ReviewCancer drug resistance (Alhambra, Calif.)2021
Regulation of cancer stem cells in triple negative breast cancer.
Review in Cancer drug resistance (Alhambra, Calif.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
66 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.
- Pooled it
- Transcriptional intermediary factor 1 gamma-based multitarget gene therapeutic strategy for triple-negative breast cancer.Signal transduction and targeted therapy · 2026Article
- Epigenetic Plasticity in Triple-Negative Breast Cancer: Mechanisms of Therapy Resistance, Biomarkers, and Therapeutic Vulnerabilities.Biomedicines · 2026Review
- CK2 in triple-negative breast cancer: oncogenic signaling networks and emerging CK2 inhibitor-based combination therapies.Clinical and experimental medicine · 2026Review
- C-MPL signaling in breast cancer: molecular mechanisms and therapeutic implications.Annals of medicine and surgery (2012) · 2026Article
- Natural Killer Cell-Derived Extracellular Vesicles Exhibit Cytotoxicity Against Bulk Tumor Cells and Cancer Stem Cells in Triple-Negative Breast Cancer.Nanomaterials (Basel, Switzerland) · 2026Article
- Repurposing Quetiapine as an Adjuvant Therapeutic Agent for Triple-Negative Breast Cancer.Radiation research · 2026Article
- Screening of kinase inhibitors in the triple negative KRAS G13D-mutated MDA-MB-231 breast cancer cell line.Scientific reports · 2026Article
- Exploring the Influence of Chemical Exposures in Breast Cancer Disparities: High-Throughput Transcriptomic Analysis in Normal Breast Cells from Diverse Donors.bioRxiv : the preprint server for biology · 2026Article
- The role of pluripotency regulators in triple-negative breast cancer immune response.Frontiers in genetics · 2026Review
- Research Progress on Signaling Pathways in Breast Cancer Bone Metastasis.Oncology research · 2026Review
- Multi-omics comprehensive analysis identified KIF22 and KRAS as highly synthetic lethal pairs for triple-negative breast cancer.Frontiers in oncology · 2026Article
- Signalling Pathways and Inhibitors in Triple Negative Breast Cancer: Current Progress.Anti-cancer agents in medicinal chemistry · 2026Review
- Tumor exosomal miR-221-3p induces glycolysis through the LIFR/GLUT1 pathway to destroy the cerebral vascular endothelial cell barrier and promote breast cancer brain metastasis.Journal of translational medicine · 2025Article
- Targeting GD2 with naxitamab overcomes GD3 synthase-driven immune suppression in triple-negative breast cancer.NPJ breast cancer · 2025Article
- IL-3/STAT5/miR-155-5p axis supports stem-related pathway reprogramming in TNBC.Breast cancer research : BCR · 2025Article
- Review
- Depleting the Action of EZH2 through PI3K-mTOR Inhibition to Overcome Metastasis and Immunotherapy Resistance in Triple-Negative Breast Cancer.Molecular cancer therapeutics · 2025Article
- Calumenin, A Calcium-Binding Modulatory Protein, Effective in Pathological Calcifications and Cancers, With Therapeutic Application Promise.FASEB bioAdvances · 2025Review
- Antibody-drug conjugates in breast cancer: mechanisms of resistance and future therapeutic perspectives.NPJ breast cancer · 2025Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.