Aggressive pulmonary adenocarcinoma with new FGFR translocation and cMET mutation not responsive to crizotinib and nintedanib treatment: a case report

Lung cancer remains one of the most common causes of cancer-related deaths (1). Adenocarcinoma is its most frequent type (2). Although lung cancer was previously thought of as a relatively homogenous disease, we now understand that it comprises subsets of diseases driven by distinct molecular changes (3). One of the most important genetic changes in tumors are driver mutations. Some of these mutations are predictive factors for targeted treatment that improves the prognosis of patients (1). Epidermal growth factor receptor, anaplastic lymphoma kinase, proto-oncogene B-Raf and proto-oncogene tyrosine-protein kinase ROS1 tyrosine kinase inhibitors (TKIs) have entered the clinical practice (3,4). Although targetable oncogene products have been found in other adenocarcinoma patients, they are not yet routinely used in clinical practice or are still under development or researched (2,3). In addition, new mutations and their combinations are being identified with the increasingly common use of NGS in clinical practice. This is in turn associated with questions on how to treat these unresearched genetic variations. We present a case of a patient with a combination of cMET mutation (exon 14 skip mutation) and a previously undescribed FGFR fusion (CHRNA6-FGFR1)