ArticleThe American journal of surgical pathology2012
Paradoxical relationship between the degree of EGFR amplification and outcome in glioblastomas.
Article in The American journal of surgical pathology, 2012. 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, 75 citations in OpenAlex.
- Prognostic value of test(s) for O6-methylguanine-DNA methyltransferase (MGMT) promoter methylation for predicting overall survival in people with glioblastoma treated with temozolomide.The Cochrane database of systematic reviews · 2021Pooled it
- Somatic copy number alterations associated with Japanese or endometriosis in ovarian clear cell adenocarcinoma.PloS one · 2015Trial
- Review
- Article
- Genomic, epigenomic and transcriptomic landscape of glioblastoma.Metabolic brain disease · 2024Review
- Molecular Profile as an Outcome Predictor in Glioblastoma along with MRI Features and Surgical Resection: A Scoping Review.International journal of molecular sciences · 2024Article
- Diagnostic utility of genetic alterations in distinguishing IDH-wildtype glioblastoma from lower-grade gliomas: Insight from next-generation sequencing analysis of 479 cases.Brain pathology (Zurich, Switzerland) · 2024Article
- Revolutionizing Brain Tumor Care: Emerging Technologies and Strategies.Biomedicines · 2024Review
- Intraventricular CARv3-TEAM-E T Cells in Recurrent Glioblastoma.The New England journal of medicine · 2024Article
- Article
- Novel sights on therapeutic, prognostic, and diagnostics aspects of non-coding RNAs in glioblastoma multiforme.Metabolic brain disease · 2023Review
- Pharmacogenomic profiling reveals molecular features of chemotherapy resistance in IDH wild-type primary glioblastoma.Genome medicine · 2023Article
- Molecular landscapes of glioblastoma cell lines revealed a group of patients that do not benefit fromFrontiers in neuroscience · 2023Article
- Distribution and favorable prognostic implication of genomic EGFR alterations in IDH-wildtype glioblastoma.Cancer medicine · 2023Article
- Genomic and Epigenomic Features of Glioblastoma Multiforme and its Biomarkers.Journal of oncology · 2022Review
- Looking Beyond the Glioblastoma Mask: Is Genomics the Right Path?Frontiers in oncology · 2022Review
- HeterogeneousCancers · 2020Article
- Spectrum of EGFR aberrations and potential clinical implications: insights from integrative pan-cancer analysis.Cancer communications (London, England) · 2020Article
- Prognostic stratification of adult primary glioblastoma multiforme patients based on their tumor gene amplification profiles.Oncotarget · 2018Article
- Prognostic significance of epidermal growth factor receptor expression in glioma patients.OncoTargets and therapy · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Glioblastoma (GBM) is the most common primary brain tumor in adults and often has amplification of the epidermal growth factor receptor (EGFR) gene. The value of EGFR as a prognostic marker in GBMs is unclear; some studies have shown an adverse correlation, whereas others have indicated a neutral or even favorable association with longer survival. Furthermore, EGFR-amplified GBMs are usually regarded as a single subgroup of tumors, although the range of EGFR copy number varies greatly. In this study, 532 GBMs were analyzed for EGFR amplification via fluorescence in situ hybridization at the time of initial diagnosis. Although there was no difference in survival by EGFR amplification (P = 0.33), stratification by the amount of EGFR amplification showed that, surprisingly, median survival was 39% longer in the high-amplifier group (EGFR:chromosome 7 ratio >20) compared to nonamplified GBMs (P = 0.03) and was 43% longer compared to GBMs with low to moderate EGFR amplification (EGFR:chromosome 7 ratio = 2 to 20; P = 0.0007). Stratifying by postsurgical treatment regimens, this difference was seen only when temozolomide (TMZ) was used; tumors without amplification and with high EGFR amplification both responded better to TMZ than those with low to moderate amplification (P = 0.01), whereas GBMs that had not been treated with adjuvant therapy nor with adjuvant therapy lacking TMZ showed no survival differences (P = 0.63 and 0.91, respectively). These results suggest that GBMs with EGFR amplification are a heterogenous group of tumors and that behavior might differ according to the degree of amplification, although not in a straightforward dose-response manner.
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.