ReviewFrontiers in pharmacology2025
An overview of mechanisms, biomarkers, and treatment strategies for acquired anti-EGFR resistance in RAS wild-type colorectal cancer.
Review in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Does the ERBB/EGF Signaling Network Serve as a Nexus for Oncogenic Signals in Uveal Melanoma?Biomolecules · 2026Review
- Development of a multi-targeted sulfonyl-bridged bisselenadiazole derivative as a potent EGFR/PI3K/AKT/mTOR modulator in lung adenocarcinoma.RSC advances · 2026Article
- Molecular Targeting of EGFR, BRAF, and HER2 Signaling in Colorectal Cancer: Contemporary Advances with Panitumumab, Encorafenib, and Tucatinib.Journal of clinical medicine · 2026Review
- Differential Tumor Response and Conversion Outcomes Associated with First-Line Biologic Strategies in Liver-LimitedOncology research · 2026Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) is a threat to public health, with a global incidence and mortality of over 1.9 million and 0.9 million people, respectively. Anti-epidermal growth factor receptor (EGFR)-based treatment is recommended for CRC with wild-type rat sarcoma (RAS). However, after continuous treatment with this regimen, acquired resistance occurs, which hampers the prognosis of patients. The median progression-free survival of patients with metastatic CRC receiving first-line anti-EGFR-based treatment is 10-13 months. The widely recognized mechanisms that induce acquired anti-EGFR resistance are related to the activation of the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR signaling pathways. In addition, novel mechanisms that induce acquired resistance, such as microsatellite stability/mismatch repair status, noncoding RNAs, the tumor microenvironment, exosome-mediated intracellular communication, and post-transcriptional modification, are being discovered. To improve personalized medication, biomarkers with predictive value for acquired anti-EGFR resistance are recognized from both tumoral samples and liquid biopsies. On the basis of the identified mechanisms, clinicians have developed several treatment strategies to cope with acquired anti-EGFR resistance. This review provides an overview of acquired anti-EGFR resistance in RAS wild-type CRC by summarizing the common genes and proteins, potential novel mechanisms, and predictive biomarkers related to acquired anti-EGFR resistance, as well as treatment strategies to address this resistance. This review may serve as a potential reference for exploring possible treatment strategies for acquired anti-EGFR resistance.
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