Han Sae-Won, Kim Hwang-Phill, Jeon Yoon Kyung, Oh Do-Youn, Lee Se-Hoon, Kim Dong-Wan, Im Seock-Ah, Chung Doo Hyun, Heo Dae Seog, Bang Yung-Jue, Kim Tae-You
Department of Internal Medicine, Seoul National University Hospital, Republic of Korea.
Lung Cancer. 2008 Jul;61(1):30-4. doi: 10.1016/j.lungcan.2007.11.014. Epub 2008 Jan 14.
Mucoepidermoid carcinoma (MEC) of lung is a rare malignancy of lung which originates from minor salivary glands of tracheobronchial tree. EGFR targeted therapy by inhibition of EGFR activation with the specific tyrosine kinase inhibitors (TKIs) has shown meaningful anti-tumor activity in patients with EGFR TK mutation and/or amplification, or in patients with adenocarcinoma. In the present study, we find that MEC has EGFR mutation in 40% (2 out of 5) of cases, and all mutations are L858R mutation. In addition, we also observed that a MEC patient well-responded to EGFR TKI in the absence of EGFR mutation or amplification. These data indicate for the first time that MEC of lung is another potential target of EGFR inhibitor, and more extended clinical investigation is warranted.
肺黏液表皮样癌(MEC)是一种罕见的肺癌,起源于气管支气管树的小唾液腺。通过使用特异性酪氨酸激酶抑制剂(TKIs)抑制表皮生长因子受体(EGFR)激活的EGFR靶向治疗,已在EGFR TK突变和/或扩增的患者或腺癌患者中显示出有意义的抗肿瘤活性。在本研究中,我们发现40%(5例中的2例)的MEC病例存在EGFR突变,且所有突变均为L858R突变。此外,我们还观察到1例MEC患者在没有EGFR突变或扩增的情况下对EGFR TKI有良好反应。这些数据首次表明,肺MEC是EGFR抑制剂的另一个潜在靶点,有必要进行更广泛的临床研究。