Clinical efficacy and drug resistance of anti-epidermal growth factor receptor therapy in colorectal

来源 :World Journal of Gastrointestinal Oncology | 被引量 : 0次 | 上传用户:m83692590
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Colorectal cancer(CRC) ranked third in cancer related death and its incidence has been increasing worldwide. In recent decades important therapeutic advances have been developed in treatment of metastatic CRC(mCRC), such as monoclonal antibodies against epidermal growth factor receptor(anti-EGFR), which provided additional clinical benefits in mCRC. However, anti-EGFR therapies have limited usage due to approximately 95% of patients with KRAS mutated mCRC do not response to anti-EGFR treatment. Thus, KRAS mutation is predictive of nonresponse to anti-EGFR therapies but it alone is not a sufficient basis to decide who should not be received such therapies because; approximately fifty percent(40%-60%) of CRC patients with wild-type KRAS mutation also have poor response to anti-EGFR based treatment. This fact leads us to suspect that there must be other molecular determinants of response to anti-EGFR therapies which have not been identified yet. Current article summarizes the clinical efficacy of anti-EGFR therapies and also evaluates its resistance mechanisms. Colorectal cancer (CRC) ranked third in cancer related death and its incidence has been increased worldwide. In recent decades, important therapeutic advances have been in treatment of metastatic CRC (mCRC), such as monoclonal antibodies against epidermal growth factor receptor (anti-EGFR ), which provided additional clinical benefits in mCRC. However, anti-EGFR therapies have limited usage due to approximately 95% of patients with KRAS mutated mCRC do not respond to anti-EGFR treatment. Thus, KRAS mutation is predictive of nonresponse to anti- EGFR therapies but it alone alone not a sufficient basis to decide who should not be received such therapies because; approximately fifty percent (40% -60%) of CRC patients with wild-type KRAS mutation also have poor responses to anti-EGFR based treatment . This fact leads us to suspect that there be other molecular determinants of response to anti-EGFR therapies which have not been identified yet. Current article summarizes the clinical eff icacy of anti-EGFR therapies and also evaluates its resistance mechanisms.
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