A systems mechanism for KRAS mutant allele–specific responses to targeted therapy
Open accessPublished version of a preprint
Abstract
A weak KRAS G13D -NF1 interaction explains why EGFR inhibitors show efficacy in certain CRC patients.
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Differential interaction kinetics between KRAS G13D and the Ras GAP NF-1 explain the sensitivity of KRAS G13D COAD tumors to anti-EGFR therapies.
“differential interaction kinetics between KRAS G13D and the Ras GAP NF-1 explain this effect22–24”
From The origins and genetic interactions of KRAS mutations are allele- and tissue-specific (2021) · cites this paper as [22]
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References 50 · Cited by 65
- Authors
- McFall, T., Diedrich, J. K., Mengistu, M., Littlechild, S. L., Paskvan, K. V., Sisk-Hackworth, L., Moresco, J. J., Shaw, A. S., & Stites, E. C.
- Affiliations
- Salk Institute for Biological Studies (US)
- Scripps Research Institute (US)
- Genentech (US)
- Department of Research Biology, Genentech, South San Francisco, CA 94080, USA.
- Corresponding author
- Stites, Edward C.
- ORCID
- Venue
- Science Signaling
- Published
- 2019-09-24
- Volume
- 12
- Issue
- 600
- ISSN
- 1937-9145 (ISSN-L)
- 1945-0877
- PMC
- PMC6864030
- OpenAlex
- W2976505807
- Cited by
- 65
- References
- 50
- Citations by year
- 2026: 6 · 2025: 9 · 2024: 9 · 2023: 7 · 2022: 12 · 2021: 13 · 2020: 6 · 2019: 1 · 2018: 1 · 2016: 1
- FWCI
- 2.65
- Type
- journal article
- Language
- en
- Open access
- green
- doi.org
- Locations
- Science Signaling (publishedVersion)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (K22CA216318, T32CA009370, P30CA014195)
- Leona M. and Harry B. Helmsley Charitable Trust
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Keywords
- KRAS mutation, targeted therapy, Ras signaling, systems biology, patient stratification, genomic medicine
- MeSH terms
- Cetuximab, Antineoplastic Agents, Immunological, Alleles, Humans, Mutation, Neurofibromatosis 1, Protein Binding, Colorectal Neoplasms, Signal Transduction, Proto-Oncogene Proteins p21(ras), Caco-2 Cells, HCT116 Cells, Cell Line, Tumor, Molecular Targeted Therapy, ErbB Receptors
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