ReviewEndocrine-related cancer2015
Identifying and targeting tumor-initiating cells in the treatment of breast cancer.
Review in Endocrine-related cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Effects of noncoding RNAs in radiotherapy response in breast cancer: a systematic review.Cell cycle (Georgetown, Tex.) · 2022Pooled it
- Promotion of breast cancer by the DNPH1 enzyme.iScience · 2026Article
- The DRP1 receptor FIS1 is critical to the expansion of triple-negative breast cancer tumor-initiating cells.Cancer cell international · 2025Article
- A positive feedback loop of OTUD1 and c-Jun driven by leptin expedites stemness maintenance in ovarian cancer.Oncogene · 2025Article
- Role and therapeutic potential of the NEDD4 family in breast cancer.Frontiers in pharmacology · 2025Review
- Visualization of Metastatic Lung Cancer with TiNIR.Tomography (Ann Arbor, Mich.) · 2023Article
- PERK signaling through C/EBPδ contributes to ER stress-induced expression of immunomodulatory and tumor promoting chemokines by cancer cells.Cell death & disease · 2021Article
- Co-dependency for MET and FGFR1 in basal triple-negative breast cancers.NPJ breast cancer · 2021Article
- Review
- Dll1Nature communications · 2021Article
- Wnt/β-Catenin Inhibition Disrupts Carboplatin Resistance in Isogenic Models of Triple-Negative Breast Cancer.Frontiers in oncology · 2021Article
- Novel C-terminal heat shock protein 90 inhibitors target breast cancer stem cells and block migration, self-renewal, and epithelial-mesenchymal transition.Molecular oncology · 2020Article
- O-GlcNAc Transferase Regulates Cancer Stem-like Potential of Breast Cancer Cells.Molecular cancer research : MCR · 2020Article
- Mechanisms of tRNA-derived fragments and tRNA halves in cancer treatment resistance.Biomarker research · 2020Review
- C/EBPδ links IL-6 and HIF-1 signaling to promote breast cancer stem cell-associated phenotypes.Oncogene · 2019Article
- Sulforaphane Suppresses the Growth of Triple-negative Breast Cancer Stem-like CellsCancer prevention research (Philadelphia, Pa.) · 2019Article
- Serum erythropoietin levels, breast cancer and breast cancer-initiating cells.Breast cancer research : BCR · 2019Article
- Hydrodynamic shear stress promotes epithelial-mesenchymal transition by downregulating ERK and GSK3β activities.Breast cancer research : BCR · 2019Article
- High collagen density augments mTOR-dependent cancer stem cells in ERα+ mammary carcinomas, and increases mTOR-independent lung metastases.Cancer letters · 2018Article
- Nicotine reduces effectiveness of doxorubicin chemotherapy and promotes CD44Experimental and therapeutic medicine · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Breast cancer is the most common cancer in women (excluding skin cancer), and it is the second leading cause of cancer-related deaths. Although conventional and targeted therapies have improved survival rates, there are still considerable challenges in treating breast cancer, including treatment resistance, disease recurrence, and metastasis. Treatment resistance can be either de novo - because of traits that tumor cells possess before treatment - or acquired - because of traits that tumor cells gain in response to treatment. A recently proposed mechanism of de novo resistance invokes the existence of a specialized subset of cancer cells defined as tumor-initiating cells (TICs), or cancer stem cells (CSCs). TICs have the capacity to self-renew and to generate new tumors that consist entirely of clonally derived cell types present in the parental tumor. There are data to suggest that TICs are resistant to many conventional cancer therapies and that they can survive treatment in spite of dramatic shrinkage of the tumor. Residual TICs can then eventually regrow, which results in disease relapse. It has also been hypothesized that TIC may be responsible for metastatic disease. If these hypotheses are correct, targeting TICs may be imperative for achieving a cure. In the present review, we discuss evidence for breast TICs and their apparent resistance to conventional chemotherapy and radiotherapy as well as to various targeted therapies. We also address the potential impact of breast TIC plasticity and metastatic potential on therapeutic strategies. Finally, we describe several genes and signaling pathways that appear to be important for TIC function and may represent promising therapeutic targets.
Indexed as
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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.