Molecular mechanisms underlying the resistance of BRAF V600E-mutant metastatic colorectal cancer to EGFR/BRAF inhibitors
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Background: Combinatorial inhibition of epidermal growth factor receptor (EGFR) and BRAF shows remarkable clinical benefits in patients with BRAF V600E-mutant metastatic colorectal cancer (mCRC). However, the tumor may inevitably develop resistance to the targeted therapy, thereby limiting the response rate and durability. This study aimed to determine the genetic alterations associated with intrinsic and acquired resistance to EGFR/BRAF inhibitors in BRAF V600E-mutant mCRC. Methods: Targeted sequencing of 520 cancer-related genes was performed in tumor tissues and in plasma samples collected from patients with BRAF V600E-mutant mCRC, who were treated with EGFR/BRAF ± MEK inhibitors, before and after the targeted treatment. Clinical benefit was defined as an objective response or a stable disease lasting longer than the median progression-free survival (PFS). Results: In all, 25 patients with BRAF V600E-mutant mCRC were included in this study. Those with RNF43 mutations ( n = 8) were more likely to achieve clinical benefit from EGFR/BRAF inhibitors than those with wild-type RNF43 (87.5% versus 37.5%, p = 0.034). Genetic alterations in receptor tyrosine kinase genes ( n = 6) were associated with worse PFS ( p = 0.005). Among the 23 patients whose disease progressed after the EGFR/BRAF-targeted therapy, at least one acquired resistance-related mutation was detected in 12 patients. Acquired mutations were most frequently observed in the mitogen-activated protein kinase pathway-related genes ( n = 9), including KRAS (G12D and Q61H/R), NRAS (Q61L/R/K and amplification), BRAF (amplification), and MEK1 (K57T). MET amplification and PIK3R1 Q579fs mutation emerged in three patients and one patient, respectively, after disease progression. Conclusion: Multiple genetic alterations are associated with clinical benefits and resistance to EGFR/BRAF inhibitors in BRAF V600E-mutant mCRC. Our findings provide novel insights into strategies for overcoming resistance to EGFR/BRAF inhibitors in patients with BRAF V600E-mutant mCRC.
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Preclinical studies show that the reactivation of the MAPK pathway is a key mechanism underlying acquired resistance to BRAF inhibitors.
“Preclinical studies show that the reactivation of the MAPK pathway is a key mechanism underlying acquired resistance to BRAF inhibitors [38,39].”
From Inhibition of fatty acid synthase enhances therapeutic efficacy and delays acquired resistance to BRAF-targeted therapy in colorectal cancer (2026) · cites this paper as [38]
The Background states that preclinical studies identify MAPK pathway reactivation as a key mechanism of acquired resistance, but specifically to combined EGFR/BRAF inhibition in BRAF V600E-mutant colorectal cancer. The claim omits those treatment and population limits, making it broader than the source supports. (LLM, conf=0.86)
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- Authors
- Xu, T., Wang, X., Wang, Z., Deng, T., Qi, C., Liu, D., Li, Y., Ji, C., Li, J., & Shen, L.
- Affiliations
- Peking University Cancer Hospital (CN)
- Tianjin Medical University Cancer Institute and Hospital (CN)
- Corresponding author
- Li, Jian
- Shen, Lin
- ORCID
- Venue
- Therapeutic Advances in Medical Oncology
- Publisher
- SAGE Publications
- Published
- 2022-01
- Volume
- 14
- Pages
- 17588359221105022-17588359221105022
- ISSN
- 1758-8340 (ISSN-L)
- 1758-8359
- PMC
- PMC9210093
- OpenAlex
- W4285228312
- Cited by
- 38
- References
- 36
- Citations by year
- 2026: 6 · 2025: 15 · 2024: 9 · 2023: 8
- FWCI
- 3.35
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Therapeutic Advances in Medical Oncology (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Chinese Society of Clinical Oncology (Y-Young2020-0516)
- Topics
- Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
- Keywords
- BRAF V600E mutation, metastatic colorectal cancer, acquired drug resistance, RNF43 mutation, MEK inhibitors, receptor tyrosine kinase mutations, KRAS mutation, NRAS mutation, BRAF amplification, MET amplification, PIK3R1 mutation, MAPK signaling, progression-free survival
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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