克拉斯
埃罗替尼
医学
表皮生长因子受体
癌症研究
病毒癌基因
肺癌
突变
腺癌
酪氨酸激酶
肿瘤科
抗性突变
吉非替尼
内科学
癌症
生物
基因
受体
结直肠癌
遗传学
聚合酶链反应
逆转录酶
作者
Biagio Ricciuti,Sara Baglivo,Vienna Ludovini,Angelo Sidoni,Giulio Metro,Marta Brambilla,Annamaria Siggillino,Maria Sole Reda,Alberto Rebonato,Daniele Maiettini,Rita Chiari
出处
期刊:Lung Cancer
[Elsevier]
日期:2018-06-01
卷期号:120: 70-74
被引量:4
标识
DOI:10.1016/j.lungcan.2018.04.002
摘要
Although epidermal growth factor receptor (EGFR) and v-Ki-ras2 Kirsten rat sarcoma viral oncogene (KRAS) mutations were thought to be mutually exclusive in patients with non-small cell lung cancer (NSCLC), the development of high sensitive large-scale mutation analysis, has increasingly shown that activating EGFR mutations occasionally coexist with other dominant genetic alterations. Herein, we discuss the case of a patient with advanced NSCLC harboring both the uncommon EGFR G719S and the KRAS G12C mutations, who was treated for 9 years with erlotinib achieving a long-term survival. In light of their rarity, multiple mutations are very challenging for the decision of tyrosine kinase inhibitors (TKIs) treatment, especially when EGFR mutations occur together with mutations known to provide resistance to EGFR TKIs, such as KRAS.
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