학술논문
A Novel MYH9-RET Fusion Occurrence and EGFR T790M Loss as an Acquired Resistance Mechanism to Osimertinib in a Patient with Lung Adenocarcinoma: A Case Report.
Document Type
Article
Source
Subject
*EPIDERMAL growth factor receptors
*NON-small-cell lung carcinoma
*ADENOCARCINOMA
*LUNGS
*HYPOKINESIA
*OSIMERTINIB
*
*
*
*
*
Language
ISSN
1178-6930
Abstract
Background: Osimertinib is a novel and irreversible epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) targeting EGFR sensitive mutations and EGFR exon20 p.T790M mutation, which demonstrated superior progression-free survival (PFS) and overall survival (OS). Case Presentation: We report a patient with lung adenocarcinoma harboring EGFR exon 19 deletion mutant treatment with icotinib. After 6 months, she developed EGFR exon20 p.T790M and then the patient received osimertinib treatment. A novel MYH9 (exon41)-RET (exon12) fusion and EGFR exon20 p.T790M loss were identified using plasma circulation tumor DNA (ctDNA) after osimertinib treatment, which led to rapid progression after osimertinib five months and suggested a potential resistance mechanism. Conclusion: Our findings expanded the spectrum of RET arrangement types and provided the basis for this hypothesis: acquired RET rearrangement and EGFR exon20 p.T790M loss potentially serve an additional resistance mechanism to osimertinib in EGFR-mutated non-small-cell lung cancer (NSCLC). [ABSTRACT FROM AUTHOR]