• 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
The biology and clinical implications of prostate cancer dormancy and metastasis.前列腺癌休眠与转移的生物学特性及临床意义
J Mol Med (Berl). 2016 Mar;94(3):259-65. doi: 10.1007/s00109-015-1353-4. Epub 2015 Oct 21.
2
Osteoblast-Secreted Factors Mediate Dormancy of Metastatic Prostate Cancer in the Bone via Activation of the TGFβRIII-p38MAPK-pS249/T252RB Pathway.成骨细胞分泌因子通过激活 TGFβRIII-p38MAPK-pS249/T252RB 通路介转移前列腺癌在骨中的休眠。
Cancer Res. 2018 Jun 1;78(11):2911-2924. doi: 10.1158/0008-5472.CAN-17-1051. Epub 2018 Mar 7.
3
Bone secreted factors induce cellular quiescence in prostate cancer cells.骨分泌因子诱导前列腺癌细胞的细胞静止。
Sci Rep. 2019 Dec 9;9(1):18635. doi: 10.1038/s41598-019-54566-4.
4
Bone Metastasis: Molecular Mechanisms Implicated in Tumour Cell Dormancy in Breast and Prostate Cancer.骨转移:乳腺癌和前列腺癌中肿瘤细胞休眠的分子机制
Curr Cancer Drug Targets. 2015;15(6):469-80. doi: 10.2174/1568009615666150506092443.
5
Tumor removal limits prostate cancer cell dissemination in bone and osteoblasts induce cancer cell dormancy through focal adhesion kinase.肿瘤切除限制了前列腺癌细胞在骨中的扩散,成骨细胞通过粘着斑激酶诱导癌细胞休眠。
J Exp Clin Cancer Res. 2023 Oct 11;42(1):264. doi: 10.1186/s13046-023-02849-0.
6
Cellular Adhesion Promotes Prostate Cancer Cells Escape from Dormancy.细胞黏附促进前列腺癌细胞脱离休眠状态。
PLoS One. 2015 Jun 19;10(6):e0130565. doi: 10.1371/journal.pone.0130565. eCollection 2015.
7
AXL Is a Putative Tumor Suppressor and Dormancy Regulator in Prostate Cancer.AXL 是前列腺癌中的一个潜在肿瘤抑制因子和休眠调控因子。
Mol Cancer Res. 2019 Feb;17(2):356-369. doi: 10.1158/1541-7786.MCR-18-0718. Epub 2018 Oct 5.
8
Detection and isolation of disseminated tumor cells in bone marrow of patients with clinically localized prostate cancer.检测和分离临床局限性前列腺癌患者骨髓中的播散肿瘤细胞。
Prostate. 2019 Oct;79(14):1715-1727. doi: 10.1002/pros.23896. Epub 2019 Aug 26.
9
The molecular function of kallikrein-related peptidase 14 demonstrates a key modulatory role in advanced prostate cancer.激肽释放酶相关肽酶 14 的分子功能在晚期前列腺癌中表现出关键的调节作用。
Mol Oncol. 2020 Jan;14(1):105-128. doi: 10.1002/1878-0261.12587. Epub 2019 Nov 28.
10
Abscisic acid regulates dormancy of prostate cancer disseminated tumor cells in the bone marrow.脱落酸调节前列腺癌细胞在骨髓中的休眠。
Neoplasia. 2021 Jan;23(1):102-111. doi: 10.1016/j.neo.2020.11.009. Epub 2020 Dec 6.

引用本文的文献

1
Abscisic acid signaling through LANCL2 and PPARγ induces activation of p38MAPK resulting in dormancy of prostate cancer metastatic cells.通过 LANCL2 和 PPARγ 的脱落酸信号传导诱导 p38MAPK 的激活,导致前列腺癌转移细胞的休眠。
Oncol Rep. 2024 Mar;51(3). doi: 10.3892/or.2024.8698. Epub 2024 Jan 12.
2
From molecular mechanisms of prostate cancer to translational applications: based on multi-omics fusion analysis and intelligent medicine.从前列腺癌的分子机制到转化应用:基于多组学融合分析与智能医学
Health Inf Sci Syst. 2023 Dec 18;12(1):6. doi: 10.1007/s13755-023-00264-5. eCollection 2024 Dec.
3
The endoplasmic reticulum stress response in prostate cancer.前列腺癌中的内质网应激反应
Nat Rev Urol. 2022 Dec;19(12):708-726. doi: 10.1038/s41585-022-00649-3. Epub 2022 Sep 27.
4
Novel Dormancy Mechanism of Castration Resistance in Bone Metastatic Prostate Cancer Organoids.骨转移前列腺癌类器官中去势抵抗的新休眠机制。
Int J Mol Sci. 2022 Mar 16;23(6):3203. doi: 10.3390/ijms23063203.
5
Prostate cancer dormancy and recurrence.前列腺癌休眠与复发。
Cancer Lett. 2022 Jan 1;524:103-108. doi: 10.1016/j.canlet.2021.09.037. Epub 2021 Oct 5.
6
Cytokeratin-positive cells in the bone marrow from patients with pancreatic, periampullary malignancy and benign pancreatic disease show no prognostic information.骨髓中细胞角蛋白阳性的细胞来自胰腺、壶腹周围恶性肿瘤和良性胰腺疾病患者,但不能提供预后信息。
BMC Cancer. 2020 Nov 16;20(1):1107. doi: 10.1186/s12885-020-07510-z.
7
Whole Organism Model to Study Molecular Mechanisms of Differentiation and Dedifferentiation.用于研究分化和去分化分子机制的全生物体模型
Biology (Basel). 2020 Apr 17;9(4):79. doi: 10.3390/biology9040079.
8
Metastatic Latency, a Veiled Threat.转移性潜伏期,一个隐藏的威胁。
Front Immunol. 2019 Aug 6;10:1836. doi: 10.3389/fimmu.2019.01836. eCollection 2019.
9
Subtypes of minimal residual disease, association with Gleason score, risk and time to biochemical failure in pT2 prostate cancer treated with radical prostatectomy.根治性前列腺切除术后pT2期前列腺癌微小残留病的亚型、与Gleason评分的关联、风险及生化复发时间
Ecancermedicalscience. 2019 Jun 6;13:934. doi: 10.3332/ecancer.2019.934. eCollection 2019.
10
Limiting tumor seeding as a therapeutic approach for metastatic disease.限制肿瘤播种作为转移性疾病的治疗方法。
Pharmacol Ther. 2019 Jul;199:117-128. doi: 10.1016/j.pharmthera.2019.03.007. Epub 2019 Mar 12.

本文引用的文献

1
Cellular Adhesion Promotes Prostate Cancer Cells Escape from Dormancy.细胞黏附促进前列腺癌细胞脱离休眠状态。
PLoS One. 2015 Jun 19;10(6):e0130565. doi: 10.1371/journal.pone.0130565. eCollection 2015.
2
Mitotic quiescence, but not unique "stemness," marks the phenotype of bone metastasis-initiating cells in prostate cancer.有丝分裂静止而非独特的“干性”标志着前列腺癌骨转移起始细胞的表型。
FASEB J. 2015 Aug;29(8):3141-50. doi: 10.1096/fj.14-266379. Epub 2015 Apr 17.
3
The epigenetic/noncoding origin of tumor dormancy.肿瘤休眠的表观遗传/非编码起源。
Trends Mol Med. 2015 Apr;21(4):206-11. doi: 10.1016/j.molmed.2015.02.005. Epub 2015 Mar 11.
4
Dormancy and growth of metastatic breast cancer cells in a bone-like microenvironment.转移性乳腺癌细胞在类骨微环境中的休眠与生长
Clin Exp Metastasis. 2015 Apr;32(4):335-44. doi: 10.1007/s10585-015-9710-9. Epub 2015 Mar 8.
5
SMAD signaling and redox imbalance cooperate to induce prostate cancer cell dormancy.SMAD信号传导与氧化还原失衡共同作用诱导前列腺癌细胞休眠。
Cell Cycle. 2015;14(8):1218-31. doi: 10.1080/15384101.2015.1014145.
6
NR2F1 controls tumour cell dormancy via SOX9- and RARβ-driven quiescence programmes.NR2F1通过SOX9和RARβ驱动的静止程序控制肿瘤细胞休眠。
Nat Commun. 2015 Jan 30;6:6170. doi: 10.1038/ncomms7170.
7
Significance of apoptotic and non-apoptotic disseminated tumor cells in the bone marrow of patients with clinically localized prostate cancer.临床局限性前列腺癌患者骨髓中凋亡和非凋亡播散肿瘤细胞的意义
Prostate. 2015 May;75(6):637-45. doi: 10.1002/pros.22947. Epub 2015 Jan 13.
8
Intrinsic TGF-β2-triggered SDF-1-CXCR4 signaling axis is crucial for drug resistance and a slow-cycling state in bone marrow-disseminated tumor cells.内源性转化生长因子-β2触发的基质细胞衍生因子-1-趋化因子受体4信号轴对骨髓播散肿瘤细胞的耐药性和慢周期状态至关重要。
Oncotarget. 2015 Jan 20;6(2):1008-19. doi: 10.18632/oncotarget.2826.
9
Bone marrow as a reservoir for disseminated tumor cells: a special source for liquid biopsy in cancer patients.骨髓作为播散肿瘤细胞的储存库:癌症患者液体活检的特殊来源。
Bonekey Rep. 2014 Nov 19;3:584. doi: 10.1038/bonekey.2014.79. eCollection 2014.
10
Forward genetic screens in mice uncover mediators and suppressors of metastatic reactivation.对小鼠进行的正向遗传学筛选揭示了转移再激活的介导因子和抑制因子。
Proc Natl Acad Sci U S A. 2014 Nov 18;111(46):16532-7. doi: 10.1073/pnas.1403234111. Epub 2014 Nov 5.

前列腺癌休眠与转移的生物学特性及临床意义

The biology and clinical implications of prostate cancer dormancy and metastasis.

作者信息

Morrissey Colm, Vessella Robert L, Lange Paul H, Lam Hung-Ming

机构信息

Department of Urology, University of Washington, 1959 Pacific Street NE, Box 356510, Seattle, WA, 98195, USA.

Department of Veterans Affairs Medical Center, 1660 S Columbian Way, Seattle, WA, 98108, USA.

出版信息

J Mol Med (Berl). 2016 Mar;94(3):259-65. doi: 10.1007/s00109-015-1353-4. Epub 2015 Oct 21.

DOI:10.1007/s00109-015-1353-4
PMID:26489605
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4803572/
Abstract

Disseminated tumor cells (DTCs) are detected early in the disease process in prostate cancer (PCa) patients and can persist after radical prostatectomy. DTCs can remain dormant in patients with no evidence of disease for a prolonged period of time only to recur 10 or more years later. Recent advances in single-cell genomics and transcriptomics have provided much needed insight into DTC biology and cancer dormancy in patients. With the development of new in vitro and preclinical models, researchers recapitulate the clinical events in patients and therefore allow further elucidation of the molecular mechanisms underlying cancer dormancy and escape. In this review, we explore novel ideas on the detection, heterogeneous transcriptomic profiles, molecular and cellular mechanisms of dormancy, and potential mechanisms underlying dormancy escape by DTCs. As such, there is hope that identifying and targeting novel dormancy-associated pathways in patients with residual disease will have significant clinical implications for the treatment of PCa patients in the future.

摘要

在前列腺癌(PCa)患者的疾病进程早期即可检测到播散肿瘤细胞(DTCs),且这些细胞在根治性前列腺切除术后仍可存活。DTCs可在无疾病证据的患者体内长期处于休眠状态,直至10年或更长时间后复发。单细胞基因组学和转录组学的最新进展为深入了解患者体内的DTC生物学特性和癌症休眠提供了急需的见解。随着新的体外和临床前模型的发展,研究人员能够重现患者的临床事件,从而进一步阐明癌症休眠和逃逸的分子机制。在这篇综述中,我们探讨了有关DTCs检测、异质转录组谱、休眠的分子和细胞机制以及休眠逃逸潜在机制的新观点。因此,有望通过识别和靶向残留疾病患者中与休眠相关的新途径,为未来PCa患者的治疗带来重大临床意义。