ArticleThe international journal of biochemistry & cell biology2012
The opposite effects of doxorubicin on bone marrow stem cells versus breast cancer stem cells depend on glucosylceramide synthase.
Article in The international journal of biochemistry & cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 44 citations in OpenAlex.
- Amifostine Attenuates Doxorubicin-Induced Subacute Hepatic and Renal Toxicity in Rats.International journal of molecular sciences · 2026Article
- Suppression of Glucosylceramide Synthase Reverses Drug Resistance in Cancer Cells Harboring Homozygous p53 Mutants.International journal of molecular sciences · 2026Article
- Ameliorative effects of agomelatine against doxorubicin-induced hepatotoxicity.BMC pharmacology & toxicology · 2025Article
- Doxorubicin Stability-indicating Method and its Main Degradation Products In vitro Toxicity.The AAPS journal · 2025Article
- Nanoparticles may influence mast cells gene expression profiles without affecting their degranulation function.Nanomedicine : nanotechnology, biology, and medicine · 2025Article
- Different Mechanisms in Doxorubicin-Induced Neurotoxicity: Impact of BRCA Mutations.International journal of molecular sciences · 2025Review
- Tumor-derived extracellular vesicles mediate cell-specific uptake and facilitate enhanced doxorubicin delivery in breast cancer.Frontiers in pharmacology · 2025Article
- Modulated Electro-Hyperthermia Accelerates Tumor Delivery and Improves Anticancer Activity of Doxorubicin Encapsulated in Lyso-Thermosensitive Liposomes in 4T1-Tumor-Bearing Mice.International journal of molecular sciences · 2024Article
- Recent Preclinical and Clinical Progress in Liposomal Doxorubicin.Pharmaceutics · 2023Review
- PhAc-ALGP-Dox, a Novel Anticancer Prodrug with Targeted Activation and Improved Therapeutic Index.Molecular cancer therapeutics · 2022Article
- Combination of Autophagy Selective Therapeutics With Doxil: An Assessment of Pathological Toxicity.Frontiers in toxicology · 2022Article
- Quercetin Alleviates the Immunotoxic Impact Mediated by Oxidative Stress and Inflammation Induced by Doxorubicin Exposure in Rats.Antioxidants (Basel, Switzerland) · 2021Article
- The inhibition of ABCB1/MDR1 or ABCG2/BCRP enables doxorubicin to eliminate liver cancer stem cells.Scientific reports · 2021Article
- Ceramide-Rubusoside Nanomicelles, a Potential Therapeutic Approach to Target Cancers Carrying p53 Missense Mutations.Molecular cancer therapeutics · 2020Article
- The Breast Cancer Stem Cells Traits and Drug Resistance.Frontiers in pharmacology · 2020Review
- Hematopoietic Stem Cells: Normal Versus Malignant.Antioxidants & redox signaling · 2018Review
- The effects of doxorubicin-loaded liposomes on viability, stem cell surface marker expression and secretion of vascular endothelial growth factor of three-dimensional stem cell spheroids.Experimental and therapeutic medicine · 2018Article
- A peptidomimetic with a chiral switch is an inhibitor of epidermal growth factor receptor heterodimerization.Oncotarget · 2017Article
- Article
- Novel Peptidomimetics for Inhibition of HER2:HER3 Heterodimerization in HER2-Positive Breast Cancer.Chemical biology & drug design · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Myelosuppression and drug resistance are common adverse effects in cancer patients with chemotherapy, and those severely limit the therapeutic efficacy and lead treatment failure. It is unclear by which cellular mechanism anticancer drugs suppress bone marrow, while drug-resistant tumors survive. We report that due to the difference of glucosylceramide synthase (GCS), catalyzing ceramide glycosylation, doxorubicin (Dox) eliminates bone marrow stem cells (BMSCs) and expands breast cancer stem cells (BCSCs). It was found that Dox decreased the numbers of BMSCs (ABCG2(+)) and the sphere formation in a dose-dependent fashion in isolated bone marrow cells. In tumor-bearing mice, Dox treatments (5mg/kg, 6 days) decreased the numbers of BMSCs and white blood cells; conversely, those treatments increased the numbers of BCSCs (CD24(-)/CD44(+)/ESA(+)) more than threefold in the same mice. Furthermore, therapeutic-dose of Dox (1mg/kg/week, 42 days) decreased the numbers of BMSCs while it increased BCSCs in vivo. Breast cancer cells, rather than bone marrow cells, highly expressed GCS, which was induced by Dox and correlated with BCSC pluripotency. These results indicate that Dox may have opposite effects, suppressing BMSCs versus expanding BCSCs, and GCS is one determinant of the differentiated responsiveness of bone marrow and cancer cells.
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.