ArticleCancer medicine2013
Phenotypic modifications in ovarian cancer stem cells following Paclitaxel treatment.
Article in Cancer medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 58 citations in OpenAlex.
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- Immune Modulation of Innate and Adaptive Responses Restores Immune Surveillance and Establishes Antitumor Immunologic Memory.Cancer immunology research · 2024Article
- Adipose microenvironment promotes hypersialylation of ovarian cancer cells.Frontiers in oncology · 2024Article
- Adipose-derived exosomal miR-421 targets CBX7 and promotes metastatic potential in ovarian cancer cells.Journal of ovarian research · 2023Article
- Adipose-derived exosomal miR-421 targets CBX7 and promotes metastatic potential in ovarian cancer cells.bioRxiv : the preprint server for biology · 2023Article
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- A Benzenesulfonamide-Based Mitochondrial Uncoupler Induces Endoplasmic Reticulum Stress and Immunogenic Cell Death in Epithelial Ovarian Cancer.Molecular cancer therapeutics · 2021Article
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- Differential expression of ABCB1, ABCG2, and KLF4 as putative indicators for paclitaxel resistance in human epithelial type 2 cells.Molecular biology reports · 2021Article
- Characteristics of CD133-Sustained Chemoresistant Cancer Stem-Like Cells in Human Ovarian Carcinoma.International journal of molecular sciences · 2020Article
- Albumin Nanoparticle of Paclitaxel (Abraxane) Decreases while Taxol Increases Breast Cancer Stem Cells in Treatment of Triple Negative Breast Cancer.Molecular pharmaceutics · 2020Article
- Transimmunization restores immune surveillance and prevents recurrence in a syngeneic mouse model of ovarian cancer.Oncoimmunology · 2020Article
- CBX7 binds the E-box to inhibit TWIST-1 function and inhibit tumorigenicity and metastatic potential.Oncogene · 2020Article
- Risk predictors of early recurrence in women with epithelial ovarian cancer in Lagos, Nigeria.The Pan African medical journal · 2020Article
- Protein kinase Cα-mediated phosphorylation of Twist1 at Ser-144 prevents Twist1 ubiquitination and stabilizes it.The Journal of biological chemistry · 2019Article
- p53-Pirh2 Complex Promotes Twist1 Degradation and Inhibits EMT.Molecular cancer research : MCR · 2019Article
- Article
- Chemoresistance in ovarian cancer: exploiting cancer stem cell metabolism.Journal of gynecologic oncology · 2018Review
- Ovarian Cancers: Genetic Abnormalities, Tumor Heterogeneity and Progression, Clonal Evolution and Cancer Stem Cells.Medicines (Basel, Switzerland) · 2018Review
- Novel approach for the detection of intraperitoneal micrometastasis using an ovarian cancer mouse model.Scientific reports · 2017Article
Corrections and comments
- Erratum issuedJoo, Won Duk [added]
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Epithelial ovarian cancer (EOC) is the most lethal gynecologic malignancy. Despite initial responsiveness, 80% of EOC patients recur and present with chemoresistant and a more aggressive disease. This suggests an underlying biology that results in a modified recurrent disease, which is distinct from the primary tumor. Unfortunately, the management of recurrent EOC is similar to primary disease and does not parallel the molecular changes that may have occurred during the process of rebuilding the tumor. We describe the characterization of unique in vitro and in vivo ovarian cancer models to study the process of recurrence. The in vitro model consists of GFP+/CD44+/MyD88+ EOC stem cells and mCherry+/CD44-/MyD88- EOC cells. The in vivo model consists of mCherry+/CD44+/MyD88+ EOC cells injected intraperitoneally. Animals received four doses of Paclitaxel and response to treatment was monitored by in vivo imaging. Phenotype of primary and recurrent disease was characterized by quantitative polymerase chain reaction (qPCR) and Western blot analysis. Using the in vivo and in vitro models, we confirmed that chemotherapy enriched for CD44+/MyD88+ EOC stem cells. However, we observed that the surviving CD44+/MyD88+ EOC stem cells acquire a more aggressive phenotype characterized by chemoresistance and migratory potential. Our results highlight the mechanisms that may explain the phenotypic heterogeneity of recurrent EOC and emphasize the significant plasticity of ovarian cancer stem cells. The significance of our findings is the possibility of developing new venues to target the surviving CD44+/MyD88+ EOC stem cells as part of maintenance therapy and therefore preventing recurrence and metastasis, which are the main causes of mortality in patients with ovarian cancer.
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