ReviewCancer science2009
Genetic alterations and signaling pathways in the evolution of gliomas.
Review in Cancer science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 210 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
210 citing papers in PubMed, 1 synthesis or guideline pooled it, 444 citations in OpenAlex.
- Relationships between PTEN gene mutations and prognosis in glioma: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Pooled it
- Gene set analysis for time-to-event outcome: comparison of a new approach based on the generalized Berk-Jones statistic with existing methods in presence of intra gene-set correlation.Briefings in bioinformatics · 2026Article
- The development of CAR T cells for patients with CNS malignancies.Nature reviews. Clinical oncology · 2026Review
- STING agonism in brain tumours: mechanisms, challenges, and therapeutic advances.Frontiers in oncology · 2026Review
- Glioblastoma at the crossroads: current understanding and future therapeutic horizons.Signal transduction and targeted therapy · 2025Review
- Analysis of the Mechanism Underlying Radiotherapy Resistance Caused by Oligodendroglia Cells in Glioblastoma by Applying the Single-cell RNA Sequencing Technology.Current medicinal chemistry · 2025Article
- Genomic Profiling in Glioma Patients to Explore Clinically Relevant Markers.International journal of molecular sciences · 2024Article
- Insight into the Role of the miR-584 Family in Human Cancers.International journal of molecular sciences · 2024Review
- A Synopsis of Biomarkers in Glioblastoma: Past and Present.Current issues in molecular biology · 2024Review
- Recurrent Glioblastoma-Molecular Underpinnings and Evolving Treatment Paradigms.International journal of molecular sciences · 2024Review
- Antitumoral Activity of the Universal Methyl DonorMolecules (Basel, Switzerland) · 2024Article
- ELAVL2 loss promotes aggressive mesenchymal transition in glioblastoma.NPJ precision oncology · 2024Article
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- Advancements in Glioma Care: Focus on Emerging Neurosurgical Techniques.Biomedicines · 2023Review
- Preclinical Development of Brain Permeable ERβ Agonist for the Treatment of Glioblastoma.Molecular cancer therapeutics · 2023Article
- Understanding Glioblastoma Signaling, Heterogeneity, Invasiveness, and Drug Delivery Barriers.International journal of molecular sciences · 2023Review
- The Spectrum of Molecular Pathways in Gliomas-An Up-to-Date Review.Biomedicines · 2023Review
- Adult IDH Wild-Type Glioblastoma Ultrastructural Investigation Suggests a Possible Correlation between Morphological Biomarkers and Ki-67 Index.Biomedicines · 2023Article
150 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gliomas are the most common primary brain tumors. They account for more than 70% of all neoplasms of the central nervous system and vary considerably in morphology, location, genetic alterations, and response to therapy. Most frequent and malignant are glioblastomas. The vast majority (>90%) develops rapidly after a short clinical history and without evidence of a less malignant precursor lesion (primary or de novo glioblastoma). Secondary glioblastomas develop more slowly through progression from low-grade or anaplastic astrocytoma. These glioblastoma subtypes constitute distinct disease entities that affect patients of different age, develop through distinct genetic pathways, show different RNA and protein expression profiles, and may differ in their response to radio- and chemotherapy. Recently, isocitrate dehydrogenase 1 (IDH1) mutations have been identified as a very early and frequent genetic alteration in the pathway to secondary glioblastomas as well as that in oligodendroglial tumors, providing the first evidence that low-grade astrocytomas and oligodendrogliomas may share common cells of origin. In contrast, primary glioblastomas very rarely contain IDH1 mutations, suggesting that primary and secondary glioblastomas may originate from different progenitor cells, despite the fact that they are histologically largely indistinguishable. In this review, we summarize the current status of genetic alterations and signaling pathways operative in the evolution of astrocytic and oligodendroglial tumors.
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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.