Targeting the PI3K-Akt pathway in human cancer
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The PI3K pathway is hyperactivated not only in GBM, but also in many other cancers including breast, ovarian, endometrial, lung, prostate, renal and lymphocyte.
“Furthermore, the PI3K pathway is hyperactivated not only in GBM, but also in many other cancers including breast, ovarian, endometrial, lung, prostate, renal and lymphocyte (5, 56–58).”
From An LXR Agonist Promotes Glioblastoma Cell Death through Inhibition of an EGFR/AKT/SREBP-1/LDLR–Dependent Pathway (2011) · cites this paper as [58]
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- Authors
- Luo, J., Manning, B. D., & Cantley, L. C.
- Affiliations
- Beth Israel Deaconess Medical Center (US)
- Corresponding author
- Cantley, Lewis C
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2003-10
- Volume
- 4
- Issue
- 4
- Pages
- 257-262
- ISSN
- 1535-6108 (ISSN-L)
- OpenAlex
- W2117263216
- Cited by
- 1,290
- References
- 5
- Citations by year
- 2026: 15 · 2025: 30 · 2024: 31 · 2023: 24 · 2022: 46 · 2021: 61 · 2020: 62 · 2019: 67 · 2018: 50 · 2017: 68 · 2016: 55 · 2015: 51 · 2014: 60 · 2013: 53 · 2012: 76
- FWCI
- 4.86
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- American Cancer Society
- National Cancer Institute (CA89021, P01CA089021)
- National Institute of General Medical Sciences (GM 41890, R01GM056203, GM 56203, R01GM041890)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Keywords
- PI3K/Akt signaling, cancer, apoptosis evasion, senescence evasion, DNA damage checkpoint, cell proliferation, oncogenic mutations, therapeutic targeting
- MeSH terms
- Animals, Cell Cycle, Cell Division, Cell Survival, Humans, Neoplasms, Neoplasms, Experimental, Phosphorylation, Proto-Oncogene Proteins, Signal Transduction, Protein Serine-Threonine Kinases, Phosphatidylinositol 3-Kinases, Models, Animal, Protein Interaction Mapping, Proto-Oncogene Proteins c-akt, Mice
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