Mutant and wild-type Ras: co-conspirators in cancer
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Summary: Although the functional interplay between mutant and wild-type Ras in driving tumor initiation and growth has been described, a clear picture of the precise ramifications and mechanisms of this association remains elusive, sometimes with conflicting conclusions. A report in this issue of Cancer Discovery tackles this question, which may have important implications for therapeutic strategies to block mutant Ras for cancer treatment. Cancer Discov; 3(1); 24–6. ©2012 AACR. See related article by Young et al., p. 112
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Combining a mutant-specific KRAS inhibitor with a SHP2 or SOS1 inhibitor could block both mutant KRAS and wild-type RAS signaling.
“A combination of a mutant specific KRAS inhibitor with either a SHP2 inhibitor or a SOS1 inhibitor could effectively block mutant KRAS and wild-type RAS signaling (12, 43, 45, 46).”
From Expanding the Reach of Precision Oncology by Drugging All <i>KRAS</i> Mutants (2022) · cites this paper as [46]
In heterozygous KRAS mutant tumor cells, RAS signaling can be supplemented and cross-regulated by RTK-WT RAS signaling.
“In heterozygous KRAS mutant tumor cells, RAS signaling can be supplemented and cross-regulated by RTK-WT RAS signaling.”
From Expanding the Reach of Precision Oncology by Drugging All <i>KRAS</i> Mutants (2022) · cites this paper as [46]
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- Authors
- Hayes, T. K., & Der, C. J.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Corresponding author
- Der, Channing J.
- Venue
- Cancer Discovery
- Published
- 2013-01-01
- Volume
- 3
- Issue
- 1
- Pages
- 24-26
- ISSN
- 2159-8274 (ISSN-L)
- 2159-8290
- PMC
- PMC3808242
- OpenAlex
- W2154115960
- Cited by
- 13
- References
- 11
- Citations by year
- 2022: 1 · 2020: 3 · 2019: 1 · 2018: 1 · 2017: 1 · 2015: 2 · 2014: 3 · 2013: 1
- FWCI
- 0.90
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Cancer Discovery (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (T32CA071341)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
- Keywords
- oncogenic Ras, RAS wild-type, tumor initiation, tumor growth, oncogenic signaling
- MeSH terms
- Humans, Neoplasms, Genes, ras, Mitogen-Activated Protein Kinases
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