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      EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy.

      Science (New York, N.Y.)

      Treatment Outcome, Sequence Deletion, metabolism, genetics, chemistry, antagonists & inhibitors, Receptor, Epidermal Growth Factor, therapeutic use, pharmacology, Quinazolines, Protein Structure, Tertiary, Protein Conformation, Phosphorylation, Mutation, Missense, Mutation, Molecular Sequence Data, Male, drug therapy, Lung Neoplasms, Japan, Humans, Genes, erbB-1, Female, Enzyme Inhibitors, Controlled Clinical Trials as Topic, Cell Line, Tumor, Carcinoma, Non-Small-Cell Lung, Antineoplastic Agents, Amino Acid Substitution, Amino Acid Sequence, Amino Acid Motifs, Adenocarcinoma, United States

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          Abstract

          Receptor tyrosine kinase genes were sequenced in non-small cell lung cancer (NSCLC) and matched normal tissue. Somatic mutations of the epidermal growth factor receptor gene EGFR were found in 15of 58 unselected tumors from Japan and 1 of 61 from the United States. Treatment with the EGFR kinase inhibitor gefitinib (Iressa) causes tumor regression in some patients with NSCLC, more frequently in Japan. EGFR mutations were found in additional lung cancer samples from U.S. patients who responded to gefitinib therapy and in a lung adenocarcinoma cell line that was hypersensitive to growth inhibition by gefitinib, but not in gefitinib-insensitive tumors or cell lines. These results suggest that EGFR mutations may predict sensitivity to gefitinib.

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          Journal
          15118125
          10.1126/science.1099314

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