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Furmonertinib activity in NSCLC Harbouring EGFR L858R and ERBB2 S310F co-mutations: a case report with literature
Shiyue Liu1, Runze Cao2, Hong Li3
1Department of Oncology, Xiangyang No.1 Peoplès Hospital, Hubei Univeristy of Medicine, XiangYang, Hubei, China.
Abstract:
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.
Insights
Concurrent EGFR and ERBB2 mutations in lung adenocarcinoma are rare. A combination of furmonertinib and radiotherapy showed a significant clinical response in a patient with these co-mutations.
Area of Science:
- Oncology
- Genetics
- Pharmacology
Background:
- Targeted therapies have improved lung adenocarcinoma (LUAD) treatment.
- Concurrent EGFR and ERBB2 mutations are rare and poorly understood, creating therapeutic uncertainty.
- Existing EGFR tyrosine kinase inhibitors (TKIs) and HER2-targeted therapies lack established efficacy for these co-mutations.
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