Concordance of predictive markers for EGFR inhibitors in primary tumors and metastases in colorectal cancer: A review
Open accessAbstract
Background.: Currently, only Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) mutational status is used as a decisional marker for epidermal growth factor receptor (EGFR) inhibitor therapy in colorectal cancer (CRC) patients. Concordance of KRAS status between primary tumors and metastases has always been considered to be close to perfect; however, cases of discordance have been reported. The actual rate of concordance of KRAS status remains unclear, as is the same for v-raf murine sarcoma viral oncogene homolog B1 (BRAF), phosphatidylinositol 3-kinase CA subunit (PIK3CA), and loss of phosphatase and tensin homologue deleted on chromosome ten (PTEN). Therefore, it is unknown whether it is necessary to perform mutational analysis on metastases instead of on (or in addition to) primary tumors. Design.: A systematic literature search was conducted to collect all studies testing concordance of KRAS in CRC, and also of BRAF, PIK3CA, and loss of PTEN. Results.: Twenty-one studies have reported concordance of KRAS, with an overall concordance rate of 93% (range, 76%–100%). Overall concordance rates of studies testing concordance of BRAF status and loss of PTEN were 98% and 68%, respectively. Three studies reported concordance of PIK3CA status (range, 89%–94%). Conclusion.: Though discordance of KRAS status does occur, it is uncommon. When considering the downsides of testing metastatic tissue in all patients along with the low incidence of discordance, we conclude that that testing the primary tumor (or whatever tissue available) is sufficient for clinical decision making on EGFR inhibitor therapy.
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The combined frequency of mutations in KRAS exons 3 and 4, and NRAS exons 2, 3, and 4 is 10-15% (approximately 20% of KRAS exon 2 wild-type cases).
“the combined frequency of mutations in KRAS exons 3 and 4, and NRAS exons 2, 3, and 4 is 10–15% (approximately 20% of KRAS exon 2 wild-type cases)”
From The Role of KRAS Mutations in Colorectal Cancer: Biological Insights, Clinical Implications, and Future Therapeutic Perspectives (2025) · cites this paper as [47]
Not only somatic mutations in KRAS codons 12 and 13 but also other hotspot mutations in KRAS exons 3 and 4, and NRAS exons 2, 3, and 4, are associated with clinical resistance to anti-EGFR therapy.
“not only somatic mutations in KRAS codons 12 and 13 but also other hotspot mutations in KRAS exons 3 and 4, and NRAS exons 2, 3, and 4, are associated with clinical resistance to anti-EGFR therapy [47]”
From The Role of KRAS Mutations in Colorectal Cancer: Biological Insights, Clinical Implications, and Future Therapeutic Perspectives (2025) · cites this paper as [47]
Among patients with confirmed RAS mutations in pre-treatment tumor tissue samples, 19% (91/478) did not exhibit RAS mutations in their plasma at the time of treatment modification. Of these, 10.2% (49/478) showed no other somatic mutations.
“among patients with confirmed RAS mutations in pre-treatment tumor tissue samples, 19% (91/478) did not exhibit RAS mutations in their plasma at the time of treatment modification. Of these, 10.2% (49/478) showed no other somatic mutations.”
From The Role of KRAS Mutations in Colorectal Cancer: Biological Insights, Clinical Implications, and Future Therapeutic Perspectives (2025) · cites this paper as [47]
Anti-EGFR antibodies are ineffective in RAS-mutant cases.
“anti-EGFR antibodies are ineffective in RAS-mutant cases”
From The Role of KRAS Mutations in Colorectal Cancer: Biological Insights, Clinical Implications, and Future Therapeutic Perspectives (2025) · cites this paper as [47]
Approximately 10% of colorectal cancer patients who were previously deemed unlikely to benefit from treatments involving anti-EGFR antibodies due to RAS mutations may actually have the potential to benefit from such therapies.
“approximately 10% of colorectal cancer patients who were previously deemed unlikely to benefit from treatments involving anti-EGFR antibodies due to RAS mutations may actually have the potential to benefit from such therapies [47]”
From The Role of KRAS Mutations in Colorectal Cancer: Biological Insights, Clinical Implications, and Future Therapeutic Perspectives (2025) · cites this paper as [47]
KRAS mutations reduce responsiveness to anti-EGFR therapies.
“resistance to certain treatments, including anti-EGFR monoclonal antibodies (panitumumab and cetuximab)”
From The Role of KRAS Mutations in Colorectal Cancer: Biological Insights, Clinical Implications, and Future Therapeutic Perspectives (2025) · cites this paper as [47]
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- Authors
- Baas, J. M., Krens, L. L., Guchelaar, H.-J., Morreau, H., & Gelderblom, H.
- Affiliations
- Leiden University Medical Center (NL)
- Corresponding author
- Morreau, Hans
- Venue
- The Oncologist
- Publisher
- Oxford University Press (OUP)
- Published
- 2011-07-08
- Volume
- 16
- Issue
- 9
- Pages
- 1239-1249
- ISSN
- 1083-7159 (ISSN-L)
- 1549-490X
- PMC
- PMC3228174
- OpenAlex
- W2160662474
- Cited by
- 89
- References
- 68
- Citations by year
- 2025: 2 · 2024: 1 · 2023: 1 · 2022: 2 · 2021: 2 · 2019: 9 · 2018: 6 · 2017: 18 · 2016: 7 · 2015: 13 · 2014: 8 · 2013: 10 · 2012: 10
- FWCI
- 0.82
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
- Locations
- The Oncologist (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Leiden Repository (Leiden University) (submittedVersion)
- Funders
- Amgen
- Topics
- Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Health Sciences › Medicine › Oncology › Colorectal Cancer Surgical Treatments
- Keywords
- colorectal cancer, EGFR inhibitors, predictive biomarkers, KRAS mutation, BRAF mutation, PIK3CA mutation, PTEN loss
- MeSH terms
- Animals, Humans, Mutation, Neoplasm Metastasis, Proto-Oncogene Proteins, Colorectal Neoplasms, Proto-Oncogene Proteins p21(ras), ras Proteins, Protein Kinase Inhibitors, ErbB Receptors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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