Wound healing and cancer stem cells: inflammation as a driver of treatment resistance in breast cancer.

Cancer growth and metastasis Pub Date : 2015-01-29 eCollection Date: 2015-01-01 DOI:10.4137/CGM.S11286
Kimberly M Arnold, Lynn M Opdenaker, Daniel Flynn, Jennifer Sims-Mourtada
{"title":"Wound healing and cancer stem cells: inflammation as a driver of treatment resistance in breast cancer.","authors":"Kimberly M Arnold,&nbsp;Lynn M Opdenaker,&nbsp;Daniel Flynn,&nbsp;Jennifer Sims-Mourtada","doi":"10.4137/CGM.S11286","DOIUrl":null,"url":null,"abstract":"<p><p>The relationship between wound healing and cancer has long been recognized. The mechanisms that regulate wound healing have been shown to promote transformation and growth of malignant cells. In addition, chronic inflammation has been associated with malignant transformation in many tissues. Recently, pathways involved in inflammation and wound healing have been reported to enhance cancer stem cell (CSC) populations. These cells, which are highly resistant to current treatments, are capable of repopulating the tumor after treatment, causing local and systemic recurrences. In this review, we highlight proinflammatory cytokines and developmental pathways involved in tissue repair, whose deregulation in the tumor microenvironment may promote growth and survival of CSCs. We propose that the addition of anti-inflammatory agents to current treatment regimens may slow the growth of CSCs and improve therapeutic outcomes. </p>","PeriodicalId":88440,"journal":{"name":"Cancer growth and metastasis","volume":"8 ","pages":"1-13"},"PeriodicalIF":0.0000,"publicationDate":"2015-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4137/CGM.S11286","citationCount":"87","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer growth and metastasis","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4137/CGM.S11286","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2015/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 87

Abstract

The relationship between wound healing and cancer has long been recognized. The mechanisms that regulate wound healing have been shown to promote transformation and growth of malignant cells. In addition, chronic inflammation has been associated with malignant transformation in many tissues. Recently, pathways involved in inflammation and wound healing have been reported to enhance cancer stem cell (CSC) populations. These cells, which are highly resistant to current treatments, are capable of repopulating the tumor after treatment, causing local and systemic recurrences. In this review, we highlight proinflammatory cytokines and developmental pathways involved in tissue repair, whose deregulation in the tumor microenvironment may promote growth and survival of CSCs. We propose that the addition of anti-inflammatory agents to current treatment regimens may slow the growth of CSCs and improve therapeutic outcomes.

Abstract Image

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
伤口愈合和癌症干细胞:炎症是乳腺癌治疗抵抗的驱动因素。
伤口愈合和癌症之间的关系早已被认识到。调节伤口愈合的机制已被证明可以促进恶性细胞的转化和生长。此外,慢性炎症与许多组织的恶性转化有关。最近,炎症和伤口愈合的通路被报道可以增加癌症干细胞(CSC)的数量。这些细胞对目前的治疗具有高度耐药性,能够在治疗后重新填充肿瘤,导致局部和全身复发。在这篇综述中,我们强调了促炎细胞因子和参与组织修复的发育途径,其在肿瘤微环境中的失调可能促进CSCs的生长和存活。我们建议在目前的治疗方案中加入抗炎剂可能会减缓CSCs的生长并改善治疗结果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Apoptosis-Induced Compensatory Proliferation in Cancer Targeting Apoptosis to Overcome Chemotherapy Resistance Metastasis: Methods and Protocols CD133 Promotes Adhesion to the Ovarian Cancer Metastatic Niche. The Impact of Radiation on the Tumor Microenvironment: Effect of Dose and Fractionation Schedules.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1