ArticleOncotarget2015
Mutant AKT1-E17K is oncogenic in lung epithelial cells.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07486648 (The Safety and Efficacy of Osimertinib Plus Capivasertib in EGFRm Advanced Non-small Cell Lung Cancer), which is not on this map. Cited by 22 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.
The Safety and Efficacy of Osimertinib Plus Capivasertib in EGFRm Advanced Non-small Cell Lung Cancer (NSCLC) Participants With PIK3CA/AKT1/PTEN Alterations Who Had Progressed on First-line Osimertinib Monotherapy or Plus Chemotherapy: a First-in-human, Phase Ib/Ⅱa Study (PRECISION)
Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Effect of AKT1 (p. E17K) Hotspot Mutation on Malignant Tumorigenesis and Prognosis.Frontiers in cell and developmental biology · 2020Pooled it
- [Variant Allele Frequency Stratification and EGFR Co-mutation Characteristics in AKT1 E17K-mutant Non-small Cell Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026Article
- AKT and DUBs: a bidirectional relationship.Cellular & molecular biology letters · 2025Review
- Article
- Novel Mutations inCurrent issues in molecular biology · 2024Article
- Assessing the validity of driver gene identification tools for targeted genome sequencing data.Bioinformatics advances · 2024Article
- The AKT1E17K Allele Promotes Breast Cancer in Mice.Cancers · 2022Article
- Upregulation of tRNA-Ser-AGA-2-1 Promotes Malignant Behavior in Normal Bronchial Cells.Frontiers in molecular biosciences · 2022Article
- AKT1 E17K Inhibits Cancer Cell Migration by Abrogating β-Catenin Signaling.Molecular cancer research : MCR · 2021Article
- Article
- Mutational drivers of cancer cell migration and invasion.British journal of cancer · 2021Review
- The Current Understanding Of Asbestos-Induced Epigenetic Changes Associated With Lung Cancer.Lung Cancer (Auckland, N.Z.) · 2020Review
- Analysis of miRNA profiles identified miR-196a as a crucial mediator of aberrant PI3K/AKT signaling in lung cancer cells.Oncotarget · 2017Article
- Activating Akt1 mutations alter DNA double strand break repair and radiosensitivity.Scientific reports · 2017Article
- Rewiring of the apoptotic TGF-β-SMAD/NFκB pathway through an oncogenic function of p27 in human papillary thyroid cancer.Oncogene · 2017Article
- Article
- Elevated expression of STIM1 is involved in lung tumorigenesis.Oncotarget · 2016Article
- Whole-exome sequencing identifies recurrent AKT1 mutations in sclerosing hemangioma of lung.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Molecular characterization of pulmonary sarcomatoid carcinoma: analysis of 33 cases.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2016Article
- AKT signaling in ERBB2-amplified breast cancer.Pharmacology & therapeutics · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hotspot E17K mutation in the pleckstrin homology domain of AKT1 occurs in approximately 0.6-2% of human lung cancers. In this manuscript, we sought to determine whether this AKT1 variant is a bona-fide activating mutation and plays a role in the development of lung cancer. Here we report that in immortalized human bronchial epithelial cells (BEAS-2B cells) mutant AKT1-E17K promotes anchorage-dependent and -independent proliferation, increases the ability to migrate, invade as well as to survive and duplicate in stressful conditions, leading to the emergency of cells endowed with the capability to form aggressive tumours at high efficiency. We provide also evidence that the molecular mechanism whereby AKT1-E17K is oncogenic in lung epithelial cells involves phosphorylation and consequent cytoplasmic delocalization of the cyclin-dependent kinase (cdk) inhibitor p27. In agreement with these results, cytoplasmic p27 is preferentially observed in primary NSCLCs with activated AKT and predicts poor survival.
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.