Effect of KRAS Mutational Status in Advanced Colorectal Cancer on the Outcomes of Anti-Epidermal Growth Factor Receptor Monoclonal Antibody Therapy: A Systematic Review and Meta-analysis

2011 ◽  
Vol 10 (1) ◽  
pp. 63-69 ◽  
Author(s):  
Albert Y. Lin ◽  
Nicholas S. Buckley ◽  
An-Ting T. Lu ◽  
Natalia B. Kouzminova ◽  
Shelley R. Salpeter
2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Kevin M. Sullivan ◽  
Peter S. Kozuch

The epidermal growth factor receptor (EGFR) pathway is a therapeutic target in the management of colorectal cancer (CRC). EGFR antagonists are active in this disease; however, only a subset of patients respond to such therapy. A Kirsten ras sarcoma viral oncogene (KRAS) wild-type (WT) status of the tumor is necessary, but possibly not sufficient, for a response to anti-EGFR monoclonal antibody therapy. Mechanisms of primary resistance to such therapy in patients harboring KRAS WT tumors are discussed. Strategies to overcome resistance to anti-EGFR monoclonal antibody therapy, including novel agents and combinations of novel therapies, are explored. Also, the use of anti-EGFR monoclonal antibodies in the adjuvant and neoadjuvant setting is reviewed.


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