SynthesisFrontiers in cell and developmental biology2020
Effect of AKT1 (p. E17K) Hotspot Mutation on Malignant Tumorigenesis and Prognosis.
Synthesis in Frontiers in cell and developmental biology, 2020. 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 35 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.
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
35 citing papers in PubMed.
- In silico discovery of natural and synthetic inhibitors targeting AKT1 in prostate cancer.Molecular diversity · 2026Article
- A powerful representation learning method for enhanced analysis of incomplete multi-omics data.NPJ systems biology and applications · 2026Article
- The Reproductive Toxicity Valuation of Deoxynivalenol: An Integrated Study from Network Toxicology, Molecular Docking, Molecular Dynamics Simulation and Single-Cell RNA Sequencing.International journal of molecular sciences · 2026Article
- Review
- Emerging Approaches in Breast Cancer: From Molecular Mechanisms to Diagnosis and Therapeutic Strategies.Oncology research · 2026Review
- Identification of Somatic and Germline Mutations Influencing Treatment Outcomes and Disease Susceptibility in Tunisian Triple-Negative Breast Cancer Using Next-Generation Sequencing.British journal of biomedical science · 2026Article
- Deciphering the Impact of AKT1 Pathogenic Variants in Juvenile Granulosa Cell Tumors Using a Drosophila Model.Molecular & cellular proteomics : MCP · 2025Article
- The potential mechanism and immunomodulatory effect of gut microbiota-derived metabolites in the treatment of gastric cancer by integrating network pharmacology and molecular docking.Clinical and experimental medicine · 2025Article
- Metastasizing Ameloblastoma Mimicking Squamous Cell Carcinoma of the Lung and Harboring an AKT1 Mutation.Head and neck pathology · 2025Article
- Physiological roles of phosphoinositides and inositol phosphates: Implications for metabolic dysfunction-associated steatotic liver disease.Clinical science (London, England : 1979) · 2025Review
- Flavonoids as Promising Akt1 Inhibitors in Cancer Medicine: Insights From Molecular Docking, Dynamics, DFT Calculations, and In Vitro Validation.Cancer reports (Hoboken, N.J.) · 2025Article
- AKT and DUBs: a bidirectional relationship.Cellular & molecular biology letters · 2025Review
- Signaling pathway dysregulation in breast cancer.Oncotarget · 2025Review
- Genomic hallmarks of endocrine therapy resistance in ER/PR+HER2- breast tumours.Communications biology · 2025Article
- The multifaceted anticancer potential of luteolin: involvement of NF-κB, AMPK/mTOR, PI3K/Akt, MAPK, and Wnt/β-catenin pathways.Inflammopharmacology · 2025Review
- Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024Review
- Predictive, preventive, and personalized medicine in breast cancer: targeting the PI3K pathway.Journal of translational medicine · 2024Review
- Meningioma: current updates on genetics, classification, and mouse modeling.Upsala journal of medical sciences · 2024Review
- Role of EGFR and FASN in breast cancer progression.Journal of cell communication and signaling · 2023Review
- Landscape of Genetic Mutations in Appendiceal Cancers.Cancers · 2023Review
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The substitution of the seventeenth amino acid glutamate by lysine in the homologous structural domain of the Akt1 gene pleckstrin is a somatic cellular mutation found in breast, colorectal, and ovarian cancers, named p. Glu17Lys or E17K. In recent years, a growing number of studies have suggested that this mutation may play a unique role in the development of tumors. In this review article, we describe how AKT1(E17K) mutations stimulate downstream signals that cause cells to emerge transformed; we explore the differential regulation and function of E17K in different physiological and pathological settings; and we also describe the phenomenon that E17K impedes tumor growth by interfering with growth-promoting and chemotherapy-resistant AKT1
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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.