ArticleHeliyon2019
Origin of mutations in genes associated with human glioblastoma multiform cancer: random polymerase errors versus deamination.
Article in Heliyon, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Metabolic Insight into Glioma Heterogeneity: Mapping Whole Exome Sequencing to In Vivo Imaging with Stereotactic Localization and Deep Learning.Metabolites · 2024Article
- HSPA5 and FGFR1 genes in the mesenchymal subtype of glioblastoma can improve a treatment efficacy.Animal cells and systems · 2024Article
- Identification and characterization of putative biomarkers and therapeutic axis in Glioblastoma multiforme microenvironment.Frontiers in cell and developmental biology · 2023Article
- Glioblastoma and Methionine Addiction.International journal of molecular sciences · 2022Review
- Single cell RNA sequencing reveals differentiation related genes with drawing implications in predicting prognosis and immunotherapy response in gliomas.Scientific reports · 2022Article
- Sex- and mutation-specific p53 gain-of-function activity in gliomagenesis.Cancer research communications · 2021Article
- The Role of Neurodevelopmental Pathways in Brain Tumors.Frontiers in cell and developmental biology · 2021Review
- Epigenetic Regulation of Circadian Rhythm and Its Possible Role in Diabetes Mellitus.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The etiology of glioblastoma multiforme (GBM), the most serious form of brain cancer, remains obscure, although it has been proposed that cancer risk is a function of random polymerase errors that occur during stem cell division and the resulting mutations in oncogenes and tumor suppressor genes. Analysis of the 8 genes (PTEN, TP53, EGFR, PIK3R1, PIK3CA, NF1, RB1, IDH1) that are mutated in at least 5% of GBM tumors indicates a non-random mutation pattern that reflects a significant role for hydrolytic deamination at CpG sites. The formation of activating mutations in some genes, e.g., IDH1, where a very limited set of mutations are oncogenic, statistically cannot involve random mutagenesis due to polymerase errors that occur during each stem cell replication. Comparison of the in vitro misincorporation tendencies of three replicative polymerases and the "random" mutation pattern in a subset of genes indicates non-polymerase based pathways are involved. Analysis of the mutation patterns shows that chemical deamination that occurs at a slow rate at each CpG is favored over random polymerase errors by a factor of more than 10 million. Therefore, if a truncating nonsense mutation in a tumor suppressor, or an activating missense mutation in an oncogene, can occur due to a C > T base substitution at a CpG sequence, it is highly favored over other mutation pathways.
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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.