ArticleOncotarget2017
Blocking epithelial-to-mesenchymal transition in glioblastoma with a sextet of repurposed drugs: the EIS regimen.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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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Who cites it
28 citing papers in PubMed, 35 citations in OpenAlex.
- Dissecting the Dual Drug Candidates Against Glioblastoma and Oligodendroglioma Through Integrated Transcriptome Analysis and Virtual Screening.Cell biochemistry and biophysics · 2025Article
- A New Adjuvant Treatment for Glioblastoma Using Aprepitant, Vortioxetine, Roflumilast and Olanzapine: The AVRO Regimen.International journal of molecular sciences · 2025Review
- Establishment of U-87MG Cellular Fibrosis as a Novel in Vitro Model to Analyze Glioblastoma Cells' Sensitivity to Temozolomide.International journal of molecular sciences · 2025Article
- Article
- Analysis of transcription profiles for the identification of master regulators as the key players in glioblastoma.Computational and structural biotechnology journal · 2024Article
- Article
- The tumor-associated fibrotic reactions in microenvironment aggravate glioma chemoresistance.Frontiers in oncology · 2024Review
- Metformin-loaded nanoerythrosomes: An erythrocyte-based drug delivery system as a therapeutic tool for glioma.Heliyon · 2023Article
- A Retrospective Study on the Role of Metformin in Colorectal Cancer Liver Metastases.Biomedicines · 2023Article
- Hedgehog signaling regulates the development and treatment of glioblastoma.Oncology letters · 2022Review
- Exploring the Mechanism of Adjuvant Treatment of Glioblastoma Using Temozolomide and Metformin.International journal of molecular sciences · 2022Article
- CD146 increases stemness and aggressiveness in glioblastoma and activates YAP signaling.Cellular and molecular life sciences : CMLS · 2022Article
- Article
- Rabeprazole has efficacy per se and reduces resistance to temozolomide in glioma via EMT inhibition.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- An Alternative Pipeline for Glioblastoma Therapeutics: A Systematic Review of Drug Repurposing in Glioblastoma.Cancers · 2021Review
- MICAL2 Promotes Proliferation and Migration of Glioblastoma Cells Through TGF-β/p-Smad2/EMT-Like Signaling Pathway.Frontiers in oncology · 2021Article
- Mesenchymal Transformation: The Rosetta Stone of Glioblastoma Pathogenesis and Therapy Resistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Review
- ELAVL1 Role in Cell Fusion and Tunneling Membrane Nanotube Formations with Implication to Treat Glioma Heterogeneity.Cancers · 2020Review
- Review
- Metformin in colorectal cancer: molecular mechanism, preclinical and clinical aspects.Journal of experimental & clinical cancer research : CR · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This paper outlines a treatment protocol to run alongside of standard current treatment of glioblastoma- resection, temozolomide and radiation. The epithelial to mesenchymal transition (EMT) inhibiting sextet, EIS Regimen, uses the ancillary attributes of six older medicines to impede EMT during glioblastoma. EMT is an actively motile, therapy-resisting, low proliferation, transient state that is an integral feature of cancers' lethality generally and of glioblastoma specifically. It is believed to be during the EMT state that glioblastoma's centrifugal migration occurs. EMT is also a feature of untreated glioblastoma but is enhanced by chemotherapy, by radiation and by surgical trauma. EIS Regimen uses the antifungal drug itraconazole to block Hedgehog signaling, the antidiabetes drug metformin to block AMP kinase (AMPK), the analgesic drug naproxen to block Rac1, the anti-fibrosis drug pirfenidone to block transforming growth factor-beta (TGF-beta), the psychiatric drug quetiapine to block receptor activator NFkB ligand (RANKL) and the antibiotic rifampin to block Wnt- all by their previously established ancillary attributes. All these systems have been identified as triggers of EMT and worthy targets to inhibit. The EIS Regimen drugs have a good safety profile when used individually. They are not expected to have any new side effects when combined. Further studies of the EIS Regimen are needed.
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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.