Clinicopathological features of younger (aged ≤ 50 years) lung adenocarcinoma patients harboring the EML4‐ALK fusion gene

Background The EML4‐ALK fusion gene has recently been identified as a driver mutation in a subset of non‐small cell lung cancers. In subsequent studies, EML4 ‐ ALK has been detected in a low percentage of patients, and was associated with a lack of EGFR or KRAS mutations, younger age, and adenocarcinoma with acinar histology. Cases with the EML4 ‐ ALK fusion gene were examined to clarify the clinicopathological characteristics of young adenocarcinoma patients. Methods Between December 1998 and May 2009, 85 patients aged ≤ 50 with lung adenocarcinoma were treated at our hospital. We examined 49 samples from adenocarcinoma patients who underwent surgical resection, chemotherapy, and/or radiotherapy for the EML4 ‐ ALK gene. None of the patients received ALK inhibitors because these drugs had not been approved in Japan before 2012. EML4 ‐ ALK fusion genes were screened using multiplex reverse‐transcription PCR assay, and were confirmed by direct sequencing. Results The EML4 ‐ ALK fusion gene was detected in five tumors (10.2%). One patient had stage IB disease, one had stage IIIA, and three had stage IV. Histologically, there was one solid adenocarcinoma, two acinar adenocarcinomas, and two papillary adenocarcinomas. EML4 ‐ ALK fusion genes were mutually exclusive to EGFR and KRAS mutations. The five‐year survival rate was 59.4% in patients without EML4 ‐ ALK fusion and was not reached in patients with EML4 ‐ ALK fusion. Conclusion The EML4 ‐ ALK fusion gene may be a strong oncogene in younger patients with lung adenocarcinoma.