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lüll HKI-272 in non small cell lung cancer Wong KKClin Cancer Res 2007[Aug]; 13 (15 Pt 2): s4593-6Somatic mutations in the kinase domain of the epidermal growth factor receptor (EGFR) gene are found in approximately 10% of lung adenocarcinomas sequenced in the United States and in approximately 30% sequenced in Asia. These mutations are associated with sensitivity to the EGFR inhibitors gefitinib and erlotinib. Many patients who initially respond to erlotinib or gefitinib subsequently relapse. Studies have identified EGFR T790M mutations in tumors from patients who initially responded and then relapsed. The T790M mutation, when combined in vitro with treatment-sensitizing EGFR mutations, permits the continued growth of tumor cells in the presence of erlotinib and gefitinib. HKI-272 is an irreversible EGFR/HER/ErbB inhibitor that has been shown to inhibit the growth of T790M mutant cells in vitro in human lung cancer cell lines and in murine cells transfected with sensitizing EGFR mutations. A phase I HKI-272 monotherapy trial in patients with solid tumors is close to completion. Preliminary analyses of the trial, presented at the 2006 annual meeting of American Society of Clinical Oncology, showed that HKI-272 can achieve stable disease control for over 6 months in some patients with non-small cell lung cancer that has progressed after treatment with gefitinib or erlotinib. A phase II trial of HKI-272 in non-small cell lung cancer patients has been initiated. HKI-272 might offer benefits to non-small cell lung cancer patients who have relapsed after an initial response to erlotinib.|Animals[MESH]|Antineoplastic Agents/*therapeutic use[MESH]|Carcinoma, Non-Small-Cell Lung/*drug therapy[MESH]|Clinical Trials as Topic[MESH]|ErbB Receptors/antagonists & inhibitors/genetics[MESH]|Genetic Predisposition to Disease[MESH]|Humans[MESH]|Lung Neoplasms/*drug therapy[MESH]|Quinolines/*therapeutic use[MESH] |