ArticleOncogene2018
A new method of identifying glioblastoma subtypes and creation of corresponding animal models.
Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 18 citations in OpenAlex.
- Multimodal survival analysis of glioblastoma using whole-slide histopathology, gene expression, clinical variables and language-model-derived mutation features.Scientific reports · 2026Article
- Intermittent fasting inhibits Tp53-driven glioma through gut microbiota-mediated methionine-mNature communications · 2026Article
- Gut microbiota induces immune-related alterations in gene expression, RNA methylation, and metabolism in glioblastoma revealed by single-cell and spatial multi-omics.Frontiers in immunology · 2026Article
- Metagenomics and transcriptomics analysis of aspartame's impact on gut microbiota and glioblastoma progression in a mouse model.Scientific reports · 2025Article
- M6A-related bioinformatics analysis indicates that LRPPRC is an immune marker for ischemic stroke.Scientific reports · 2024Article
- Impact of endogenous viral elements on glioma clinical phenotypes by inducing OCT4 in the host.Frontiers in cellular and infection microbiology · 2024Article
- Alternative Polyadenylation Regulatory Factors Signature for Survival Prediction in Kidney Renal Cell Carcinoma.Cancer informatics · 2024Article
- Enhancing nasopharyngeal carcinoma cell radiosensitivity by suppressing AKT/mTOR via CENP-N knockdown.Journal of translational medicine · 2023Article
- Identifying Potential Tumor Antigens and Antigens-Related Subtypes in Hepatocellular Carcinoma for mRNA Vaccine Development.Journal of oncology · 2022Article
- Mechanistic models of signaling pathways deconvolute the glioblastoma single-cell functional landscape.NAR cancer · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) accounts for up to 50% of brain parenchymal tumors. It is the most malignant type of brain cancer with very poor survival and limited remedies. Cancer subtyping is important for cancer research and therapy. Here, we report a new subtyping method for GBM based on the genetic alterations of CDKN2A and TP53 genes. CDKN2A and TP53 are the most frequently mutated genes with mutation rates of 60 and 30%, respectively. We found that patients with deletion of CDKN2A possess worse survival than those with TP53 mutation. Interestingly, survival of patients with both TP53 mutation and CDKN2A deletion is no worse than for those with only one of these genetic alterations, but similar to those with TP53 mutation alone. Next, we investigated differences in the gene expression profile between TP53 and CDKN2A samples. Consistent with the survival data, the samples with both TP53 mutation and CDKN2A deletion showed a gene expression profile similar to those samples with TP53 mutation alone. Finally, we found that activation of RAS pathway plus Cdkn2a/b silencing can induce GBM, in a similar way to tumor induction by RAS activation plus TP53 silencing. In conclusion, we show that the genetic alterations of CDKN2A and TP53 may be used to stratify GBM, and the new animal models matching this stratification method were generated.
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.