• 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
Translation of DNA Damage Response Inhibitors as Chemoradiation Sensitizers From the Laboratory to the Clinic.将 DNA 损伤反应抑制剂作为化学放射增敏剂从实验室到临床的转化。
Int J Radiat Oncol Biol Phys. 2021 Dec 1;111(5):e38-e53. doi: 10.1016/j.ijrobp.2021.07.1708. Epub 2021 Aug 1.
2
The role of DNA damage response in chemo- and radio-resistance of cancer cells: Can DDR inhibitors sole the problem?DNA 损伤反应在癌细胞的化疗和放疗抵抗中的作用:DDR 抑制剂能否解决这个问题?
DNA Repair (Amst). 2021 May;101:103074. doi: 10.1016/j.dnarep.2021.103074. Epub 2021 Feb 18.
3
The complementarity of DDR, nucleic acids and anti-tumour immunity.DDR、核酸和抗肿瘤免疫的互补性。
Nature. 2023 Jul;619(7970):475-486. doi: 10.1038/s41586-023-06069-6. Epub 2023 Jul 19.
4
DNA topoisomerase I-targeting drugs as radiation sensitizers.靶向DNA拓扑异构酶I的药物作为辐射增敏剂
Oncology (Williston Park). 1999 Oct;13(10 Suppl 5):39-46.
5
Targeting the DNA damage response for cancer therapy.针对癌症治疗的 DNA 损伤反应。
Biochem Soc Trans. 2023 Feb 27;51(1):207-221. doi: 10.1042/BST20220681.
6
Targeting DNA Damage Response in Prostate and Breast Cancer.针对前列腺癌和乳腺癌中的DNA损伤反应
Int J Mol Sci. 2020 Nov 4;21(21):8273. doi: 10.3390/ijms21218273.
7
Identification of novel radiosensitizers in a high-throughput, cell-based screen for DSB repair inhibitors.在基于细胞的高通量筛选中鉴定用于DNA双链断裂修复抑制剂的新型放射增敏剂。
Mol Cancer Ther. 2015 Feb;14(2):326-42. doi: 10.1158/1535-7163.MCT-14-0765. Epub 2014 Dec 15.
8
A high content clonogenic survival drug screen identifies mek inhibitors as potent radiation sensitizers for KRAS mutant non-small-cell lung cancer.一项高内涵克隆形成存活药物筛选将MEK抑制剂鉴定为KRAS突变型非小细胞肺癌的有效辐射增敏剂。
J Thorac Oncol. 2014 Jul;9(7):965-973. doi: 10.1097/JTO.0000000000000199.
9
Synergistic Effect of a Mesothelin-Targeted Th Conjugate in Combination with DNA Damage Response Inhibitors in Ovarian Cancer Xenograft Models.一种针对间皮素的 Th 偶联物与 DNA 损伤反应抑制剂联合在卵巢癌异种移植模型中的协同效应。
J Nucl Med. 2019 Sep;60(9):1293-1300. doi: 10.2967/jnumed.118.223701. Epub 2019 Mar 8.
10
G2/M Checkpoint Abrogation With Selective Inhibitors Results in Increased Chromatid Breaks and Radiosensitization of 82-6 hTERT and RPE Human Cells.G2/M 检验点阻断联合选择性抑制剂导致 82-6 hTERT 和 RPE 人细胞染色单体断裂增加和放射增敏。
Front Public Health. 2021 May 28;9:675095. doi: 10.3389/fpubh.2021.675095. eCollection 2021.

引用本文的文献

1
Targeting Monounsaturated Fatty Acid Metabolism for Radiosensitization of KRAS Mutant 3D Lung Cancer Models.针对单不饱和脂肪酸代谢以增强KRAS突变型3D肺癌模型的放射敏感性
Mol Cancer Ther. 2025 Jun 4;24(6):920-930. doi: 10.1158/1535-7163.MCT-24-0213.
2
Challenges and opportunities for early phase clinical trials of novel drug-radiotherapy combinations: recommendations from NRG Oncology, the American Society for Radiation Oncology (ASTRO), the American College of Radiology (ACR), the Sarah Cannon Research Institute, and the American College of Radiation Oncology (ACRO).新型药物联合放疗的早期临床试验面临的挑战与机遇:美国肿瘤放射治疗协作组(NRG Oncology)、美国放射肿瘤学会(ASTRO)、美国放射学院(ACR)、Sarah Cannon 研究所以及美国放射肿瘤学会(ACRO)的建议。
Lancet Oncol. 2024 Oct;25(10):e489-e500. doi: 10.1016/S1470-2045(24)00264-X.
3
Tumor Heterogeneity Research and Innovation in Biologically Based Radiation Therapy From the National Cancer Institute Radiation Research Program Portfolio.来自美国国立癌症研究所放射研究项目组合的肿瘤异质性研究与基于生物学的放射治疗创新。
J Clin Oncol. 2022 Jun 10;40(17):1861-1869. doi: 10.1200/JCO.21.02579. Epub 2022 Mar 4.
4
Contribution of Lipid Oxidation and Ferroptosis to Radiotherapy Efficacy.脂质氧化和铁死亡对放疗疗效的贡献。
Int J Mol Sci. 2021 Nov 22;22(22):12603. doi: 10.3390/ijms222212603.

本文引用的文献

1
Progress towards a clinically-successful ATR inhibitor for cancer therapy.用于癌症治疗的临床成功的 ATR 抑制剂的研究进展。
Curr Res Pharmacol Drug Discov. 2021 Feb 5;2:100017. doi: 10.1016/j.crphar.2021.100017. eCollection 2021.
2
Clinical Candidates Targeting the ATR-CHK1-WEE1 Axis in Cancer.针对癌症中ATR-CHK1-WEE1轴的临床候选药物
Cancers (Basel). 2021 Feb 14;13(4):795. doi: 10.3390/cancers13040795.
3
3D Tumor Models and Their Use for the Testing of Immunotherapies.3D 肿瘤模型及其在免疫疗法测试中的应用。
Front Immunol. 2020 Dec 10;11:603640. doi: 10.3389/fimmu.2020.603640. eCollection 2020.
4
Combinatorial Efficacy of Olaparib with Radiation and ATR Inhibitor Requires PARP1 Protein in Homologous Recombination-Proficient Pancreatic Cancer.奥拉帕利联合放疗和 ATR 抑制剂的组合疗效需要同源重组修复有效的胰腺癌细胞中的 PARP1 蛋白。
Mol Cancer Ther. 2021 Feb;20(2):263-273. doi: 10.1158/1535-7163.MCT-20-0365. Epub 2020 Dec 2.
5
Reprogramming the tumour microenvironment by radiotherapy: implications for radiotherapy and immunotherapy combinations.放疗对肿瘤微环境的重编程:对放疗与免疫治疗联合应用的启示
Radiat Oncol. 2020 Nov 4;15(1):254. doi: 10.1186/s13014-020-01678-1.
6
The clonogenic assay: robustness of plating efficiency-based analysis is strongly compromised by cellular cooperation.集落形成分析:基于贴壁效率的分析稳健性受到细胞合作的严重影响。
Radiat Oncol. 2020 Oct 29;15(1):248. doi: 10.1186/s13014-020-01697-y.
7
Minimum Information for Reporting on the Comet Assay (MIRCA): recommendations for describing comet assay procedures and results.彗星试验报告最低信息量要求 (MIRCA):彗星试验程序和结果描述的建议。
Nat Protoc. 2020 Dec;15(12):3817-3826. doi: 10.1038/s41596-020-0398-1. Epub 2020 Oct 26.
8
Targeting DNA Damage Response and Replication Stress in Pancreatic Cancer.靶向胰腺癌中的DNA损伤反应与复制应激
Gastroenterology. 2021 Jan;160(1):362-377.e13. doi: 10.1053/j.gastro.2020.09.043. Epub 2020 Oct 9.
9
Cell Cycle Checkpoints Cooperate to Suppress DNA- and RNA-Associated Molecular Pattern Recognition and Anti-Tumor Immune Responses.细胞周期检查点协同作用抑制 DNA 和 RNA 相关分子模式识别和抗肿瘤免疫反应。
Cell Rep. 2020 Sep 1;32(9):108080. doi: 10.1016/j.celrep.2020.108080.
10
Harnessing DNA Replication Stress for Novel Cancer Therapy.利用 DNA 复制应激进行新型癌症治疗。
Genes (Basel). 2020 Aug 25;11(9):990. doi: 10.3390/genes11090990.

将 DNA 损伤反应抑制剂作为化学放射增敏剂从实验室到临床的转化。

Translation of DNA Damage Response Inhibitors as Chemoradiation Sensitizers From the Laboratory to the Clinic.

机构信息

Department of Radiation Oncology, University of Michigan Medical School and Rogel Cancer Center, Ann Arbor, Michigan.

Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.

出版信息

Int J Radiat Oncol Biol Phys. 2021 Dec 1;111(5):e38-e53. doi: 10.1016/j.ijrobp.2021.07.1708. Epub 2021 Aug 1.

DOI:10.1016/j.ijrobp.2021.07.1708
PMID:34348175
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8602768/
Abstract

Combination therapies with agents targeting the DNA damage response (DDR) offer an opportunity to selectively enhance the therapeutic index of chemoradiation or eliminate use of chemotherapy altogether. The successful translation of DDR inhibitors to clinical use requires investigating both their direct actions as (chemo)radiosensitizers and their potential to stimulate tumor immunogenicity. Beginning with high-throughput screening using both viability and DNA damage-reporter assays, followed by validation in gold-standard radiation colony-forming assays and in vitro assessment of mechanistic effects on the DDR, we describe proven strategies and methods leading to the clinical development of DDR inhibitors both with radiation alone and in combination with chemoradiation. Beyond these in vitro studies, we discuss the impact of key features of human xenograft and syngeneic mouse models on the relevance of in vivo tumor efficacy studies, particularly with regard to the immunogenic effects of combined therapy with radiation and DDR inhibitors. Finally, we describe recent technological advances in radiation delivery (using the small animal radiation research platform) that allow for conformal, clinically relevant radiation therapy in mouse models. This overall approach is critical to the successful clinical development and ultimate Food and Drug Administration approval of DDR inhibitors as (chemo)radiation sensitizers.

摘要

联合作用于 DNA 损伤反应(DDR)的治疗药物为选择性提高放化疗疗效指数或完全消除化疗提供了机会。要成功地将 DDR 抑制剂转化为临床应用,需要研究它们作为(化疗)放射增敏剂的直接作用及其刺激肿瘤免疫原性的潜力。我们首先使用高通量筛选方法,包括细胞活力和 DNA 损伤报告基因检测,然后在金标准放射集落形成测定和体外评估对 DDR 的机制作用中进行验证,描述了导致 DDR 抑制剂的临床开发的经过验证的策略和方法,包括单独应用放射疗法和联合放化疗。除了这些体外研究,我们还讨论了人异种移植和同源小鼠模型的关键特征对体内肿瘤疗效研究的相关性的影响,特别是关于联合应用放射和 DDR 抑制剂的免疫治疗效果。最后,我们描述了放射传递的最新技术进展(使用小动物放射研究平台),该技术可在小鼠模型中实现适形、临床相关的放射治疗。这种整体方法对于 DDR 抑制剂作为(化疗)放射增敏剂的成功临床开发和最终获得美国食品和药物管理局的批准至关重要。