ReviewWorld journal of gastroenterology2016
Mechanisms of resistance to anti-epidermal growth factor receptor inhibitors in metastatic colorectal cancer.
Review in World journal of gastroenterology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
75 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Systematic literature review and meta-analysis of HER2 amplification, overexpression, and positivity in colorectal cancer.JNCI cancer spectrum · 2024Pooled it
- Do cancer biomarkers make targeted therapies cost-effective? A systematic review in metastatic colorectal cancer.PloS one · 2018Pooled it
- Amivantamab Monotherapy in ChemorefractoryJournal of clinical oncology : official journal of the American Society of Clinical Oncology · 2026Trial
- Metastatic Colorectal Cancer Treatment Response Evaluation by Ultra-Deep Sequencing of Cell-Free DNA and Matched White Blood Cells.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Trial
- Mutation burden and other molecular markers of prognosis in colorectal cancer treated with curative intent: results from the QUASAR 2 clinical trial and an Australian community-based series.The lancet. Gastroenterology & hepatology · 2018Trial
- Disrupting KRAS-AGO2 interaction: a dual-pronged strategy to sensitize chemo-immunotherapy in KRAS-mutated colorectal cancer.Apoptosis : an international journal on programmed cell death · 2026Article
- Overcoming Resistance to Anti-EGFR Therapies: Mechanisms of Cetuximab and Panitumumab Resistance and Emerging Combination Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- EGFR Signaling in Colorectal Cancer: Novel Therapeutic Strategies, Predictive Biomarkers, and Counteracting Treatment Resistance.International journal of molecular sciences · 2026Review
- Review
- BCL-xL as a therapeutic target in cetuximab-refractory colorectal cancer.Cell death & disease · 2026Article
- Wide-Field Optical Redox Imaging with Leading-Edge Detection Enables Assessment of Treatment Response and Heterogeneity in Patient-Derived Cancer Organoids.Cancer research · 2025Article
- Impact of Human Epidermal Growth Factor Receptor 2 in Patients With Metastatic Colorectal Cancer Treated With Chemotherapy Plus Bevacizumab or Anti-EGFRs: Exploratory Analysis of Eight Randomized Trials.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2025Article
- Targeting endothelial growth factor receptor in thyroid cancer: current concepts and future directions.Medical oncology (Northwood, London, England) · 2025Review
- Experimental System Design and Modelling of EGFR Extracellular Domain and Its Mutant Binding to Antibody Interacting Partner.International journal of molecular sciences · 2025Article
- Tumour mutational burden using a targeted panel approach for comprehensive tumour profiling focusing on colorectal cancer.Hereditary cancer in clinical practice · 2025Review
- Precision medicine in colorectal cancer: genomics profiling and targeted treatment.Frontiers in pharmacology · 2025Review
- Article
- Combined KRAS and TP53 mutation in patients with colorectal cancer enhance chemoresistance to promote postoperative recurrence and metastasis.BMC cancer · 2024Article
- Thymol-loaded liposomes effectively induced apoptosis and decreased EGFR expression in colorectal cancer cells.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Therapeutic strategies targeting the epidermal growth factor receptor signaling pathway in metastatic colorectal cancer.World journal of gastrointestinal oncology · 2024Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The prognosis of patients with metastatic colorectal cancer (mCRC) remain poor despite the impressive improvement of treatments observed over the last 20 years that led to an increase in median overall survival from 6 mo, with the only best supportive care, to approximately 30 mo with the introduction of active chemotherapy drugs and targeted agents. The monoclonal antibodies (moAbs) cetuximab and panitumumab, directed against the epidermal growth factor receptor (EGFR), undoubtedly represent a major step forward in the treatment of mCRC, given the relevant efficacy in terms of progression-free survival, overall survival, response rate, and quality of life observed in several phase III clinical trials among different lines of treatment. However, the anti-EGFR moAbs were shown only to be effective in a subset of patients. For instance, KRAS and NRAS mutations have been identified as biomarkers of resistance to these drugs, improving the selection of patients who might derive a benefit from these treatments. Nevertheless, several other alterations might affect the response to these drugs, and unfortunately, even the responders eventually become resistant by developing secondary (or acquired) resistance in approximately 13-18 mo. Several studies highlighted that the landscape of responsible alterations of both primary and acquired resistance to anti-EGFR drugs biochemically converge into MEK-ERK and PIK3CA-AKT pathways. In this review, we describe the currently known mechanisms of primary and acquired resistance to anti-EGFR moAbs together with the various strategies evaluated to prevent, overcame or revert them.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.