Abstract
Colorectal cancer remains a major cause of morbidity and mortality worldwide despite substantial improvement in the standard of care. Although surgical resection in selected patients may potentially be curative, systemic therapy is the only choice of treatment for most patients with metastatic colorectal cancer. Anti-epidermal growth factor receptor (anti-EGFR) monoclonal antibody has established its role in the systemic therapy of metastatic colorectal cancer through multiple well-designed clinical trials and yet, the optimal use of anti-EGFR monoclonal antibody is undefined. This article serves to review the available evidence for anti-EGFR monoclonal antibodies and to speculate optimal strategy for their uses.
Highlights
Colorectal cancer is the third most common cancer in men and the second in women worldwide
With the use of chemotherapy in metastatic colorectal cancer, it was shown that the exact sequence of chemotherapeutic agents used did not affect outcomes [45] as long as patients were exposed to all active agents [46]
The ability to select patients according to KRAS mutational status has revolutionalized the field of personalized therapy in the treatment of metastatic colorectal cancer
Summary
Colorectal cancer is the third most common cancer in men and the second in women worldwide. The principal modality of treatment for patients with metastatic disease is systemic therapy and approved sole or combination options include: 5fluorouracil, capecitabine, oxaliplatin, irinotecan, bevacizumab, cetuximab and panitumumab. Among all these options, only the anti-epidermal growth factor receptor (anti-EGFR) monoclonal antibodies, cetuximab and panitumumab, have proven efficacy in early as well as late lines of therapy. Being the first receptor identified in the family, EGFR is known as the type I receptor tyrosine kinase or ErbB1/HER1. EGFR forms homo- or heterodimers with other members of the ErbB family resulting in autophosphorylation of the intracellular domain and subsequent activation of downstream intracellular signaling cascade [5,6]. The Ras/Raf/ mitogen-activated protein kinase (MAPK), the PI3K/AKT and the Jak2/Stat pathways are major downstream signaling pathways that are crucial for cancer cell proliferation, survival, invasion, metastasis and neo-angiogenesis [7]
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