ReviewNeuro-oncology2010
Inherited predisposition to glioma.
Review in Neuro-oncology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.
- Pooled it
- Tempered optimism: Advances in the precision medicine era for pediatric low-grade glioma.Neuro-oncology · 2026Review
- Systemic Drug Effects in Vortioxetine-Induced Time-Series Datasets.International journal of molecular sciences · 2026Article
- Medical comorbidities prognosticate survival in glioblastoma.BJC reports · 2025Article
- Key genes altered in glioblastoma based on bioinformatics (Review).Oncology letters · 2025Review
- Metformin and glioma: Targeting metabolic dysregulation for enhanced therapeutic outcomes.Translational oncology · 2025Review
- Principles in the Management of Glioblastoma.Genes · 2024Review
- Risk of subsequent gliomas and meningiomas among 69,460 5-year survivors of childhood and adolescent cancer in Europe: the PanCareSurFup study.British journal of cancer · 2024Article
- Unusual presentation of glioblastoma in the brainstem: a case report of a diffuse pontine glioblastoma multiforme and surgical management.Frontiers in oncology · 2024Article
- Prevalence of pathogenic germline variants in adult-type diffuse glioma.Neuro-oncology practice · 2023Article
- Evaluating the Utilization of Ethylenediaminetetraacetic Acid as a Treatment Supplement for Gliomas.Cureus · 2022Review
- Article
- Liquid Biopsy in Glioblastoma.Cancers · 2022Review
- Tumour immune landscape of paediatric high-grade gliomas.Brain : a journal of neurology · 2021Review
- Article
- POT1 Regulates Proliferation and Confers Sexual Dimorphism in Glioma.Cancer research · 2021Article
- Diagnosis and Individualized Treatment of Three Primary Malignant Tumors: A Case Report.Breast cancer (Dove Medical Press) · 2021Article
- Characteristics of IDH-mutant gliomas with non-canonical IDH mutation.Journal of neuro-oncology · 2021Article
- Second primary cancers in long-term survivors of glioblastoma.Neuro-oncology practice · 2019Article
- Genetic and molecular epidemiology of adult diffuse glioma.Nature reviews. Neurology · 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
4 authors at 3 institutions in 2 countries.
Funding
Abstract
In gliomas, germline gene alterations play a significant role during malignant transformation of progenitor glial cells, at least for families with occurrence of multiple cancers or with specific hereditary cancer syndromes. Scientific evidence during the last few years has revealed several constitutive genetic abnormalities that may influence glioma formation. These germline abnormalities are manifested as either gene polymorphisms or hemizygous mutations of key regulatory genes that are involved either in DNA repair or in apoptosis. Such changes, among others, include hemizygous alterations of the neurofibromatosis 1 (NF1) and p53 genes that are involved in apoptotic pathways, and alterations in multiple DNA repair genes such as mismatch repair (MMR) genes, x-ray cross-complementary genes (XRCC), and O6-methylguanine-DNA methyltransferase (MGMT) genes. Subsequent cellular changes include somatic mutations in cell cycle regulatory genes and genes involved in angiogenesis and invasion, leading eventually to tumor formation in various stages. Future molecular diagnosis may identify new genomic regions that could harbor genes important for glioma predisposition and aid in the early diagnosis of these patients and genetic counseling of their families.
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.