ReviewInternational journal of molecular sciences2020
The PI3K-Akt-mTOR Signaling Pathway in Human Acute Myeloid Leukemia (AML) Cells.
Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 214 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
214 citing papers in PubMed, 1 synthesis or guideline pooled it, 334 citations in OpenAlex.
- Prognostic significance ofBMJ open · 2023Pooled it
- NUC-7738 regulates β-catenin signalling resulting in reduced proliferation and self-renewal of AML cells.PloS one · 2022Trial
- The Inv(16) Oncogene CBFB::MYH11 is Required for the Survival of Leukemia Cells in the Blood and Spleen, but not the Bone Marrow.Oncogene · 2026Article
- Revisiting retinoic acid in AML therapy: mechanisms of action and rational combination strategies.British journal of cancer · 2026Review
- Piper nigrum Has an Antitumor Effect Through Regulation of the Phosphatidylinositol 3-Kinase Signaling Pathway in a Murine Model of Acute Myeloid Leukemia.Phytotherapy research : PTR · 2026Article
- CREB1 and GSK3 Isoforms as Potential Adaptive Signaling Nodes in PI3K/Akt/mTOR Inhibitor Treated Philadelphia Chromosome-Positive B-ALL.International journal of molecular sciences · 2026Article
- PI3Kδ inhibitor YY‑20394 is effective alone or in combination with Bcl‑2 inhibitor ABT199 in acute myeloid leukemia cells.Oncology reports · 2026Article
- Emetine and Its Derivatives as Anticancer Agents Targeting the PI3K/AKT/mTOR Pathway: A Narrative Review of Mechanisms, Pharmacology, and Clinical Insights.Journal of cellular and molecular medicine · 2026Review
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- Quercetin targets IGF1 signaling in gastric cancer: a synergy of network pharmacology, molecular simulations, and in vitro functional assays.Journal of computer-aided molecular design · 2026Article
- MSLN expression predicts a high risk of EMD in AML by promoting cell adhesion and metastasis via interaction with MUC16.Blood advances · 2026Article
- Apoptosis-related gene model predicts the prognosis in patients with acute myeloid leukemia.Blood science (Baltimore, Md.) · 2026Article
- Zanubrutinib enhances CD19 CAR T killing of B-cell lymphoma by inhibiting BTK phosphorylation, regulating PI3K/AKT/mTOR pathway, and promoting autophagy.Blood science (Baltimore, Md.) · 2026Article
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- Assessing current capabilities for incorporating lipidomics in multiomics data integration.Briefings in bioinformatics · 2026Review
- Integrated Analysis of the mTOR Signaling Pathway Mediated by the ORF3 Protein of Swine Hepatitis E Virus in HepG2 Cells via a circRNA-miRNA Network.Veterinary sciences · 2026Article
- Isoalantolactone induces AML pyroptosis and potentiatesActa pharmaceutica Sinica. B · 2026Article
- Leveraging Deep Learning to Construct a Programmed Cell Death-Driven Prognostic Signature in Acute Myeloid Leukemia.Current issues in molecular biology · 2026Article
154 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
4 authors at 2 institutions in 1 country.
Funding
Abstract
Acute myeloid leukemia (AML) is a heterogeneous group of diseases characterized by uncontrolled proliferation of hematopoietic stem cells in the bone marrow. Malignant cell growth is characterized by disruption of normal intracellular signaling, caused by mutations or aberrant external signaling. The phosphoinositide 3-kinase (PI3K)-Akt-mammalian target of rapamycin (mTOR) pathway (PI3K-Akt-mTOR pathway) is among one of the intracellular pathways aberrantly upregulated in cancers including AML. Activation of this pathway seems important in leukemogenesis, and given the central role of this pathway in metabolism, the bioenergetics of AML cells may depend on downstream signaling within this pathway. Furthermore, observations suggest that constitutive activation of the PI3K-Akt-mTOR pathway differs between patients, and that increased activity within this pathway is an adverse prognostic parameter in AML. Pharmacological targeting of the PI3K-Akt-mTOR pathway with specific inhibitors results in suppression of leukemic cell growth. However, AML patients seem to differ regarding their susceptibility to various small-molecule inhibitors, reflecting biological heterogeneity in the intracellular signaling status. These findings should be further investigated in both preclinical and clinical settings, along with the potential use of this pathway as a prognostic biomarker, both in patients receiving intensive curative AML treatment and in elderly/unfit receiving AML-stabilizing treatment.
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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.