PARD3-ALK: A novel ALK fusion gene identified in a patient with lung adenocarcinoma

In non-small cell lung cancer (NSCLC), anaplastic lymphoma kinase (ALK) rearrangement is the key targetable oncogenic event. NSCLC patients with ALK rearrangements benefit from ALK tyrosine kinase inhibitors (ALK-TKIs), such as crizotinib, ceritinib, alectinib, brigatinib, lorlatinib [ [1] Katayama R. Therapeutic strategies and mechanisms of drug resistance in anaplastic lymphoma kinase (ALK)-rearranged lung cancer. Pharmacol. Ther. 2017; 177: 1-8 Crossref PubMed Scopus (19) Google Scholar ]. EML4-ALK is the most common type of ALK rearrangement; however, with the development of next generation sequencing (NGS), diverse ALK fusion partner genes have been identified, such as EML6, FBXO11, and CUX1 [ [2] Lin H. Ren G. Liang X. A novel EML6-ALK FBXO11-ALK double fusion variant in lung adenocarcinoma and response to Crizotinib. J. Thorac. Oncol. 2018; 13: e234-e236 Abstract Full Text Full Text PDF PubMed Scopus (6) Google Scholar , [3] Zhang M. Wang Q. Ding Y. Wang G. Chu Y. He X. et al. CUX1-ALK, a novel ALK rearrangement that responds to crizotinib in non-small cell lung cancer. J. Thorac. Oncol. 2018; 13: 1792-1797 Abstract Full Text Full Text PDF PubMed Scopus (13) Google Scholar ]. Here, we report a case of lung adenocarcinoma which carries a novel partition-defective 3 (PARD3)-ALK gene fusion identified by NGS.