ReviewJournal of clinical medicine2020
Targeting PI3K/Akt/mTOR in AML: Rationale and Clinical Evidence.
Review in Journal of clinical medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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
78 citing papers in PubMed, 120 citations in OpenAlex.
- Pan-Cancer Analysis of the Immunomodulatory Roles and Prognostic Value of PDXP and Experimental Verification in SKCM.Cancer medicine · 2026Article
- PI3Kδ inhibitor YY‑20394 is effective alone or in combination with Bcl‑2 inhibitor ABT199 in acute myeloid leukemia cells.Oncology reports · 2026Article
- Mitochondrial RNA helicase DDX28 promotes cell cycle and DNA repair programs and shapes an immunosuppressive microenvironment in acute myeloid leukemia.Translational oncology · 2026Article
- Investigation of the expression and potential mechanistic role of BYSL in acute myeloid leukemia.Clinical and experimental medicine · 2026Article
- The correlation between characteristics and pharmacological effects of monoterpene glycosides and tannins in Radix Paeoniae Alba.Journal of pharmaceutical analysis · 2026Review
- Review
- Deciphering Multitarget Mechanisms of Cardiac Glycosides in Acute Myeloid Leukemia Using a Network Pharmacology and Molecular Docking.Drug design, development and therapy · 2026Article
- DC-STAMP activates the PI3K/AKT/mTOR signaling pathway to regulate PANoptosis in acute myeloid leukemia.PloS one · 2026Article
- Senescence of bone marrow mesenchymal stromal cells: a narrative review of mechanisms, functional consequences, and rejuvenation strategies for age-related disorders.Stem cell research & therapy · 2025Review
- Inhibition of PI3K/AKT/mTOR signaling enhances autophagy in HL-60 acute myeloid leukemia cells: An integrative bioinformatic and in vitro study.Biochemistry and biophysics reports · 2025Article
- Network pharmacology, molecular docking, and experimental validation-based approach to explore the mechanism of action of ginsenoside Rh4 on acute myeloid leukemia cells.Medical oncology (Northwood, London, England) · 2025Article
- NaCells · 2025Article
- Unveiling the role of microRNAs, the PI3K/AKT pathway, and their associations in various types of leukemia: a comprehensive review.Blood research · 2025Review
- Machine Learning-Based Predictive Modeling Maximizes the Efficacy of mTOR/p53 Co-Targeting Therapy Against AML.Cancer science · 2025Article
- Integrated metabolomic and transcriptomic analysis identifies adipogenic differentiation of mesenchymal stem cells as a driver of chemoresistance in acute myeloid leukemia.Journal of experimental & clinical cancer research : CR · 2025Article
- Article
- Targeting the mTOR Signaling Pathway Through miR-100 and miR-101 in De Novo Acute Myeloid Leukemia: Implications for Therapeutic Intervention.Cancer reports (Hoboken, N.J.) · 2025Article
- diffGEK: differential gene expression kinetics.Bioinformatics (Oxford, England) · 2025Article
- Identification of CD84 as a potent survival factor in acute myeloid leukemia.The Journal of clinical investigation · 2025Article
- DyNDG: Identifying Leukemia-related Genes Based on Time-series Dynamic Network by Integrating Differential Genes.Genomics, proteomics & bioinformatics · 2025Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Acute myeloid leukemia (AML) is a highly heterogeneous hematopoietic malignancy characterized by excessive proliferation and accumulation of immature myeloid blasts in the bone marrow. AML has a very poor 5-year survival rate of just 16% in the UK; hence, more efficacious, tolerable, and targeted therapy is required. Persistent leukemia stem cell (LSC) populations underlie patient relapse and development of resistance to therapy. Identification of critical oncogenic signaling pathways in AML LSC may provide new avenues for novel therapeutic strategies. The phosphatidylinositol-3-kinase (PI3K)/Akt and the mammalian target of rapamycin (mTOR) signaling pathway, is often hyperactivated in AML, required to sustain the oncogenic potential of LSCs. Growing evidence suggests that targeting key components of this pathway may represent an effective treatment to kill AML LSCs. Despite this, accruing significant body of scientific knowledge, PI3K/Akt/mTOR inhibitors have not translated into clinical practice. In this article, we review the laboratory-based evidence of the critical role of PI3K/Akt/mTOR pathway in AML, and outcomes from current clinical studies using PI3K/Akt/mTOR inhibitors. Based on these results, we discuss the putative mechanisms of resistance to PI3K/Akt/mTOR inhibition, offering rationale for potential candidate combination therapies incorporating PI3K/Akt/mTOR inhibitors for precision medicine in AML.
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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 Socratic graph.