ArticleOncotarget2014
Epigenetic suppression of EGFR signaling in G-CIMP+ glioblastomas.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Evaluating the transcriptional fidelity of cancer models.Genome medicine · 2021Article
- PI3Kγ inhibition suppresses microglia/TAM accumulation in glioblastoma microenvironment to promote exceptional temozolomide response.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Expression and pharmacological inhibition of TrkB and EGFR in glioblastoma.Molecular biology reports · 2020Article
- Glioblastomas located in proximity to the subventricular zone (SVZ) exhibited enrichment of gene expression profiles associated with the cancer stem cell state.Journal of neuro-oncology · 2020Article
- The proneural gene ASCL1 governs the transcriptional subgroup affiliation in glioblastoma stem cells by directly repressing the mesenchymal gene NDRG1.Cell death and differentiation · 2019Article
- Mapping of genomic EGFRvIII deletions in glioblastoma: insight into rearrangement mechanisms and biomarker development.Neuro-oncology · 2018Article
- The angiogenic switch leads to a metabolic shift in human glioblastoma.Neuro-oncology · 2017Article
- The Hippo transducer TAZ promotes cell proliferation and tumor formation of glioblastoma cells through EGFR pathway.Oncotarget · 2016Article
- Differential localization of glioblastoma subtype: implications on glioblastoma pathogenesis.Oncotarget · 2016Article
- Genetic biomarkers of drug response for small-molecule therapeutics targeting the RTK/Ras/PI3K, p53 or Rb pathway in glioblastoma.CNS oncology · 2016Review
- IDH mutation and MGMT promoter methylation in glioblastoma: results of a prospective registry.Oncotarget · 2015Article
- Dynamic epigenetic regulation of glioblastoma tumorigenicity through LSD1 modulation of MYC expression.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Insights into the clinical value of cyclin-dependent kinase 5 in glioma: a retrospective study.World journal of surgical oncology · 2015Article
- Article
- Genetic and clinical characteristics of primary and secondary glioblastoma is associated with differential molecular subtype distribution.Oncotarget · 2015Article
- EGFR promoter exhibits dynamic histone modifications and binding of ASH2L and P300 in human germinal matrix and gliomas.Epigenetics · 2015Article
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The intrinsic signaling cascades and cell states associated with the Glioma CpG Island Methylator Phenotype (G-CIMP) remain poorly understood. Using published mRNA signatures associated with EGFR activation, we demonstrate that G-CIMP+ tumors harbor decreased EGFR signaling using three independent datasets, including the Chinese Glioma Genome Atlas(CGGA; n=155), the REMBRANDT dataset (n=288), and The Cancer Genome Atlas (TCGA; n=406). Additionally, an independent collection of 25 fresh-frozen glioblastomas confirmed lowered pERK levels in G-CIMP+ specimens (p<0.001), indicating suppressed EGFR signaling. Analysis of TCGA glioblastomas revealed that G-CIMP+ glioblastomas harbored lowered mRNA levels for EGFR and H-Ras. Induction of G-CIMP+ state by exogenous expression of a mutated isocitrate dehydrogenase 1, IDH1-R132H, suppressed EGFR and H-Ras protein expression as well as pERK accumulation in independent glioblastoma models. These suppressions were associated with increased deposition of the repressive histone markers, H3K9me3 and H3K27me3, in the EGFR and H-Ras promoter regions. The IDH1-R132H expression-induced pERK suppression can be reversed by exogenous expression of H-RasG12V. Finally, the G-CIMP+ Ink4a-Arf-/- EGFRvIII glioblastoma line was more resistant to the EGFR inhibitor, Gefitinib, relative to its isogenic G-CIMP- counterpart. These results suggest that G-CIMP epigenetically regulates EGFR signaling and serves as a predictive biomarker for EGFR inhibitors in glioblastoma patients.
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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.