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Lgr5+ stem cells are indispensable for radiation-induced intestinal regeneration.Lgr5+ 干细胞对于辐射诱导的肠道再生是不可或缺的。
Cell Stem Cell. 2014 Feb 6;14(2):149-59. doi: 10.1016/j.stem.2013.11.008. Epub 2013 Dec 12.
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Induction of intestinal stem cells by R-spondin 1 and Slit2 augments chemoradioprotection.R 型分泌蛋白 1 和 Slit2 诱导肠干细胞增强放化疗保护作用。
Nature. 2013 Sep 5;501(7465):107-11. doi: 10.1038/nature12416. Epub 2013 Jul 31.
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Heparin-binding EGF-like growth factor (HB-EGF) protects the intestines from radiation therapy-induced intestinal injury.肝素结合表皮生长因子样生长因子 (HB-EGF) 可保护肠道免受放疗引起的肠道损伤。
J Pediatr Surg. 2013 Jun;48(6):1316-22. doi: 10.1016/j.jpedsurg.2013.03.030.
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Keratinocyte growth factor pretreatment prevents radiation-induced intestinal damage in a mouse model.角质形成细胞生长因子预处理可预防小鼠模型中辐射诱导的肠道损伤。
Scand J Gastroenterol. 2013 Apr;48(4):419-26. doi: 10.3109/00365521.2013.772227. Epub 2013 Mar 7.
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Systematic review of agents for the management of gastrointestinal mucositis in cancer patients.系统评价癌症患者胃肠道黏膜炎管理中的药物。
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Crypt base columnar stem cells in small intestines of mice are radioresistant.小鼠小肠隐窝柱状干细胞具有辐射抗性。
Gastroenterology. 2012 Nov;143(5):1266-1276. doi: 10.1053/j.gastro.2012.07.106. Epub 2012 Jul 27.
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Pharmacological targeting of the thrombomodulin-activated protein C pathway mitigates radiation toxicity.靶向血栓调节蛋白激活蛋白 C 通路的药物治疗可减轻辐射毒性。
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Cancer treatment and survivorship statistics, 2012.癌症治疗与生存统计,2012 年。
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PLoS One. 2012;7(3):e33044. doi: 10.1371/journal.pone.0033044. Epub 2012 Mar 27.
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Anti-ceramide antibody prevents the radiation gastrointestinal syndrome in mice.抗神经酰胺抗体可预防小鼠放射性胃肠综合征。
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放射性肠病——发病机制、治疗与预防

Radiation enteropathy--pathogenesis, treatment and prevention.

作者信息

Hauer-Jensen Martin, Denham James W, Andreyev H Jervoise N

机构信息

Surgical Service, Central Arkansas Veterans Healthcare System and Division of Radiation Health, University of Arkansas for Medical Sciences, 4301 West Markham, Little Rock, AR 72205, USA.

Department of Radiation Oncology, University of Newcastle, Newcastle, NSW 2308, Australia.

出版信息

Nat Rev Gastroenterol Hepatol. 2014 Aug;11(8):470-9. doi: 10.1038/nrgastro.2014.46. Epub 2014 Apr 1.

DOI:10.1038/nrgastro.2014.46
PMID:24686268
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4346191/
Abstract

Changes in cancer incidence and mortality have been modest during the past several decades, but the number of cancer survivors has almost tripled during the same period. With an increasing cohort of cancer survivors, efforts to prevent, diagnose and manage adverse effects of cancer therapy, in general, and those of radiation therapy specifically, have intensified. Many cancer survivors have undergone radiation therapy of tumours in the pelvis or abdomen, thus rendering the bowel at risk of injury. In fact, the current prevalence of patients who have long-term radiation-induced intestinal adverse effects exceeds that of IBD. Considerable progress towards reducing toxicity of radiation therapy has been made by the introduction of so-called dose-sculpting treatment techniques, which enable precise delivery of the radiation beam. Moreover, new insights into the underlying pathophysiology have resulted in an improved understanding of mechanisms of radiation-induced bowel toxicity and in development of new diagnostic strategies and management opportunities. This Review discusses the pathogenesis of early and delayed radiation-induced bowel toxicity, presents current management options and outlines priorities for future research. By adding insight into molecular and cellular mechanisms of related bowel disorders, gastroenterologists can substantially strengthen these efforts.

摘要

在过去几十年中,癌症发病率和死亡率的变化不大,但同期癌症幸存者的数量几乎增加了两倍。随着癌症幸存者群体的不断扩大,总体上预防、诊断和管理癌症治疗(特别是放射治疗)不良反应的工作力度加大。许多癌症幸存者接受过盆腔或腹部肿瘤的放射治疗,从而使肠道有受伤风险。事实上,目前长期存在放射诱导肠道不良反应的患者患病率超过了炎症性肠病。通过引入所谓的剂量塑形治疗技术,在降低放射治疗毒性方面取得了相当大的进展,该技术能够精确地输送辐射束。此外,对潜在病理生理学的新认识增进了对放射诱导肠道毒性机制的理解,并推动了新诊断策略和管理方法的发展。本综述讨论了早期和迟发性放射诱导肠道毒性的发病机制,介绍了当前的管理选择,并概述了未来研究的重点。通过深入了解相关肠道疾病的分子和细胞机制,胃肠病学家可以大力加强这些工作。