• 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

利用具有共存致癌驱动因素的癌细胞中的信号重排。

Exploiting signaling rewiring in cancer cells with co-existing oncogenic drivers.

机构信息

Department of Pathology, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.

Department of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center, University of Torino, Torino, Italy.

出版信息

Mol Oncol. 2023 Nov;17(11):2215-2217. doi: 10.1002/1878-0261.13547. Epub 2023 Oct 31.

DOI:10.1002/1878-0261.13547
PMID:37872865
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10620112/
Abstract

The development of tailored therapies designed to specifically target driver oncogenes has initiated a revolutionary era in cancer biology. The availability of a growing number of selective inhibitors has generated novel experimental and clinical paradigms. These represent an opportunity and a challenge for researchers and clinicians to delve deeper into the intricate dynamics of cancer development and response to treatment. By directly inhibiting key driver oncogenes involved in tumor initiation and progression, scientists have an unprecedented opportunity to conduct longitudinal and clonal evolutionary studies of how cancer cells adapt, rewire, and exploit conflictive or overlapping signaling dependencies in response to treatment in vitro and in vivo. This challenge has to be progressively resolved to discover more effective and personalized cancer therapies.

摘要

针对驱动致癌基因的靶向治疗方法的发展,开创了癌症生物学的新纪元。越来越多的选择性抑制剂的出现,产生了新的实验和临床范例。这为研究人员和临床医生提供了一个机会和挑战,让他们深入研究癌症发展和对治疗反应的复杂动态。通过直接抑制肿瘤起始和进展中涉及的关键驱动致癌基因,科学家们有机会以前所未有的方式进行纵向和克隆进化研究,了解癌细胞如何适应、重新布线以及在体外和体内对治疗做出反应时利用冲突或重叠的信号依赖性。为了发现更有效和个性化的癌症治疗方法,这个挑战必须逐步得到解决。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a101/10620112/0363b24784f5/MOL2-17-2215-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a101/10620112/0363b24784f5/MOL2-17-2215-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a101/10620112/0363b24784f5/MOL2-17-2215-g002.jpg

相似文献

1
Exploiting signaling rewiring in cancer cells with co-existing oncogenic drivers.利用具有共存致癌驱动因素的癌细胞中的信号重排。
Mol Oncol. 2023 Nov;17(11):2215-2217. doi: 10.1002/1878-0261.13547. Epub 2023 Oct 31.
2
Identification of oncogenic driver mutations by genome-wide CRISPR-Cas9 dropout screening.通过全基因组CRISPR-Cas9敲除筛选鉴定致癌驱动突变。
BMC Genomics. 2016 Sep 9;17(1):723. doi: 10.1186/s12864-016-3042-2.
3
Focus issue: From genomic mutations to oncogenic pathways.重点议题:从基因突变到致癌途径。
Sci Signal. 2013 Mar 26;6(268):eg3. doi: 10.1126/scisignal.2004149.
4
RAS-mediated oncogenic signaling pathways in human malignancies.人类恶性肿瘤中 RAS 介导的致癌信号通路。
Semin Cancer Biol. 2019 Feb;54:1-13. doi: 10.1016/j.semcancer.2018.03.001. Epub 2018 Mar 7.
5
A compendium of mutational cancer driver genes.癌症驱动基因突变综合分析
Nat Rev Cancer. 2020 Oct;20(10):555-572. doi: 10.1038/s41568-020-0290-x. Epub 2020 Aug 10.
6
Pan-cancer proteogenomics connects oncogenic drivers to functional states.泛癌蛋白质基因组学将致癌驱动因素与功能状态联系起来。
Cell. 2023 Aug 31;186(18):3921-3944.e25. doi: 10.1016/j.cell.2023.07.014. Epub 2023 Aug 14.
7
SB Driver Analysis: a Sleeping Beauty cancer driver analysis framework for identifying and prioritizing experimentally actionable oncogenes and tumor suppressors.SB 驱动子分析:一种用于识别和优先考虑具有实验可操作性的致癌基因和抑癌基因的沉睡美人癌症驱动子分析框架。
Nucleic Acids Res. 2018 Sep 19;46(16):e94. doi: 10.1093/nar/gky450.
8
Rapid testing of candidate oncogenes and tumour suppressor genes in signal transduction and neoplastic transformation.在信号转导和肿瘤转化中候选癌基因和肿瘤抑制基因的快速检测。
Adv Biol Regul. 2022 Jan;83:100841. doi: 10.1016/j.jbior.2021.100841. Epub 2021 Nov 23.
9
Identification of druggable cancer driver genes amplified across TCGA datasets.在TCGA数据集中鉴定出扩增的可靶向癌症驱动基因。
PLoS One. 2014 May 29;9(5):e98293. doi: 10.1371/journal.pone.0098293. eCollection 2014.
10
Recurrent copy number gains drive PKCι expression and PKCι-dependent oncogenic signaling in human cancers.反复出现的拷贝数增益驱动 PKCι 的表达和 PKCι 依赖的致癌信号在人类癌症中。
Adv Biol Regul. 2020 Dec;78:100754. doi: 10.1016/j.jbior.2020.100754. Epub 2020 Sep 12.

本文引用的文献

1
Systematic profiling of conditional pathway activation identifies context-dependent synthetic lethalities.条件性通路激活的系统分析确定了上下文依赖性的合成致死性。
Nat Genet. 2023 Oct;55(10):1709-1720. doi: 10.1038/s41588-023-01515-7. Epub 2023 Sep 25.
2
Real-world circulating tumor DNA analysis depicts resistance mechanism and clonal evolution in ALK inhibitor-treated lung adenocarcinoma patients.真实世界循环肿瘤 DNA 分析描绘了 ALK 抑制剂治疗的肺腺癌患者的耐药机制和克隆进化。
ESMO Open. 2022 Feb;7(1):100337. doi: 10.1016/j.esmoop.2021.100337. Epub 2022 Feb 2.
3
Oncogenic switch and single-agent MET inhibitor sensitivity in a subset of -mutant lung cancer.
MET 外显子 14 跳跃突变型肺癌对致癌开关和单药 MET 抑制剂的敏感性。
Sci Transl Med. 2021 Sep;13(609):eabb3738. doi: 10.1126/scitranslmed.abb3738. Epub 2021 Sep 1.
4
Acquired Resistance to KRAS Inhibition in Cancer.癌症中对 KRAS 抑制的获得性耐药。
N Engl J Med. 2021 Jun 24;384(25):2382-2393. doi: 10.1056/NEJMoa2105281.
5
Co-occurrence and mutual exclusivity: what cross-cancer mutation patterns can tell us.共现与互斥:跨癌种突变模式能告诉我们什么。
Trends Cancer. 2021 Sep;7(9):823-836. doi: 10.1016/j.trecan.2021.04.009. Epub 2021 May 22.
6
Thinking Differently about Cancer Treatment Regimens.从不同角度思考癌症治疗方案。
Cancer Discov. 2021 May;11(5):1016-1023. doi: 10.1158/2159-8290.CD-20-1187. Epub 2021 Mar 1.
7
A model for RAS mutation patterns in cancers: finding the sweet spot.癌症中 RAS 突变模式的模型:寻找最佳切点。
Nat Rev Cancer. 2018 Dec;18(12):767-777. doi: 10.1038/s41568-018-0076-6.
8
In vivo oncogenic conflict triggered by co-existing KRAS and EGFR activating mutations in lung adenocarcinoma.肺腺癌中同时存在的KRAS和EGFR激活突变引发的体内致癌冲突。
Oncogene. 2017 Apr 20;36(16):2309-2318. doi: 10.1038/onc.2016.385. Epub 2016 Oct 24.
9
Excess of NPM-ALK oncogenic signaling promotes cellular apoptosis and drug dependency.NPM-ALK致癌信号的过度激活会促进细胞凋亡和药物依赖性。
Oncogene. 2016 Jul 21;35(29):3854-3865. doi: 10.1038/onc.2015.456. Epub 2015 Dec 14.
10
Evidence that synthetic lethality underlies the mutual exclusivity of oncogenic KRAS and EGFR mutations in lung adenocarcinoma.合成致死性是肺腺癌中致癌性KRAS和EGFR突变相互排斥的基础的证据。
Elife. 2015 Jun 5;4:e06907. doi: 10.7554/eLife.06907.