Oncogenic kinase signalling.
Abstract
Protein-tyrosine kinases (PTKs) are important regulators of intracellular signal-transduction pathways mediating development and multicellular communication in metazoans. Their activity is normally tightly controlled and regulated. Perturbation of PTK signalling by mutations and other genetic alterations results in deregulated kinase activity and malignant transformation. The lipid kinase phosphoinositide 3-OH kinase (PI(3)K) and some of its downstream targets, such as the protein-serine/threonine kinases Akt and p70 S6 kinase (p70S6K), are crucial effectors in oncogenic PTK signalling. This review emphasizes how oncogenic conversion of protein kinases results from perturbation of the normal autoinhibitory constraints on kinase activity and provides an update on our knowledge about the role of deregulated PI(3)K/Akt and mammalian target of rapamycin/p70S6K signalling in human malignancies.
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Alterations to the activity of some kinases, especially those with oncogenic or tumor-suppressive functions, have the potential to promote malignant signaling and drive the development and progression of many kinds of cancers, including prostate cancer.
“Alterations to the activity of some kinases, especially to those with oncogenic or tumor-suppressive functions, has the potential to promote malignant signaling and drive the development and progression of many kinds of cancers, including prostate (42).”
From Minireview: Alternative Activation Pathways for the Androgen Receptor in Prostate Cancer (2011) · cites this paper as [42]
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- Authors
- Blume-Jensen, P., & Hunter, T.
- Affiliations
- Salk Institute for Biological Studies (US)
- ORCID
- Hunter, Tony
- Venue
- Nature
- Published
- 2001-05-01
- Volume
- 411
- Issue
- 6835
- Pages
- 355-365
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W1639582946
- Cited by
- 3,738
- References
- 93
- Citations by year
- 2026: 48 · 2025: 69 · 2024: 87 · 2023: 102 · 2022: 103 · 2021: 114 · 2020: 121 · 2019: 118 · 2018: 105 · 2017: 119 · 2016: 131 · 2015: 156 · 2014: 186 · 2013: 185 · 2012: 200
- FWCI
- 12.95
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- 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 › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- tyrosine kinase, oncogenic signaling, signal transduction, phosphatidylinositol 3-kinase, Akt, p70 S6 kinase, mTOR, kinase autoinhibition, malignant transformation, human malignancies
- MeSH terms
- Animals, Humans, Mutation, Neoplasms, Oncogenes, Protein-Tyrosine Kinases, Signal Transduction, Oncogene Proteins, Retroviridae Proteins, Oncogenic, Phosphatidylinositol 3-Kinases, Ribosomal Protein S6 Kinases, Receptor Protein-Tyrosine Kinases, Oncogene Protein v-akt
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