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Mucoepidermoid carcinoma of lung: potential target of EGFR-directed treatment
Sae-Won Han1, Hwang-Phill Kim, Yoon Kyung Jeon
1Department of Internal Medicine, Seoul National University Hospital, Republic of Korea.
Abstract:
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.
Insights
Mucoepidermoid carcinoma (MEC) of the lung shows EGFR mutations in 40% of cases. Lung MEC may respond to EGFR tyrosine kinase inhibitors (TKIs), warranting further clinical studies.
Area of Science:
- Oncology
- Pulmonology
- Molecular Biology
Background:
- Mucoepidermoid carcinoma (MEC) of the lung is a rare lung malignancy originating from the tracheobronchial tree's minor salivary glands.
- Epidermal Growth Factor Receptor (EGFR) targeted therapy using tyrosine kinase inhibitors (TKIs) is effective in specific lung cancer subtypes.
Observation:
- This study investigated EGFR mutations and TKI response in lung MEC.
- EGFR mutations were identified in 40% of the studied MEC cases, specifically the L858R mutation.
- One MEC patient demonstrated a positive response to EGFR TKI treatment despite lacking EGFR mutation or amplification.
Findings:
- Lung MEC exhibits EGFR mutations, with L858R being the predominant type observed.
- EGFR TKIs show potential therapeutic efficacy in lung MEC, even in cases without detectable EGFR mutations or amplification.
Implications:
- Lung MEC represents a novel potential target for EGFR inhibitor therapy.
- These findings support further clinical investigation into the use of EGFR TKIs for treating lung MEC.
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