- Author:
Seung Hun JANG
1
Author Information
- Publication Type:Review
- Keywords: Receptor, Epidermal Growth Factor; Carcinoma, Non-Small Cell Lung; Drug Therapy
- MeSH: Carcinoma, Non-Small-Cell Lung*; Clone Cells; Drug Therapy; Humans; Phosphotransferases; Prognosis; Receptor, Epidermal Growth Factor; Tumor Burden
- From:Tuberculosis and Respiratory Diseases 2014;76(1):8-14
- CountryRepublic of Korea
- Language:English
- Abstract: Non-small cell lung cancer harboring epidermal growth factor receptor (EGFR) sensitizing mutations has a distinct disease entity. Patients with this cancer have better prognosis, and frequently achieve long-term survival. EGFR-tyrosine kinase inhibitor (TKI) is the drug of choice for this cancer; but the disease inevitably progresses, after durable response. The tumor is a mixture of EGFR-TKI sensitive clones and resistant clones, regardless of their molecular mechanisms. EGFR-TKI sensitive clones are very susceptible to this drug, but rarely eradicated; so, withdrawal of the drug permits rapid regrowth of drug sensitive clones, possibly causing "disease flare." Re-administration or continuation of EGFR-TKI can effectively suppress the expansion of drug sensitive clones, even when the total tumor volume continuously increases. Chemotherapy can definitely prolong the survival of patients experiencing EGFR-TKI failure. Prospective clinical trials are warranted to compare efficacies of chemotherapeutic agents. A few retrospective studies suggested that a taxane-based regimen may be superior to others. Here, we reviewed therapeutic options and clinical evidence about this unique disease entity.