Selecting Patients for Epidermal Growth Factor Receptor Inhibitor Treatment: A FISH Story or a Tale of Mutations?

摘要: The two articles that appear in this issue of the Journal Clinical Oncology provide additional information about role mutated epidermal growth factor receptor (EGFR) and gene copy number EGFR response, time to progression, survival patients with non–small-cell lung cancer treated gefitinib. article by Takano et al includes on 66 (NSCLC) from Japan whose tumors underwent sequencing exons 18 24 determination quantitative, real-time polymerase chain reaction (PCR). Hirsch extends these observations assessed fluorescence situ hybridization (FISH) its relationship an subset 81 bronchioloalveolar carcinoma (BAC). reinforces FISH assessing outcome following treatment gefitinib, while provides evidence presence mutations EGFR—rather than number—is more important determining gefitinib therapy. Although both used as tyrosine kinase inhibitor (EGFR-TKI), some Editorial will include other EGFR-TKI commonly for NSCLC, erlotinib. research community is appropriately left wonder if mutations, number, immunohistochemistry or a combination tests should be help predict which are most likely respond therapy, done identify appropriate candidates It point out there different end points successful treatment, minority demonstrating partial response erlotinib greater proportion prolonged stable disease ultimately contribute benefit. In addition Oncology, manuscripts Asia group University Colorado particularly pertinent whether story tale both. data somatic NSCLC consistent have appeared 2005. These studies been limited Korea, where detected approximately three times often United States Europe. design was similar. were retrospectively identified, their tumor retrieved banks previous resection biopsy, all DNA extracted blocks. differences rates, those without highly statistically significant (P .0053 0.0001, respectively; Table 1). study also confirmed increased mutation frequency specific subgroups patients, namely nonsmokers BAC features. addition, described (exon 19 deletions, L858R G719S/C) previously identified dramatic clinical responses when Three (L703V, E709K, S768I), but occurred concert one above, JOURNAL OF CLINICAL ONCOLOGY E D I T O R A L VOLUME 23 NUMBER 28 OCTOBER 1 2005