ReviewNeurosurgical review2003
Genes and pathways driving glioblastomas in humans and murine disease models.
Review in Neurosurgical review, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 67 citations in OpenAlex.
- Review
- Non-coding RNAs as Key Regulators of the Notch Signaling Pathway in Glioblastoma: Diagnostic, Prognostic, and Therapeutic Targets.CNS & neurological disorders drug targets · 2024Review
- Therapeutic Potential of Thymoquinone in Glioblastoma Treatment: Targeting Major Gliomagenesis Signaling Pathways.BioMed research international · 2018Review
- Nanomedicine associated with photodynamic therapy for glioblastoma treatment.Biophysical reviews · 2017Review
- Expression pattern of BCCIP in hepatocellular carcinoma is correlated with poor prognosis and enhanced cell proliferation.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Differential proteomics analysis of low- and high-grade of astrocytoma using iTRAQ quantification.OncoTargets and therapy · 2016Article
- Growth factor dependent regulation of centrosome function and genomic instability by HuR.Biomolecules · 2015Article
- Anti-tumor effect of a novel PI3-kinase inhibitor, SF1126, in (12) V-Ha-Ras transgenic mouse glioma model.Cancer cell international · 2014Article
- Article
- ProBDNF and its receptors are upregulated in glioma and inhibit the growth of glioma cells in vitro.Neuro-oncology · 2013Article
- Gene therapy and targeted toxins for glioma.Current gene therapy · 2011Review
- The G1359A-CNR1 gene polymorphism is associated to glioma in Spanish patients.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2010Article
- Notch signaling in glioblastoma: a developmental drug target?BMC medicine · 2010Review
- FasL and FADD delivery by a glioma-specific and cell cycle-dependent HSV-1 amplicon virus enhanced apoptosis in primary human brain tumors.Molecular cancer · 2010Article
- Article
- Alterations of BCCIP, a BRCA2 interacting protein, in astrocytomas.BMC cancer · 2009Article
- Multiparameter computational modeling of tumor invasion.Cancer research · 2009Article
- Loss of heterozygosity of TRIM3 in malignant gliomas.BMC cancer · 2009Article
- siRNA Down-regulation of the PATZ1 Gene in Human Glioma Cells Increases Their Sensitivity to Apoptotic Stimuli.Cancer therapy · 2008Article
- Roles of BCCIP in chromosome stability and cytokinesis.Oncogene · 2007Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human malignant gliomas arise from neural progenitor cells and/or dedifferentiated astrocytes. By now, they are genetically so well characterized that several murine glioma models have emerged that faithfully reiterate the typical histological features of the disease. In experimental animals, only one or two elements of the growth factor/Ras, PI3K/PTEN/PKB, p53/ARF/HDM2, and p16/Rb/cyclinD/CDK4 pathways are targeted. In human gliomas, many additional genes and pathways are targeted due to a most severe mutator phenotype that leads to the accumulation of countless epigenetic and genetic alterations. Changes that convey a growth advantage are selected for, leading to overgrowth of precursor cell populations with increasingly malignant tumor cell clones. While murine models represent a powerful tool for elucidating the role of genetic pathways, mechanisms of response and resistance to new therapeutic agents might be fundamentally different due to the high degree of genomic instability in the human disease. In fact, little is known about the molecular causes of genomic instability involved in gliomas, except for the rare Turcot's syndrome, O(6)-methylguanine-DNA methyltransferase, and the apurinic/apyrimidinic endonuclease Ape-1. Novel approaches that selectively exploit fundamental metabolic differences between tumor and normal cells have to consider these fundamental differences between human disease and presently available, highly sophisticated animal models.
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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.