OBJECTIVE: The echinoderm microtubule associated protein-like 4 
(EML4)-anaplastic lymphoma kinase (ALK) fusion gene was identified in patients 
with non-small cell lung cancer. To the best of our knowledge, there are only 
three cell lines harboring the EML4-ALK fusion gene, which have contributed to 
the development of therapeutic strategies. Therefore, we tried to establish a 
new lung cancer cell line harboring EML4-ALK.
METHODS: A 61-year-old Japanese female presented with chest discomfort. She was 
diagnosed with left lung adenocarcinoma with T4N3M1 Stage IV. Although she was 
treated with chemotherapy, her disease progressed with massive pleural effusion. 
Because the EML4-ALK rearrangement was found in a biopsied specimen using 
fluorescence in situ hybridization, she was treated with crizotinib. She did 
well for 3 months.
RESULTS: Tumor cells were obtained from the malignant pleural effusion before 
treatment with crizotinib. Cells continued to proliferate substantially for 
several weeks. The cell line was designated ABC-11. The EML4-ALK fusion protein 
and genes were identified in ABC-11 cells using fluorescence in situ 
hybridization and immunohistochemistry, respectively. ABC-11 cells were 
sensitive to crizotinib and next-generation ALK inhibitors (ceritinib and 
AP26113), as determined by a 
3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. 
Phosphorylated ALK protein and its downstream signaling were suppressed by 
treatment with crizotinib in western blotting. Furthermore, we could transplant 
ABC-11 cells subcutaneously into BALB/c nu/nu mice.
CONCLUSIONS: We successfully established a new lung adenocarcinoma cell line 
harboring the EML4-ALK fusion gene. This cell line could contribute to future 
research of EML4-ALK-positive lung cancer both in vivo and in vitro.