Conclusions

The promise of target-based therapies for treatment of cancer is a tantalizing one. Ideally, the hope is to identify a unitary oncogenic driving force in a given patient and treat the disease with a potent and highly selective inhibitor. Such ideals have come close to fruition with the introduction of selective EGFR TKIs such as gefitinib and erlotinib which exhibit remarkable and specific efficacy, albeit for a small subset of NSCLC patients. These TKIs have not only aided in the treatment of NSCLC, but have also helped to reveal a pharmacogenomic profile of response leading to the identification of onco-genic EGFR mutations, approximately 20 years after the avian erythroblastosis virus was found to express transforming genes homologous to EGFR. Thus, it appears that ErbB family proteins should be attractive targets for drug discovery efforts, in NSCLC as well as other solid tumors.

Primary and acquired resistance to EGFR TKIs has forced researchers to identify alternative targets or therapeutic strategies that may aid in targeting EGFR mutants in cancer. The major challenges that are manifest in this arena include the full understanding of the molecular and cellular basis for primary and acquired resistance, such as the identification of oncogenic determinants that may drive EGFR-independent cancer cell growth and survival. Such challenges are only now being addressed at the basic science level, and it is only a matter of time until these findings are translated into clinical practice.

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