医学
蛋白酪氨酸激酶
肿瘤科
表皮生长因子受体抑制剂
表皮生长因子受体
酪氨酸激酶
养生
靶向治疗
内科学
肺癌
腺癌
吉非替尼
奥西默替尼
突变
酪氨酸激酶抑制剂
精密医学
癌症研究
生物信息学
个性化医疗
治疗方法
肺
梅德林
后天抵抗
临床试验
化疗
激酶
基因组测序
作者
Shiyue Liu,Runze Cao,Hong Li,Dongdong Zhang
标识
DOI:10.1080/1120009x.2025.2580760
摘要
While targeted therapies have remarkably transformed the landscape of lung adenocarcinoma (LUAD) management, the clinical implications of concurrent mutations in EGFR and ERBB2 remain inadequately understood due to their exceptional rarity in patients. This lack of understanding leads to significant uncertainty regarding therapeutic strategies for individuals with such co-mutations, as neither single-agent EGFR tyrosine kinase inhibitors (TKIs) nor HER2-targeted therapies have demonstrated established efficacy in this specific molecular context. Here, we present a compelling case involving a 61-year-old female patient diagnosed with advanced LUAD, with both EGFR L858R (exon 21) and ERBB2 S310F mutations identified through comprehensive next-generation sequencing (NGS). The patient received a treatment regimen consisting of the third-generation EGFR TKI furmonertinib, combined with localized radiotherapy, which resulted in a marked and significant clinical response. Our findings indicate that furmonertinib may effectively address the therapeutic uncertainties associated with EGFR/ERBB2 co-mutations, presenting a promising clinically actionable strategy while we continue to await the advent of more personalized and tailored treatment solutions.
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