ArticleCells2019
Identification and Characterization of a New Platinum-Induced TP53 Mutation in MDAH Ovarian Cancer Cells.
Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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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.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Dual inhibition of mTOR and HSP90 enhances cisplatin efficacy and overcomes resistance in ovarian cancer.Cell death & disease · 2026Article
- USP1 deubiquitinates PARP1 to regulate its trapping and PARylation activity.Science advances · 2024Article
- Prognostic value of baseline genetic features and newly identified TP53 mutations in advanced breast cancer.Molecular oncology · 2022Article
- Triptolide promotes degradation of the unfolded gain-of-function Tp53Translational lung cancer research · 2022Article
- Platinum-resistant ovarian cancer: From drug resistance mechanisms to liquid biopsy-based biomarkers for disease management.Seminars in cancer biology · 2021Review
- HSP90 identified by a proteomic approach as druggable target to reverse platinum resistance in ovarian cancer.Molecular oncology · 2021Article
- New Insights into Therapy-Induced Progression of Cancer.International journal of molecular sciences · 2020Review
- Clinical, Genomic, and Pharmacological Study ofCancers · 2020Article
- Purified Tea (International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Platinum-based chemotherapy is the therapy of choice for epithelial ovarian cancer (EOC). Acquired resistance to platinum (PT) is a frequent event that leads to disease progression and predicts poor prognosis. To understand possible mechanisms underlying acquired PT-resistance, we have recently generated and characterized three PT-resistant isogenic EOC cell lines. Here, we more deeply characterize several PT-resistant clones derived from MDAH-2774 cells. We show that, in these cells, the increased PT resistance was accompanied by the presence of a subpopulation of multinucleated giant cells. This phenotype was likely due to an altered progression through the M phase of the cell cycle and accompanied by the deregulated expression of genes involved in M phase progression known to be target of mutant TP53. Interestingly, we found that PT-resistant MDAH cells acquired in the TP53 gene a novel secondary mutation (i.e., S185G) that accompanied the R273H typical of MDAH cells. The double p53
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Registered trials
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