ReviewJournal of cancer research and clinical oncology2015
Current clinical regulation of PI3K/PTEN/Akt/mTOR signalling in treatment of human cancer.
Review in Journal of cancer research and clinical oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 1 of them a synthesis that pooled it.
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
92 citing papers in PubMed, 1 synthesis or guideline pooled it, 172 citations in OpenAlex.
- Pooled it
- Recent progress and therapeutic strategies in the treatment of cervical neuroendocrine neoplasms (Review).International journal of molecular medicine · 2026Review
- The mechanism of the PI3K-AKT-mTOR signaling pathway in renal cell carcinoma: current developments and future prospects.Frontiers in oncology · 2026Review
- Expression Analysis of the orphan receptors GPR161, GPR132, GPR20, and GPR139 in patients with cervicitis and low-grade, and high-grade squamous intraepithelial lesions.Genetics and molecular biology · 2026Article
- ESE-1 Regulates CREB-Mediated PTEN Expression to Activate the PI3K/Akt Pathway and Promote High-Glucose-Induced Endothelial Cell Injury.Current medical science · 2025Article
- Potential role of thymoquinone to treat gastrointestinal cancers: insights into its molecular mechanisms.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- NSAID-encapsulated nanoparticles as a targeted therapeutic platform for modulating chronic inflammation and inhibiting cancer progression: a review.Inflammopharmacology · 2025Review
- A bibliometric analysis of the application of the PI3K-AKT-mTOR signaling pathway in cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Targeted therapy of cancer stem cells: inhibition of mTOR in pre-clinical and clinical research.Cell death & disease · 2024Review
- Signaling pathways activated and regulated by stem cell-derived exosome therapy.Cell & bioscience · 2024Review
- Chlorogenic Acid and Cinnamaldehyde in Combination Inhibit Metastatic Traits and Induce Apoptosis via Akt Downregulation in Breast Cancer Cells.International journal of molecular sciences · 2024Article
- Article
- The relationship between nonsteroidal anti-inflammatory drugs and cancer incidence: An umbrella review.Heliyon · 2024Review
- Circular RNA ZBTB46 depletion alleviates the progression of Atherosclerosis by regulating the ubiquitination and degradation of hnRNPA2B1 via the AKT/mTOR pathway.Immunity & ageing : I & A · 2023Article
- MDiscover oncology · 2023Article
- Therapeutic Targets of Monoclonal Antibodies Used in the Treatment of Cancer: Current and Emerging.Biomedicines · 2023Review
- RUNX1 Upregulation Causes Mitochondrial Dysfunction via Regulating the PI3K-Akt Pathway in iPSC from Patients with Down Syndrome.Molecules and cells · 2023Article
- Integrated network-based multiple computational analyses for identification of co-expressed candidate genes associated with neurological manifestations of COVID-19.Scientific reports · 2022Article
- Polyphenols in Ilex latifolia Thunb. inhibit human lung cancer cell line A549 by regulation of the PI3K-Akt signaling pathway.BMC complementary medicine and therapies · 2022Article
- mTOR Signaling Components in Tumor Mechanobiology.International journal of molecular sciences · 2022Review
32 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposePTEN is an essential tumour suppressor gene which encodes a phosphatase protein that antagonises the PI3K/Akt/mTOR antiapoptotic pathway. Impairment of this tumour suppressor pathway potentially becomes a causal factor for development of malignancies. This review aims to assess current understanding of mechanisms of dysfunction involving the PI3K/PTEN/Akt/mTOR pathway linked to tumorigenesis and evaluate the evidence for targeted therapy directed at this signalling axis.
methodsRelevant articles in scientific databases were identified using a combination of search terms, including "malignancies", "targeted therapy", "PTEN", and "combination therapy". These databases included Medline, Embase, Cochrane Review, Pubmed, and Scopus.
resultsPI3K/PTEN expression is frequently deregulated in a majority of malignancies through genetic, epigenetic, and post-transcriptional modifications. This contributes to the upregulation of the PI3K/Akt/mTOR pathway which has been the focus of intense clinical studies. Targeted agents aimed at this pathway offer a novel treatment approach in a variety of haematologic malignancies and solid tumours. Compared to single-agent use, greater response rates were obtained in combination regimens, supporting further investigation of suitable drug combinations in a broad spectrum of malignancies.
conclusionActivation of the PI3K/PTEN/Akt/mTOR pathway is implicated both in the pathogenesis of malignancies and development of resistance to anticancer therapies. Therefore, PI3K/Akt/mTOR inhibitors are a promising therapeutic option, in association with systemic cytotoxic and biological therapies, to enable sustained clinical outcomes in cancer treatment. Therapeutic strategies could be tailored according to appropriate biomarkers and patient-specific mutation profiles to maximise benefit of combination therapies.
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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.