The DOI matches its Crossref record; 159 of the 160 references it cites were found in a registry or an index.
Targeting PI3K signalling in cancer: opportunities, challenges and limitations
Abstract
There are ample genetic and laboratory studies that suggest the PI3K-Akt pathway is vital to the growth and survival of cancer cells. Inhibitors targeting this pathway are entering the clinic at a rapid pace. In this Review, the therapeutic potential of drugs targeting PI3K-Akt signalling for the treatment of cancer is discussed. I focus on the advantages and drawbacks of different treatment strategies for targeting this pathway, the cancers that might respond best to these therapies and the challenges and limitations that confront their clinical development.
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“AKT, through a series of complex signal transduction cascades, leads to the activation of the mTOR1 complex (Engelman, 2009).”
From Dasatinib sensitizes KRAS mutant colorectal tumors to cetuximab (2011) · cites this paper as Engelman, 2009
In the citing paper
“These include mutation and/or amplification of the genes encoding the PI3K catalytic subunits p110α (PIK3CA) and p110β (PIK3CB), the PI3K regulatory subunit p85α (PIK3R1), the PI3K effectors AKT1, AKT2, and PDK1, and loss of the lipid phosphatases PTEN and INPP4B [reviewed in (Engelman, 2009)].”
From ERBB Receptors: From Oncogene Discovery to Basic Science to Mechanism-Based Cancer Therapeutics (2014) · cites this paper as Engelman, 2009
In the citing paper
“Somatic alterations in the PI3K/AKT pathway are the most frequent in breast cancer, occurring in approximately 30% of HER2+ tumors.”
From ERBB Receptors: From Oncogene Discovery to Basic Science to Mechanism-Based Cancer Therapeutics (2014) · cites this paper as Engelman, 2009
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Metadata
- Authors
- Engelman, J. A.
- Affiliations
- Massachusetts General Hospital (US)
- Corresponding author
- Engelman, Jeffrey A.
- ORCID
- Engelman, Jeffrey A.
- Venue
- Nature Reviews Cancer
- Published
- 2009-08
- Volume
- 9
- Issue
- 8
- Pages
- 550-562
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- OpenAlex
- W1977267072
- Cited by
- 2,445
- References
- 160
- Citations by year
- 2026: 60 · 2025: 71 · 2024: 75 · 2023: 102 · 2022: 90 · 2021: 125 · 2020: 146 · 2019: 127 · 2018: 163 · 2017: 172 · 2016: 159 · 2015: 210 · 2014: 211 · 2013: 221 · 2012: 184
- FWCI
- 13.17
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Cancer (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- 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, Lipids, and Metabolism
- Keywords
- PI3K/Akt signaling, PI3K inhibitors, AKT inhibitors, cancer therapy, targeted therapy, drug development, tumor cell survival, treatment resistance
- MeSH terms
- Antineoplastic Agents, Humans, Neoplasms, Protein Kinases, Signal Transduction, Phosphatidylinositol 3-Kinases, Protein Kinase Inhibitors, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases
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