi: 10.1016/j.ajpath.2014.01.013. Epub 2014 Mar 12.
3
Constitutive activation and targeted disruption of signal transducer and activator of transcription 3 (Stat3) in mouse epidermis reveal its critical role in UVB-induced skin carcinogenesis.小鼠表皮中信号转导和转录激活因子3(Stat3)的组成性激活和靶向破坏揭示了其在紫外线B诱导的皮肤癌发生中的关键作用。
Oncogene. 2009 Feb 19;28(7):950-60. doi: 10.1038/onc.2008.453. Epub 2009 Jan 12.
4
UV-induced ablation of the epidermal basal layer including p53-mutant clones resets UV carcinogenesis showing squamous cell carcinomas to originate from interfollicular epidermis.UV 诱导的表皮基底层消融,包括 p53 突变克隆,重置了 UV 致癌作用,表明鳞状细胞癌起源于毛囊间表皮。
Carcinogenesis. 2012 Mar;33(3):714-20. doi: 10.1093/carcin/bgs004. Epub 2012 Jan 6.
5
UV-Induced Molecular Signaling Differences in Melanoma and Non-melanoma Skin Cancer.紫外线诱导的黑色素瘤和非黑色素瘤皮肤癌中的分子信号差异
Adv Exp Med Biol. 2017;996:27-40. doi: 10.1007/978-3-319-56017-5_3.
6
Stochastic fate of p53-mutant epidermal progenitor cells is tilted toward proliferation by UV B during preneoplasia.在癌前病变过程中,UVB 会使 p53 突变的表皮祖细胞向增殖方向倾斜。
Proc Natl Acad Sci U S A. 2010 Jan 5;107(1):270-5. doi: 10.1073/pnas.0909738107. Epub 2009 Dec 15.
7
Lgr6+ stem cells and their progeny in mouse epidermis under regimens of exogenous skin carcinogenesis, and their absence in ensuing skin tumors.外源性皮肤致癌作用机制下小鼠表皮中的Lgr6 +干细胞及其后代,以及它们在随后发生的皮肤肿瘤中的缺失。
Oncotarget. 2016 Dec 27;7(52):86740-86754. doi: 10.18632/oncotarget.13436.
8
Basal cell carcinomas arise from hair follicle stem cells in Ptch1(+/-) mice.基底细胞癌起源于 Ptch1(+/-) 小鼠的毛囊干细胞。
Cancer Cell. 2011 Jan 18;19(1):114-24. doi: 10.1016/j.ccr.2010.11.007. Epub 2011 Jan 6.
9
Molecular mechanisms underlying chemopreventive activities of glycyrrhizic acid against UVB-radiation-induced carcinogenesis in SKH-1 hairless mouse epidermis.甘草酸抑制 UVB 辐射诱导的 SKH-1 无毛小鼠表皮癌变的化学预防作用的分子机制。
Radiat Res. 2011 Aug;176(2):177-86. doi: 10.1667/rr2510.1. Epub 2011 May 5.
10
Wounding enhances epidermal tumorigenesis by recruiting hair follicle keratinocytes.创伤通过招募毛囊角质形成细胞促进表皮肿瘤发生。
Proc Natl Acad Sci U S A. 2011 Mar 8;108(10):4099-104. doi: 10.1073/pnas.1014489108. Epub 2011 Feb 14.

引用本文的文献

1
Transcriptional Signature for Dysplastic Epidermal Development in Human Premalignant Skin.人类癌前皮肤发育异常的转录特征
J Invest Dermatol. 2025 Apr 23. doi: 10.1016/j.jid.2025.04.006.
2
Trial protocol for SiroSkin: a randomised double-blind placebo-controlled trial of topical sirolimus in chemoprevention of facial squamous cell carcinomas in solid organ transplant recipients.西罗肤美:一项随机双盲安慰剂对照研究,评估外用西罗莫司预防实体器官移植受者面部鳞状细胞癌的临床试验方案。
Trials. 2024 Nov 22;25(1):789. doi: 10.1186/s13063-024-08619-3.
3
Epidermal mutation accumulation in photodamaged skin is associated with skin cancer burden and can be targeted through ablative therapy.
光损伤皮肤中表皮突变的积累与皮肤癌负担有关,可以通过消融疗法来靶向治疗。
Sci Adv. 2023 May 10;9(19):eadf2384. doi: 10.1126/sciadv.adf2384.
4
Binary organization of epidermal basal domains highlights robustness to environmental exposure.表皮基底层的二元组织突出了对环境暴露的稳健性。
EMBO J. 2022 Sep 15;41(18):e110488. doi: 10.15252/embj.2021110488. Epub 2022 Aug 10.
5
Multicolor strategies for investigating clonal expansion and tissue plasticity.多色策略用于研究克隆扩增和组织可塑性。
Cell Mol Life Sci. 2022 Feb 20;79(3):141. doi: 10.1007/s00018-021-04077-1.
6
Whole-mount staining coupled to a UV-inducible basal cell carcinoma murine model.全组织染色结合 UV 诱导的基底细胞癌小鼠模型。
STAR Protoc. 2021 Feb 5;2(1):100329. doi: 10.1016/j.xpro.2021.100329. eCollection 2021 Mar 19.