ArticleProceedings of the National Academy of Sciences of the United States of America2019
A cell type-selective apoptosis-inducing small molecule for the treatment of brain cancer.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 35 citations in OpenAlex.
- A Novel Class of Multi-substituted Diaryl Scaffold Derivatives Inhibit Glioblastoma Progression by Targeting CD155.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Design, Synthesis, and Biological Evaluation of Naphthoquinone Salts as Anticancer Agents.Molecules (Basel, Switzerland) · 2025Article
- Analysis of cuproptosis-related genes in prognosis and immune infiltration in grade 4 diffuse gliomas.Heliyon · 2024Article
- Small Molecule Inhibitors Targeting the "Undruggable" Survivin: The Past, Present, and Future from a Medicinal Chemist's Perspective.Journal of medicinal chemistry · 2023Review
- A Cell Type Selective YM155 Prodrug Targets Receptor-Interacting Protein Kinase 2 to Induce Brain Cancer Cell Death.Journal of the American Chemical Society · 2023Article
- RIPK2: a promising target for cancer treatment.Frontiers in pharmacology · 2023Review
- Pyroptosis-related prognosis model, immunocyte infiltration characterization, and competing endogenous RNA network of glioblastoma.BMC cancer · 2022Article
- Wasl is crucial to maintain microglial core activities during glioblastoma initiation stages.Glia · 2022Article
- Molecular Subtypes and Prognostic Signature of Pyroptosis-Related lncRNAs in Glioma Patients.Frontiers in oncology · 2022Article
- Identification and Validation of Inflammatory Response-Related Gene Signatures to Predict the Prognosis of Neuroblastoma.International journal of genomics · 2022Article
- Glioblastoma and the search for non-hypothesis driven combination therapeutics in academia.Frontiers in oncology · 2022Review
- Limb-bud and heart development (LBH) contributes to glioma progression in vitro and in vivo.FEBS open bio · 2022Article
- A computational guided, functional validation of a novel therapeutic antibody proposes Notch signaling as a clinical relevant and druggable target in glioma.Scientific reports · 2020Article
- Modulating microenvironments for treating glioblastoma.Current tissue microenvironment reports · 2020Article
- System-based approaches as prognostic tools for glioblastoma.BMC cancer · 2019Review
- Antitumor effect of TW-37, a BH3 mimetic in human oral cancer.Laboratory animal research · 2019Article
- Valproic Acid Enhanced Apoptosis by Promoting Autophagy Via Akt/mTOR Signaling in Glioma.Cell transplantationArticle
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 7 institutions in 3 countries.
Funding
Abstract
Glioblastoma multiforme (GBM; grade IV astrocytoma) is the most prevalent and aggressive form of primary brain cancer. A subpopulation of multipotent cells termed GBM cancer stem cells (CSCs) play a critical role in tumor initiation, tumor maintenance, metastasis, drug resistance, and recurrence following surgery. Here we report the identification of a small molecule, termed RIPGBM, from a cell-based chemical screen that selectively induces apoptosis in multiple primary patient-derived GBM CSC cultures. The cell type-dependent selectivity of this compound appears to arise at least in part from redox-dependent formation of a proapoptotic derivative, termed cRIPGBM, in GBM CSCs. cRIPGBM induces caspase 1-dependent apoptosis by binding to receptor-interacting protein kinase 2 (RIPK2) and acting as a molecular switch, which reduces the formation of a prosurvival RIPK2/TAK1 complex and increases the formation of a proapoptotic RIPK2/caspase 1 complex. In an orthotopic intracranial GBM CSC tumor xenograft mouse model, RIPGBM was found to significantly suppress tumor formation in vivo. Our chemical genetics-based approach has identified a drug candidate and a potential drug target that provide an approach to the development of treatments for this devastating disease.
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.