ArticleBritish journal of cancer2010
Activating K-Ras mutations outwith 'hotspot' codons in sporadic colorectal tumours - implications for personalised cancer medicine.
Article in British journal of cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 4 of them syntheses that pooled it.
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95 citing papers in PubMed, 4 syntheses or guidelines pooled it, 178 citations in OpenAlex.
- Schimmelpenning-Feuerstein-Mims syndrome: a systematic review of clinical cases to identify genotype-phenotype associations.Frontiers in medicine · 2025Pooled it
- Standards for the classification of pathogenicity of somatic variants in cancer (oncogenicity): Joint recommendations of Clinical Genome Resource (ClinGen), Cancer Genomics Consortium (CGC), and Variant Interpretation for Cancer Consortium (VICC).Genetics in medicine : official journal of the American College of Medical Genetics · 2022Guideline
- Signal transduction pathway mutations in gastrointestinal (GI) cancers: a systematic review and meta-analysis.Scientific reports · 2020Pooled it
- MicroRNA-binding site polymorphisms and risk of colorectal cancer: A systematic review and meta-analysis.Cancer medicine · 2019Pooled it
- Blood-based detection of RAS mutations to guide anti-EGFR therapy in colorectal cancer patients: concordance of results from circulating tumor DNA and tissue-based RAS testing.Molecular oncology · 2017Trial
- KRAS codon 12 and 13 mutations in relation to disease-free survival in BRAF-wild-type stage III colon cancers from an adjuvant chemotherapy trial (N0147 alliance).Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Trial
- KRAS-targeted therapies in colorectal cancer: a systematic analysis of mutations, inhibitors, and clinical trials.NPJ precision oncology · 2025Article
- Functional Analysis of Rare RAS Variants of Unknown Significance.Cancer research communications · 2025Article
- Search for Mutations Connected With Non-Response to Anti-EGFR Therapy in mCRC in the Morphologically Defined Regions of Primary Tumours.Cancer medicine · 2025Article
- A sequencing-based screening method identifies regulators of EGFR signaling from nonviable mutants inScience signaling · 2025Article
- KRAS Mutation Subtypes and Their Association with Other Driver Mutations in Oncogenic Pathways.Cells · 2024Review
- Lymph node and bone metastasis of pulmonary intestinal adenocarcinoma: A case report.Oncology letters · 2023Article
- Article
- Review
- Whole-cell energy modeling reveals quantitative changes of predicted energy flows in RAS mutant cancer cell lines.iScience · 2023Article
- Molecular-Targeted Therapy for Tumor-Agnostic Mutations in Acute Myeloid Leukemia.Biomedicines · 2022Review
- Clinicopathologic and Molecular Characterization of Epstein-Barr Virus-positive Plasmacytoma.The American journal of surgical pathology · 2022Article
- SFPQ promotes RAS-mutant cancer cell growth by modulating 5'-UTR mediated translational control of CK1α.NAR cancer · 2022Article
- Functional and biological heterogeneity of KRASScience signaling · 2022Article
- Crucial Role of OncogenicCells · 2022Review
35 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundResponse to EGFR-targeted therapies in colorectal cancer patients has been convincingly associated with Kirsten-Ras (K-Ras) mutation status. Current mandatory mutation testing for patient selection is limited to the K-Ras 'hotspot' codons 12 and 13.
methodsColorectal tumours (n=106) were screened for additional K-Ras mutations, phenotypes compared in transformation and Ras GTPase activating assays and gene and pathway changes induced by individual K-Ras mutants identified by microarray analysis. Taqman-based gene copy number and FISH analyses were used to investigate K-Ras gene amplification.
resultsFour additional K-Ras mutations (Leu(19)Phe (1 out of 106 tumours), Lys(117)Asn (1 out of 106), Ala(146)Thr (7 out of 106) and Arg(164)Gln (1 out of 106)) were identified. Lys(117)Asn and Ala(146)Thr had phenotypes similar to the hotspot mutations, whereas Leu(19)Phe had an attenuated phenotype and the Arg(164)Gln mutation was phenotypically equivalent to wt K-Ras. We additionally identified a new K-Ras gene amplification event, present in approximately 2% of tumours.
conclusionsThe identification of mutations outwith previously described hotspot codons increases the K-Ras mutation burden in colorectal tumours by one-third. Future mutation screening to facilitate optimal patient selection for treatment with EGFR-targeted therapies should therefore be extended to codon 146, and in addition should consider the unique molecular signatures associated with individual K-Ras mutations.
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