ArticleMolecular cancer2007
Molecular signatures define two main classes of meningiomas.
Article in Molecular cancer, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The prognostic role of Ki-67/MIB-1 in meningioma: A systematic review with meta-analysis.Medicine · 2020Pooled it
- Clinical implementation of integrated molecular-morphologic risk prediction for meningioma.Brain pathology (Zurich, Switzerland) · 2023Article
- Review
- Meningiomas: An Overview of the Landscape of Copy Number Alterations in Samples from an Admixed Population.Journal of oncology · 2020Article
- Expression and prognostic value of brain and acute leukemia, cytoplasmic in meningiomas.Chinese medical journal · 2019Article
- Simultaneous analysis of miRNA-mRNA in human meningiomas by integrating transcriptome: A relationship between PTX3 and miR-29c.BMC cancer · 2017Article
- Article
- Transcriptomic analysis of aggressive meningiomas identifies PTTG1 and LEPR as prognostic biomarkers independent of WHO grade.Oncotarget · 2016Article
- Microarray Expression Data Identify DCC as a Candidate Gene for Early Meningioma Progression.PloS one · 2016Article
- Review
- Lyophilized brain tumor specimens can be used for histologic, nucleic acid, and protein analyses after 1 year of room temperature storage.Journal of neuro-oncology · 2013Article
- Tumor prognostic factors and the challenge of developing predictive factors.Current oncology reports · 2013Article
- Atypical meningioma of sylvian fissure with a 20-year history: a rare case report.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2012Article
- Alternative splicing of CHEK2 and codeletion with NF2 promote chromosomal instability in meningioma.Neoplasia (New York, N.Y.) · 2012Article
- Analysis of transforming growth factor β receptor expression and signaling in higher grade meningiomas.Journal of neuro-oncology · 2011Article
- Tumor grade-related NDRG2 gene expression in primary and recurrent intracranial meningiomas.Journal of neuro-oncology · 2011Article
- Gene expression profiling of meningiomas: current status after a decade of microarray-based transcriptomic studies.Acta neurochirurgica · 2011Review
- Tumor profiling: development of prognostic and predictive factors to guide brain tumor treatment.Current oncology reports · 2011Review
- DNA microarray analysis identifies CKS2 and LEPR as potential markers of meningioma recurrence.The oncologist · 2011Article
- Identification of gene markers associated with aggressive meningioma by filtering across multiple sets of gene expression arrays.Journal of neuropathology and experimental neurology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMeningiomas are common brain tumors that are classified into three World Health Organization grades (benign, atypical and malignant) and are molecularly ill-defined tumors. The purpose of this study was identify molecular signatures unique to the different grades of meningiomas and to unravel underlying molecular mechanisms driving meningioma tumorigenesis.
resultsWe have used a combination of gene expression microarrays and array comparative genomic hybridization (aCGH) to show that meningiomas of all three grades fall into two main molecular groups designated 'low-proliferative' and 'high-proliferative' meningiomas. While all benign meningiomas fall into the low-proliferative group and all malignant meningiomas fall into the high-proliferative group, atypical meningiomas distribute into either one of these groups. High-proliferative atypical meningiomas had an elevated median MIB-1 labeling index and a greater frequency of copy number aberrations (CNAs) compared to low-proliferative atypical meningiomas. Additionally, losses on chromosome 6q, 9p, 13 and 14 were found exclusively in the high-proliferative meningiomas. We have identified genes that distinguish benign low-proliferative meningiomas from malignant high-proliferative meningiomas and have found that gain of cell-proliferation markers and loss of components of the transforming growth factor-beta signaling pathway were the major molecular mechanisms that distinguish these two groups.
conclusionCollectively, our data suggests that atypical meningiomas are not a molecularly distinct group but are similar to either benign or malignant meningiomas. It is anticipated that identified molecular and CNA markers will potentially be more accurate prognostic markers of meningiomas.
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.