Regulation of cancer stem cells in triple negative breast cancer.

IF 4.6 Q1 ONCOLOGY
癌症耐药(英文) Pub Date : 2021-06-19 eCollection Date: 2021-01-01 DOI:10.20517/cdr.2020.106
Norman Fultang, Madhuparna Chakraborty, Bela Peethambaran
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引用次数: 0

Abstract

Triple Negative Breast Cancer (TNBC) is the most lethal subtype of breast cancer. Despite the successes of emerging targeted therapies, relapse, recurrence, and therapy failure rates in TNBC significantly outpace other subtypes of breast cancer. Mounting evidence suggests accumulation of therapy resistant Cancer Stem Cell (CSC) populations within TNBCs contributes to poor clinical outcomes. These CSCs are enriched in TNBC compared to non-TNBC breast cancers. The mechanisms underlying CSC accumulation have been well-characterized and discussed in other reviews. In this review, we focus on TNBC-specific mechanisms that allow the expansion and activity of self-renewing CSCs. We highlight cellular signaling pathways and transcription factors, specifically enriched in TNBC over non-TNBC breast cancer, contributing to stemness. We also analyze publicly available single-cell RNA-seq data from basal breast cancer tumors to highlight the potential of emerging bioinformatic approaches in identifying novel drivers of stemness in TNBC and other cancers.

肿瘤干细胞在三阴性乳腺癌中的调控作用
癌症三阴性(TNBC)是癌症最致命的亚型。尽管新出现的靶向治疗取得了成功,但TNBC的复发率、复发率和治疗失败率显著高于其他类型的癌症。越来越多的证据表明,TNBC中耐药癌症干细胞(CSC)群体的积累导致了不良的临床结果。与非TNBC乳腺癌相比,这些CSC在TNBC中富集。CSC积累的机制已经在其他综述中得到了很好的描述和讨论。在这篇综述中,我们重点关注TNBC的特定机制,这些机制允许自我更新的CSC的扩展和活动。我们强调了细胞信号通路和转录因子,它们在非TNBC乳腺癌症的TNBC中特别富集,有助于干性。我们还分析了来自癌症基底肿瘤的公开可用的单细胞RNA-seq数据,以强调新兴的生物信息学方法在确定TNBC和其他癌症干燥的新驱动因素方面的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
6.60
自引率
0.00%
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