Kobayashi Susumu, Boggon Titus J, Dayaram Tajhal, Jänne Pasi A, Kocher Olivier, Meyerson Matthew, Johnson Bruce E, Eck Michael J, Tenen Daniel G, Halmos Balázs
Division of Hematology/Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, USA.
N Engl J Med. 2005 Feb 24;352(8):786-92. doi: 10.1056/NEJMoa044238.
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.
在对苯胺喹唑啉表皮生长因子受体(EGFR)抑制剂有反应的非小细胞肺癌患者的标本中,已鉴定出EGFR基因的突变。尽管对此类抑制剂有显著反应,但大多数患者最终都会复发。耐药机制尚不清楚。在此,我们报告一例EGFR突变、对吉非替尼敏感的晚期非小细胞肺癌患者,该患者在接受吉非替尼治疗两年完全缓解后复发。复发时其肿瘤活检标本中EGFR基因的DNA序列显示存在第二个点突变,导致EGFR第790位氨基酸由苏氨酸变为甲硫氨酸。结构建模和生化研究表明,这第二个突变导致了吉非替尼耐药。