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      EGFR mutation and resistance of non-small-cell lung cancer to gefitinib.

      The New England journal of medicine

      Aged, Antineoplastic Agents, adverse effects, therapeutic use, Biopsy, Carcinoma, Non-Small-Cell Lung, diagnosis, drug therapy, genetics, DNA, Neoplasm, Drug Resistance, Neoplasm, Humans, Lung Neoplasms, Male, Models, Structural, Molecular Structure, Neoplasm Recurrence, Local, pathology, Point Mutation, Quinazolines, chemistry, metabolism, RNA, Neoplasm, Receptor, Epidermal Growth Factor, antagonists & inhibitors, Sequence Analysis, DNA, Sequence Analysis, RNA

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          Abstract

          Mutations of the epidermal growth factor receptor (EGFR) gene have been identified in specimens from patients with non-small-cell lung cancer who have a response to anilinoquinazoline EGFR inhibitors. Despite the dramatic responses to such inhibitors, most patients ultimately have a relapse. The mechanism of the drug resistance is unknown. Here we report the case of a patient with EGFR-mutant, gefitinib-responsive, advanced non-small-cell lung cancer who had a relapse after two years of complete remission during treatment with gefitinib. The DNA sequence of the EGFR gene in his tumor biopsy specimen at relapse revealed the presence of a second point mutation, resulting in threonine-to-methionine amino acid change at position 790 of EGFR. Structural modeling and biochemical studies showed that this second mutation led to gefitinib resistance. Copyright 2005 Massachusetts Medical Society.

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          Journal
          15728811
          10.1056/NEJMoa044238

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