AI Article Synopsis
- Anti-EGFR monoclonal antibody treatment has shown success in patients with chemotherapy-resistant or metastatic colorectal cancer, but not all patients respond effectively.
- Resistance to anti-EGFR treatment may be linked to various biomarkers beyond just KRAS mutations, including molecular interactions within the EGFR pathway, though this area remains under-researched and inconsistent.
- Clinical trials, like the AIO KRK-0306, raise questions about existing guidelines for evaluating treatment response, highlighting the challenges and limitations in the current understanding and effectiveness of anti-EGFR therapies.
Article Abstract
Anti-epidermal growth-factor receptor (EGFR) monoclonal antibody (MoAb) treatment for chemotherapy refractory or metastatic colorectal cancer has obtained great achievement. However, not every colorectal patient responds to such molecular-targeted agent well. Biomarkers associated with anti-EGFR resistance are not limited to KRAS mutation up to now. It was recently reported that cross-talking molecular effectors interacted with EGFR-related pathway were also negative predictor for anti-EGFR treatment. However, the limited data, controversial results, and contradictories between in vitro and clinical studies restrict the clinical application of these new biomarkers. Although the current theory of tumor microenvironment supported the application of multi-target treatment, the results from the clinical studies were less than expected. Moreover, WHO or RECIST guideline for response assessment in anti-EGFR MoAb treatment was also queried by recent AIO KRK-0306 trial. This review focuses on these controversies, contradictories, and limitations, in order to uncover the unmet needs in current status of anti-EGFR MoAb treatment in colorectal cancer.
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| http://dx.doi.org/10.1007/s00280-014-2489-6 | DOI Listing |
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