Lung adenocarcinoma with EGFR 19Del and an ALK rearrangement benefits from alectinib instead of an EGFR-TKI: A case report

Rationale: A remarkable concurrence of an EGFR mutation and an EML4-ALK fusion (double positive) occasionally occurs within a narrow number of patients. Previous studies using targeted therapy on EGFR/ALK co-mutated patients have commonly focused on single tyrosine kinase inhibitors (TKIs) or on the sequential use of EGFR-TKIs and ALK-TKIs. At present, no consensus exists regarding the treatment of patients with double positive mutations. The effectiveness of precision therapy also remains unknown. Patient concerns: A 53-year-old female non-smoker who described recurrent coughing and blood in her sputum over a month-long interval was examined at a local hospital. Diagnosis: Using computed tomography (CT) and positron emission tomography CT (PET-CT), the patient was diagnosed with Stage IVb lung adenocarcinoma (T4N3M1). Interventions: The patient had a novel ALK-RAB10 rearrangement identified using DNA sequencing, which, at the transcript level, was actually a canonical ALK fusion that caused a response to alectinib therapy. Outcomes: The patient has achieved partial remission (PR), with a progression free survival (PFS) of 16 months, and continues to benefit. Lessons: Our results may indicate differential sensitivities to TKIs in patients harboring an EGFR mutation and an ALK rearrangement. Our patient's response to alectinib, instead of to EGFR-TKIs, may lead to an expanded list of alectinib beneficiaries who have rare gene co-alterations in lung adenocarcinoma.

Automated summary

This study found differential sensitivities to tyrosine kinase inhibitors (TKIs) in lung adenocarcinoma patients with EGFR mutations and ALK rearrangements, suggesting the efficacy of alectinib in this patient population. The results of this study are clinically significant for precision therapy in lung adenocarcinoma patients.