Tumor: Stroma Interaction and Cancer.

Q2 Medicine
Michael P Rogers, Zhiyong Mi, Neill Y Li, Philip Y Wai, Paul C Kuo
{"title":"Tumor: Stroma Interaction and Cancer.","authors":"Michael P Rogers,&nbsp;Zhiyong Mi,&nbsp;Neill Y Li,&nbsp;Philip Y Wai,&nbsp;Paul C Kuo","doi":"10.1007/978-3-030-91311-3_2","DOIUrl":null,"url":null,"abstract":"<p><p>The understanding of how normal cells transform into tumor cells and progress to invasive cancer and metastases continues to evolve. The tumor mass is comprised of a heterogeneous population of cells that include recruited host immune cells, stromal cells, matrix components, and endothelial cells. This tumor microenvironment plays a fundamental role in the acquisition of hallmark traits, and has been the intense focus of current research. A key regulatory mechanism triggered by these tumor-stroma interactions includes processes that resemble epithelial-mesenchymal transition, a physiologic program that allows a polarized epithelial cell to undergo biochemical and cellular changes and adopt mesenchymal cell characteristics. These cellular adaptations facilitate enhanced migratory capacity, invasiveness, elevated resistance to apoptosis, and greatly increased production of ECM components. Indeed, it has been postulated that cancer cells undergo epithelial-mesenchymal transition to invade and metastasize.In the following discussion, the physiology of chronic inflammation, wound healing, fibrosis, and tumor invasion will be explored. The key regulatory cytokines, transforming growth factor β and osteopontin, and their roles in cancer metastasis will be highlighted.</p>","PeriodicalId":36906,"journal":{"name":"Experientia supplementum (2012)","volume":"113 ","pages":"59-87"},"PeriodicalIF":0.0000,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experientia supplementum (2012)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/978-3-030-91311-3_2","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 1

Abstract

The understanding of how normal cells transform into tumor cells and progress to invasive cancer and metastases continues to evolve. The tumor mass is comprised of a heterogeneous population of cells that include recruited host immune cells, stromal cells, matrix components, and endothelial cells. This tumor microenvironment plays a fundamental role in the acquisition of hallmark traits, and has been the intense focus of current research. A key regulatory mechanism triggered by these tumor-stroma interactions includes processes that resemble epithelial-mesenchymal transition, a physiologic program that allows a polarized epithelial cell to undergo biochemical and cellular changes and adopt mesenchymal cell characteristics. These cellular adaptations facilitate enhanced migratory capacity, invasiveness, elevated resistance to apoptosis, and greatly increased production of ECM components. Indeed, it has been postulated that cancer cells undergo epithelial-mesenchymal transition to invade and metastasize.In the following discussion, the physiology of chronic inflammation, wound healing, fibrosis, and tumor invasion will be explored. The key regulatory cytokines, transforming growth factor β and osteopontin, and their roles in cancer metastasis will be highlighted.

肿瘤:间质相互作用与癌症。
对正常细胞如何转化为肿瘤细胞并进展为侵袭性癌症和转移的理解在不断发展。肿瘤肿块由异质细胞群组成,包括募集的宿主免疫细胞、基质细胞、基质成分和内皮细胞。这种肿瘤微环境在标志性特征的获得中起着至关重要的作用,是当前研究的热点。由这些肿瘤-间质相互作用触发的关键调控机制包括类似于上皮-间质转化的过程,这是一种允许极化上皮细胞经历生化和细胞变化并采用间质细胞特征的生理程序。这些细胞适应有助于增强迁移能力,侵袭性,提高对凋亡的抵抗力,并大大增加ECM成分的产生。事实上,已经假设癌细胞经过上皮-间质转化来侵袭和转移。在接下来的讨论中,我们将探讨慢性炎症、伤口愈合、纤维化和肿瘤侵袭的生理机制。重点介绍肿瘤转移过程中关键的调节细胞因子转化生长因子β和骨桥蛋白在肿瘤转移中的作用。
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 求助全文
来源期刊
Experientia supplementum (2012)
Experientia supplementum (2012) Medicine-Medicine (all)
CiteScore
3.30
自引率
0.00%
发文量
24
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信