ReviewContemporary oncology (Poznan, Poland)2015
Regulation of breast cancer stem cell features.
Review in Contemporary oncology (Poznan, Poland), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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
39 citing papers in PubMed, 57 citations in OpenAlex.
- Implications of Mineralization Biomarkers in Breast Cancer Outcomes Beyond Calcifications.International journal of molecular sciences · 2025Article
- Multifaceted role ofMedComm · 2024Review
- The Epigenetic Modifiers HDAC2 and HDAC7 Inversely Associate with Cancer Stemness and Immunity in Solid Tumors.International journal of molecular sciences · 2024Article
- Long Noncoding RNAs CAT2064 and CAT2042 may Function as Diagnostic Biomarkers for Prostate Cancer by Affecting Target MicrorRNAs.Indian journal of clinical biochemistry : IJCB · 2024Article
- Bromodomain (BrD) Family Members as Regulators of Cancer Stemness-A Comprehensive Review.International journal of molecular sciences · 2023Review
- The association between bromodomain proteins and cancer stemness in different solid tumor types.International journal of cancer · 2022Article
- Tumour Stem Cells in Breast Cancer.International journal of molecular sciences · 2022Review
- Chelerythrine Chloride Inhibits Stemness of Melanoma Cancer Stem-Like Cells (CSCs) Potentially via Inducing Reactive Oxygen Species and Causing Mitochondria Dysfunction.Computational and mathematical methods in medicine · 2022Article
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- Investigation of the efficacy of paclitaxel on some miRNAs profiles in breast cancer stem cells.Turkish journal of biology = Turk biyoloji dergisi · 2021Article
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- The role of TRIM family proteins in the regulation of cancer stem cell self-renewal.Stem cells (Dayton, Ohio) · 2020Review
- Phenotypic and microRNA characterization of the neglected CD24+ cell population in MCF-7 breast cancer 3-dimensional spheroid culture.Journal of the Chinese Medical Association : JCMA · 2020Article
- NQO1 is Required for β-Lapachone-Mediated Downregulation of Breast-Cancer Stem-Cell Activity.International journal of molecular sciences · 2018Article
- Cancer Stem Cell Phenotypes in ERMolecular cancer research : MCR · 2018Article
- Breast cancer lung metastasis: Molecular biology and therapeutic implications.Cancer biology & therapy · 2018Review
- Effects of miRNAs on functions of breast cancer stem cells and treatment of breast cancer.OncoTargets and therapy · 2018Review
- The complexity of TRIM28 contribution to cancer.Journal of biomedical science · 2017Review
- Isoform expression patterns of EPHA10 protein mediate breast cancer progression by regulating the E-Cadherin and β-catenin complex.Oncotarget · 2017Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer stem cells (CSCs) are rare, tumour-initiating cells that exhibit stem cell properties: capacity of self-renewal, pluripotency, highly tumorigenic potential, and resistance to therapy. Cancer stem cells have been characterised and isolated from many cancers, including breast cancer. Developmental pathways, such as the Wnt/β-catenin, Notch/γ-secretase/Jagged, Shh (sonic hedgehog), and BMP signalling pathways, which direct proliferation and differentiation of normal stem cells, have emerged as major signalling pathways that contribute to the self-renewal of stem and/or progenitor cells in a variety of organs and cancers. Deregulation of these signalling pathways is frequently linked to an epithelial-mesenchymal transition (EMT), and breast CSCs often possess properties of cells that have undergone the EMT process. Signalling networks mediated by microRNAs and EMT-inducing transcription factors tie the EMT process to regulatory networks that maintain "stemness". Recent studies have elucidated epigenetic mechanisms that control pluripotency and stemness, which allows an assessment on how embryonic and normal tissue stem cells are deregulated during cancerogenesis to give rise to CSCs. Epigenetic-based mechanisms are reversible, and the possibility of "resetting" the abnormal cancer epigenome by applying pharmacological compounds targeting epigenetic enzymes is a promising new therapeutic strategy. Chemoresistance of CSCs is frequently driven by various mechanisms, including aberrant expression/activity of ABC transporters, aldehyde dehydrogenase and anti-oncogenic proteins (i.e. BCL2, B-cell lymphoma-2), enhanced DNA damage response, activation of pro-survival signalling pathways, and epigenetic deregulations. Despite controversy surrounding the CSC hypothesis, there is substantial evidence for their role in cancer, and a number of drugs intended to specifically target CSCs have entered clinical trials.
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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.