Published online Jan 15, 2016. doi: 10.4251/wjgo.v8.i1.1
Peer-review started: April 24, 2015
First decision: September 2, 2015
Revised: November 12, 2015
Accepted: December 7, 2015
Article in press: December 8, 2015
Published online: January 15, 2016
Processing time: 266 Days and 16.6 Hours
Core tip: Molecular targeting agents, such as monoclonal antibodies against epidermal growth factor receptor (anti-EGFR), provide additional clinical benefits in metastatic colorectal cancer (CRC). However, anti-EGFR therapies have limited usage due to approximately 95% of patients with KRAS mutated metastatic CRC 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.
