ArticleAmerican journal of cancer research2011
Akt signaling is required for glioblastoma maintenance in vivo.
Article in American journal of cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
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.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- A Review of the Anticancer Properties of Cedrol and its Molecular Mechanisms.Anti-cancer agents in medicinal chemistry · 2026Review
- Structure-based drug design of small molecule AKT1 inhibitors to treat glioma.Journal of computer-aided molecular design · 2025Article
- Article
- LncRNA CASC2 Inhibits Progression of Glioblastoma by Regulating the Expression of AKT in T98G Cell Line, Treated by TMZ and Thiosemicarbazone Complex.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- Article
- Receptor tyrosine kinase-Ras-PI 3 kinase-Akt signaling network in glioblastoma multiforme.Medical oncology (Northwood, London, England) · 2018Review
- Novel internal regulators and candidate miRNAs within miR-379/miR-656 miRNA cluster can alter cellular phenotype of human glioblastoma.Scientific reports · 2018Article
- Glioblastoma: new therapeutic strategies to address cellular and genomic complexity.Oncotarget · 2018Review
- Resistance mechanisms to genetic suppression of mutant NRAS in melanoma.Melanoma research · 2017Article
- 5-Aminolevulinic Acid Guided Sampling of Glioblastoma Microenvironments Identifies Pro-Survival Signaling at Infiltrative Margins.Scientific reports · 2017Article
- Article
- Penfluridol suppresses glioblastoma tumor growth by Akt-mediated inhibition of GLI1.Oncotarget · 2017Article
- Inhibition of the PI3K/AKT/mTOR Pathway in Solid Tumors.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2016Review
- Inhibition of Autophagy by Chloroquine Enhances the Antitumor Efficacy of Sorafenib in Glioblastoma.Cellular and molecular neurobiology · 2016Article
- Review
- Aplysin induces apoptosis in glioma cells through HSP90/AKT pathway.Experimental biology and medicine (Maywood, N.J.) · 2015Article
- Overexpressed let-7a inhibits glioma cell malignancy by directly targeting K-ras, independently of PTEN.Neuro-oncology · 2013Article
- Akt signaling accelerates tumor recurrence following ras inhibition in the context of ink4a/arf loss.Genes & cancer · 2013Article
- Anti-cancer Therapies in High Grade Gliomas.Current proteomics · 2013Article
- Sorafenib selectively depletes human glioblastoma tumor-initiating cells from primary cultures.Cell cycle (Georgetown, Tex.) · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Glioblastoma multiforme (GBM) can be induced in mice through the combined expression of activated forms of KRas and Akt in glial progenitor cells. We have previously demonstrated that KRas is required for the maintenance of these tumors in vivo as inhibition of KRas expression resulted in apoptotic tumor regression and significantly increased survival. To determine the reliance of these tumors on Akt signaling in vivo, we generated a viral vector that allows the expression of Akt to be controlled post-delivery. Survival rates were compared between those animals with continued Akt expression and animals in which expression of Akt was suppressed. Although a fifth of the tumors were refractory to treatment, inhibition of Akt significantly increased the survival of tumor-bearing mice and nearly a fourth of the mice remained in remission four months after the treatment period. These data suggest that Akt is required for glioblastoma maintenance in the context of activated Ras and that loss of Akt expression results in increased survival; therefore, the PI3K/AKT signaling pathway is a viable therapeutic target in this context.
Identifiers
21796274PMC3142953W50744607What 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.