ArticleThe American journal of pathology2017
AKT Hyperactivation and the Potential of AKT-Targeted Therapy in Diffuse Large B-Cell Lymphoma.
Article in The American journal of pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 59 citations in OpenAlex.
- Efficacy and Safety of Capivasertib (AZD5363), a Potent, Oral Pan-AKT Inhibitor, in Patients with Relapsed or Refractory B-cell Non-Hodgkin Lymphoma (CAPITAL).Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Trial
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- Nootkatone as a multi-target modulator of the PD-L1/PD-1 signaling in pancreatic cancer: network pharmacology, docking, molecular dynamics, and DFT analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Proinflammatory GSDMD activation in live macrophages and DLBCL cells marks cognate interactions and better prognosis.Blood advances · 2026Article
- Chidamide and anlotinib synergistically inhibit high grade B-cell lymphomas via PI3K/AKT signaling pathway.Scientific reports · 2025Article
- The metabolic role of lactate dehydrogenase in the growth of diffuse large B cell lymphoma.Annals of hematology · 2025Article
- Potent combination benefit of the AKT inhibitor capivasertib and the BCL-2 inhibitor venetoclax in diffuse large B cell lymphoma.Leukemia · 2024Article
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- The Role of the Akt Signaling Pathway in Sjögren's Syndrome.Mediterranean journal of rheumatology · 2023Article
- A combination of BR101801 and venetoclax enhances antitumor effect in DLBCL cells via c-Myc/Bcl-2/Mcl-1 triple targeting.American journal of cancer research · 2023Article
- Pyrimidine-5-carbonitrile based potential anticancer agents as apoptosis inducers through PI3K/AKT axis inhibition in leukaemia K562.Journal of enzyme inhibition and medicinal chemistry · 2022Article
- Prognostic significance of BLK expression in R-CHOP treated diffuse large B-cell lymphoma.Journal of pathology and translational medicine · 2022Article
- Systems Drug Discovery for Diffuse Large B Cell Lymphoma Based on Pathogenic Molecular Mechanism via Big Data Mining and Deep Learning Method.International journal of molecular sciences · 2022Article
- Altered pathways and targeted therapy in double hit lymphoma.Journal of hematology & oncology · 2022Review
- AKT Isoforms in the Immune Response in Cancer.Current topics in microbiology and immunology · 2022Article
- Transcriptomics-Based Investigation of Molecular Mechanisms Underlying Apoptosis Induced by ZnO Nanoparticles in Human Diffuse Large B-Cell Lymphoma.International journal of nanomedicine · 2022Article
- Chemoprevention of 4NQO-Induced Mouse Tongue Carcinogenesis by AKT Inhibitor through the MMP-9/RhoC Signaling Pathway and Autophagy.Analytical cellular pathology (Amsterdam) · 2022Article
- Cooperative miRNA-dependent PTEN regulation drives resistance to BTK inhibition in B-cell lymphoid malignancies.Cell death & disease · 2021Article
Corrections and comments
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Authors and funding
23 authors at 13 institutions in 8 countries.
Funding
Abstract
AKT signaling is important for proliferation and survival of tumor cells. The clinical significance of AKT activation in diffuse large B-cell lymphoma (DLBCL) is not well analyzed. Here, we assessed expression of phosphorylated AKT (p-AKT) in 522 DLBCL patients. We found that high levels of p-AKT nuclear expression, observed in 24.3% of the study cohort, were associated with significantly worse progression-free survival and Myc and Bcl-2 overexpression. However, multivariate analysis indicated that AKT hyperactivation was not an independent factor. miRNA profiling analysis demonstrated that 63 miRNAs directly or indirectly related to the phosphatidylinositol 3-kinase/AKT/mechanistic target of rapamycin pathway were differentially expressed between DLBCLs with high and low p-AKT nuclear expression. We further targeted AKT signaling using a highly selective AKT inhibitor MK-2206 in 26 representative DLBCL cell lines and delineated signaling alterations using a reverse-phase protein array. MK-2206 treatment inhibited lymphoma cell viability, and MK-2206 sensitivity correlated with AKT activation status in DLBCL cells. On MK-2206 treatment, p-AKT levels and downstream targets of AKT signaling were significantly decreased, likely because of the decreased feedback repression; Rictor and phosphatidylinositol 3-kinase expression and other compensatory pathways were also induced. This study demonstrates the clinical and therapeutic implications of AKT hyperactivation in DLBCL and suggests that AKT inhibitors need to be combined with other targeted agents for DLBCL to achieve optimal clinical efficacy.
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