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Cited by 543PI3K/AKT/mTOR signaling in cancerMetabolism, Diabetes, and CancerAdvanced Breast Cancer Therapies

Targeting the PI3K signaling pathway in cancer

Open access
Wong, Kwok-Kin, Engelman, Jeffrey A, Cantley, Lewis C·2010·Current Opinion in Genetics & Development
DOI 10.1016/j.gde.2009.11.002PMC PMC2822054
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Abstract

The phosphoinositide 3-kinase (PI3K) pathway is activated in a variety of different human cancers, and inhibitors of this pathway are under active development as anti-cancer therapeutics. In this review, we discuss the data supporting the use of PI3K pathway inhibitors in genetically and clinically defined cancers. This review focuses on their efficacy as single agents and in combination with other targeted therapies, specifically those targeting the MEK-ERK signaling pathway.

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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 [56]

    The Introduction describes widespread PI3K pathway activation in cancer and identifies breast, prostate and brain cancers; the section on concurrent alterations also identifies endometrial cancer, and the paper discusses PI3K-driven lung cancer. The passages do not establish the claim for ovarian, renal or lymphocyte cancers specifically. Page numbers are not available in our copy. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • 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 [5]

    The Introduction (page unavailable) describes PI3K-pathway activation across many cancers and identifies pathway-related alterations in breast, prostate and brain cancers; it also discusses endometrial and lung cancers. Our copy does not substantiate the full list: the searched passages do not identify ovarian, renal or lymphocyte cancers as examples of PI3K-pathway hyperactivation. (LLM, conf=0.85)

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Cites

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Research works printed but not linked: 26

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Sorted by citations

Authors
Wong, K.-K., Engelman, J. A., & Cantley, L. C.
Affiliations
  • Harvard University (US)
  • Beth Israel Deaconess Medical Center (US)
Corresponding author
Wong, Kwok-Kin
ORCID
Venue
Current Opinion in Genetics & Development
Publisher
Elsevier BV
Published
2010-02
Volume
20
Issue
1
Pages
87-90
ISSN
0959-437X (ISSN-L)
DOI
10.1016/j.gde.2009.11.002
PMC
PMC2822054
OpenAlex
W2077223675
Cited by
543
References
6
Citations by year
2026: 5 · 2025: 9 · 2024: 20 · 2023: 17 · 2022: 20 · 2021: 29 · 2020: 25 · 2019: 30 · 2018: 26 · 2017: 32 · 2016: 48 · 2015: 49 · 2014: 52 · 2013: 67 · 2012: 63
FWCI
2.91
Type
journal article
Language
en
Open access
Licence
Locations
  • Current Opinion in Genetics & Development (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Cancer Institute (R01CA122794, R01CA140594, P01CA089021, K08CA120060, R01CA137008)
  • National Institute of General Medical Sciences (R01GM056203, R01GM036624, 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
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Advanced Breast Cancer Therapies
Keywords
PI3K signaling, PI3K inhibitors, cancer therapy, MEK/ERK signaling, combination therapy, targeted cancer therapy
MeSH terms
Phosphoinositide-3 Kinase Inhibitors, Antineoplastic Agents, Antineoplastic Combined Chemotherapy Protocols, Humans, Neoplasms, Signal Transduction, Receptor, ErbB-2, Erb-b2 Receptor Tyrosine Kinases, Phosphatidylinositol 3-Kinases, MAP Kinase Kinase Kinases

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