Clinical Epidemiology and Ageing

[Lung adenocarcinoma with concomitant EGFR mutation and ALK rearrangement].

Caliez J, Monnet I, Pujals A, Rousseau-Bussac G, Jabot L, Boudjemaa A, Leroy K, Chouaid C Rev Mal Respir. 2017;34(5):576-580.

<p><b>INTRODUCTION: </b>Among patients with non-small-cell lung cancer, coexistence of EGFR mutation and ALK rearrangement is rare. We describe the clinical features of two patients with this double anomaly.</p><p><b>CASE REPORTS: </b>A 62-year-old Caucasian non-smoking woman was diagnosed with cT4N0M0 lung adenocarcinoma. Initial biopsy showed EGFR mutation and ALK rearrangement. She received cisplatin-gemcitabine, followed by 17 months of gemcitabine. Owing to progression, she received erlotinib for 14 months, then paclitaxel for 6 months and finally crizotinib. A partial response was achieved and maintained for 24 months. A 45-year-old Caucasian woman, light smoker, was diagnosed with cT2N3M0 lung adenocarcinoma. Only EGFR mutation was found on initial analysis. She underwent treatment with cisplatin-gemcitabine and thoracic radiotherapy. Progression occurred after 8 months and afatinbib was started. Eight months later, progression was observed with a neoplasic pleural effusion in which tumor cells expressing ALK rearrangement were found. A new FISH analysis was performed on the initial tumor but did not find this rearrangement. Despite a third line of crizotinib, the patient died one month later.</p><p><b>DISCUSSION: </b>The literature shows 45 other cases of these two abnormalities, observed either from the start or during follow-up. EGFR's TKI were almost always given before ALK's TKI.</p><p><b>CONCLUSIONS: </b>Therapeutic strategy needs to be clarified in cases of double alteration. With regard to the second patient, appearance of ALK rearrangement may constitute a resistance mechanism to EGFR's TKI.</p>

MeSH terms: Adenocarcinoma; Adenocarcinoma of Lung; Anaplastic Lymphoma Kinase; Antineoplastic Combined Chemotherapy Protocols; Cisplatin; Crizotinib; ErbB Receptors; Erlotinib Hydrochloride; Female; Humans; Lung Neoplasms; Middle Aged; Mutation; Paclitaxel; Pyrazoles; Pyridines; Receptor Protein-Tyrosine Kinases; Translocation, Genetic
DOI: 10.1016/j.rmr.2016.08.002