ReviewMolecular cancer research : MCR2021
Emerging Roles for AKT Isoform Preference in Cancer Progression Pathways.
Review in Molecular cancer research : MCR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 68 citations in OpenAlex.
- Identification of novel loci regulating circulating melatonin and its causal relationship with hypertension.Human genetics · 2026Article
- ProteoForge: An Imputation-Aware Framework for Differential Proteoform Discovery in Bottom-Up Proteomics.Journal of proteome research · 2026Article
- Network pharmacology and experimental evaluation of Sanwei Tanxiang Tangsan in doxorubicin-induced heart failure.Journal of cardiothoracic surgery · 2026Article
- Exploration of the effect and mechanism ofOncology letters · 2026Article
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- Article
- Triptonide Suppresses AML via PI3K/AKT Signaling: A Network Pharmacology Approach Validated by Molecular Docking and Experimental Studies.Current issues in molecular biology · 2026Article
- Genomic Evaluation of Canine Prostatic Carcinomas as a Model for the Human Disease: or 'UC or not UC - that is the question'.Veterinary and comparative oncology · 2025Article
- Spirulina and exercise: a two-pronged approach to mitigating oxidative stress in colorectal cancer.Molecular biology reports · 2025Review
- Endometrial cancer: from clinical reality to molecular treatment.Discover oncology · 2025Review
- Targeting the AKT/mTOR pathway attenuates the metastatic potential of colorectal carcinoma circulating tumor cells in a murine xenotransplantation model.Molecular oncology · 2025Article
- Kinome Reprogramming of G2/M Kinases and Repression of MYCN Contribute to Superior Efficacy of Lorlatinib in ALK-Driven Neuroblastoma.Molecular cancer therapeutics · 2025Article
- The Role of PI3K/AKT/mTOR Signaling in Tumor Radioresistance and Advances in Inhibitor Research.International journal of molecular sciences · 2025Review
- Akt isoform specificity drives intrinsic immune regulation during HSV-1 infection.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The roles of AKT isoforms in decidualization and embryo implantation using a Progesterone Receptor-Cre mouse model†.Biology of reproduction · 2025Article
- A Novel Molecular Profile of Hormone-Sensitive Prostate Cancer Defines High Risk Patients.Cancer medicine · 2025Article
- Pharmacogenomic andFrontiers in pharmacology · 2025Article
- [High expression of CRTAC1 promotes proliferation, migration and immune cell infiltration of gastric cancer by regulating the PI3K/AKT signaling pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- AXL-TBK1 driven AKT3 activation promotes metastasis.Science signaling · 2024Article
- AKT kinases as therapeutic targets.Journal of experimental & clinical cancer research : CR · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The phosphoinositol-3 kinase (PI3K)-AKT pathway is one of the most mutated in human cancers, predominantly associated with the loss of the signaling antagonist, PTEN, and to lesser extents, with gain-of-function mutations in PIK3CA (encoding PI3K-p110α) and AKT1. In addition, most oncogenic driver pathways activate PI3K/AKT signaling. Nonetheless, drugs targeting PI3K or AKT have fared poorly against solid tumors in clinical trials as monotherapies, yet some have shown efficacy when combined with inhibitors of other oncogenic drivers, such as receptor tyrosine kinases or nuclear hormone receptors. There is growing evidence that AKT isoforms, AKT1, AKT2, and AKT3, have different, often distinct roles in either promoting or suppressing specific parameters of oncogenic progression, yet few if any isoform-preferred substrates have been characterized. This review will describe recent data showing that the differential activation of AKT isoforms is mediated by complex interplays between PTEN, PI3K isoforms and upstream tyrosine kinases, and that the efficacy of PI3K/AKT inhibitors will likely depend on the successful targeting of specific AKT isoforms and their preferred pathways.
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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.