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Updated: Sep 22, 2025

Isolation and Functional Assessment of Human Breast Cancer Stem Cells from Cell and Tissue Samples
Published on: October 2, 2020
Regulation of cancer stem cells in triple negative breast cancer
Norman Fultang1, Madhuparna Chakraborty2, Bela Peethambaran2
1Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19140, USA.
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.
Insights
Triple Negative Breast Cancer (TNBC) is aggressive, with high relapse rates due to therapy-resistant cancer stem cells (CSCs). This review details TNBC-specific mechanisms driving CSC expansion and activity, offering new therapeutic targets.
Area of Science:
- Oncology
- Cancer Biology
- Genomics
Background:
- Triple Negative Breast Cancer (TNBC) is the most lethal breast cancer subtype.
- High rates of relapse, recurrence, and therapy failure in TNBC compared to other subtypes.
- Therapy-resistant Cancer Stem Cell (CSC) populations are implicated in poor TNBC outcomes and are enriched in TNBC.
Purpose of the Study:
- To focus on TNBC-specific mechanisms driving Cancer Stem Cell (CSC) expansion and self-renewal.
- To highlight cellular signaling pathways and transcription factors enriched in TNBC that contribute to stemness.
- To explore the potential of bioinformatic approaches, like single-cell RNA-seq, in identifying novel stemness drivers in TNBC.
Main Methods:
- Literature review focusing on TNBC-specific CSC mechanisms.
- Analysis of cellular signaling pathways and transcription factors.
- Bioinformatic analysis of publicly available single-cell RNA-seq data from basal breast cancer tumors.
Main Results:
- TNBC exhibits unique mechanisms for CSC expansion and activity compared to other breast cancers.
- Specific signaling pathways and transcription factors are identified as key drivers of stemness in TNBC.
- Single-cell RNA-seq data analysis reveals potential novel drivers of stemness.
Conclusions:
- Understanding TNBC-specific CSC mechanisms is crucial for improving treatment outcomes.
- Targeting identified pathways and factors could lead to novel therapeutic strategies for TNBC.
- Bioinformatic approaches show promise in uncovering new targets for TNBC and other cancers.
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