ArticleOncotarget2016
Epithelioid peritoneal mesothelioma: a hybrid phenotype within a mesenchymal-epithelial/epithelial-mesenchymal transition framework.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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.
The trial behind it
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- FASN for diffuse malignant peritoneal mesothelioma: a prognostic biomarker after CRS+HIPEC and a therapeutic target.Journal of translational medicine · 2026Article
- Major response of a peritoneal mesothelioma to nivolumab and ipilimumab: a case report, molecular analysis and review of literature.Frontiers in oncology · 2024Article
- Review
- Hand2 delineates mesothelium progenitors and is reactivated in mesothelioma.Nature communications · 2022Article
- Molecular Pathways in Peritoneal Mesothelioma: A Minireview of New Insights.Frontiers in oncology · 2022Review
- Biological basis for novel mesothelioma therapies.British journal of cancer · 2021Review
- The Role of Alternative Lengthening of Telomeres Mechanism in Cancer: Translational and Therapeutic Implications.Cancers · 2020Review
- Fluorescence in situ hybridization (FISH) provides estimates of minute and interstitial BAP1, CDKN2A, and NF2 gene deletions in peritoneal mesothelioma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020Article
- Molecular Signatures for Combined Targeted Treatments in Diffuse Malignant Peritoneal Mesothelioma.International journal of molecular sciences · 2019Article
- Splicing modulation as novel therapeutic strategy against diffuse malignant peritoneal mesothelioma.EBioMedicine · 2019Article
- Complex Immune Contextures Characterise Malignant Peritoneal Mesothelioma: Loss of Adaptive Immunological Signature in the More Aggressive Histological Types.Journal of immunology research · 2018Article
- Mesothelial to mesenchyme transition as a major developmental and pathological player in trunk organs and their cavities.Communications biology · 2018Review
- CBX7 negatively regulates migration and invasion in glioma via Wnt/β-catenin pathway inactivation.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
18 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to reconsider the biological characteristics of epithelioid malignant peritoneal mesothelioma (E-MpM) in the light of new concepts about epithelial mesenchymal transition and mesenchymal epithelial reverse transition (EMT/MErT) and the role of epigenetic reprogramming in this context. To this end we profiled surgical specimens and derived cells cultures by a number of complementary approaches i.e. immunohistochemistry, immunofluorescence, in situ hybridization, biochemistry, pluripotent stem cell arrays, treatments with cytokines, growth factors and specific inhibitors.The analyses of the surgical specimens showed that i) EZH2 is expressed throughout the spectrum of MpM, ii) that E-MpM (including the high-grade undifferentiated form) are characterised by c-MYC and miRNA 17-5p expression, and iii) that progression to sarcomatoid MpM is dictated by EMT regulators. They also showed that E-MpM expressed c-MET and are enriched in E- and P-cadherins- and VEGFR2-expressing CSCs, thus strongly supporting a role for MErT reprogramming in endowing E-MpM tumour cells with stemness and plasticity, and hence with a drug resistant phenotype. The cell culture-based experiments confirmed the stemness traits and plasticity of E-MpM, and support the view that EZH2 is a druggable target in this tumor.
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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.