The DOI matches its Crossref record; 0 of the 52 references it cites were found in a registry or an index.
PI3King the Lock: Targeting the PI3K/Akt/mTOR Pathway as a Novel Therapeutic Strategy in Neuroblastoma
Abstract
Neuroblastoma is the most common extracranial cancer in childhood. High-risk neuroblastoma continues to have a poor prognosis and there is an urgent need to design biologically based therapies that specifically target the pathways responsible for malignant transformation and progression. One such pathway is the PI3K/Akt/mTOR pathway. In this article we outline the evidence for aberrant activation of the PI3K/Akt/mTOR pathway in neuroblastoma and discuss the possible mechanisms which mediate it. We also discuss the development of treatments targeting this pathway in neuroblastoma and the challenges that must be overcome before such treatments can enter routine clinical practice.
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“ROS are known to hyperactivate PI3K/Akt/mTOR (Phosphoinositide 3-Kinases/Protein kinase B/mammalian Target Of Rapamycin), an intracellular pathway playing an important role in cell cycle regulation, specifically proliferation, cancer, and longevity (King et al. 2015).”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as King et al. 2015
Citations
Cites
Neuroblastoma: biological insights into a clinical enigma. Nat Rev Cancer.
Brodeur (2003)
UnresolvedDevelopment of treatment strategies for advanced neuroblastoma. Int J Clin Oncol.
Hara (2012)
Unresolved. The International Neuroblastoma Risk Group (INRG) classification system: an INRG Task Force report. J Clin Oncol.
Cohn (2009)
Unresolved. Association of phosphatidylinositol kinase activity with polyoma middle-T competent for transformation. Nature.
Whitman (1985)
UnresolvedPI3K signalling: the path to discovery and understanding. Nat Rev Mol Cell Biol.
Vanhaesebroeck (2012)
Unresolved. Dissecting the PI3K signaling axis in pediatric solid tumors: novel targets for clinical integration. Front Oncol.
Loh (2013)
UnresolvedOvercoming acquired resistance to anticancer therapy: focus on the PI3KAKTmTOR pathway. Cancer Chemother Pharmacol.
Burris (2013)
Unresolved. N-myc is a novel regulator of PI3K-mediated VEGF expression in neuroblastoma. Oncogene.
Kang (2008)
Unresolved. Activation of Akt predicts poor outcome in neuroblastoma. Cancer Res.
Opel (2007)
Unresolved. Inhibitors of mammalian target of rapamycin downregulate MYCN protein expression and inhibit neuroblastoma growth in vitro and in vivo. Oncogene.
Johnsen (2008)
Unresolved
Cited by
Sorted by citations
Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging
Jomova, K., Raptova, R., Alomar, S. Y., Alwasel, S. H., Nepovimova, E., Kuca, K., & Valko, M. (2023) · Archives of Toxicology · doi:10.1007/s00204-023-03562-9 · Cited by 2,638
Tewari, D., Patni, P., Bishayee, A., Sah, A. N., & Bishayee, A. (2019) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2019.12.008 · Cited by 659
The role of TGF-β/SMAD4 signaling in cancer
Zhao, M., Mishra, L., & Deng, C.-X. (2018) · International Journal of Biological Sciences · doi:10.7150/ijbs.23230 · Cited by 631
“(PIP3), which then phosphorylates and activates AKT, and makes it localize on the plasma membrane [46].”
BackgroundEpithelial-mesenchymal transition in tissue repair and fibrosis
Stone, R. C., Pastar, I., Ojeh, N. O., Chen, V., Liu, S., Garzon, K. I., & Tomic‐Canic, M. (2016) · Cell and Tissue Research · doi:10.1007/s00441-016-2464-0 · Cited by 591
“Additionally, the c-Met-PI3K/ AKT pathway influences the cell cycle, proliferation, and quiescence (King et al. 2015), and PI3K-activated mTORC2 is one of the driving factors for the phenotypic transition in EMT, whereas mTORC1 encourages cell growth and movement (Lamouille et al. 2012; Lamouille…”
BackgroundPI3K/Akt signaling transduction pathway, erythropoiesis and glycolysis in hypoxia (Review)
Xie, Y., Shi, X., Sheng, K., Han, G., Li, W., Zhao, Q., Jiang, B., Feng, J., Li, J., & Gu, Y. (2018) · Molecular Medicine Reports · doi:10.3892/mmr.2018.9713 · Cited by 505
Metadata
- Authors
- King, D., Yeomanson, D., & Bryant, H. E.
- Affiliations
- Sheffield Children's Hospital (GB)
- Venue
- Journal of Pediatric Hematology/Oncology
- Published
- 2015-05
- Volume
- 37
- Issue
- 4
- Pages
- 245-251
- ISSN
- 1077-4114 (ISSN-L)
- OpenAlex
- W1974245465
- Cited by
- 248
- References
- 52
- Citations by year
- 2026: 10 · 2025: 19 · 2024: 31 · 2023: 24 · 2022: 26 · 2021: 29 · 2020: 29 · 2019: 25 · 2018: 22 · 2017: 22 · 2016: 11
- FWCI
- 2.46
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Pediatric Hematology/Oncology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Neuroblastoma Research and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Health Sciences › Medicine › Clinical Neurology › Neurofibromatosis and Schwannoma Cases
- Keywords
- neuroblastoma, PI3K/AKT/mTOR pathway, high-risk neuroblastoma, PI3K inhibitors, AKT inhibitors, mTOR inhibitors, targeted therapy, childhood cancer
- MeSH terms
- Mechanistic Target of Rapamycin Complex 1, Mechanistic Target of Rapamycin Complex 2, Phosphoinositide-3 Kinase Inhibitors, Animals, Humans, Neuroblastoma, Signal Transduction, Phosphatidylinositol 3-Kinases, Multiprotein Complexes, Protein Kinase Inhibitors, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases
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