Open AccessSmall non‐mucinous bronchioloalveolar carcinoma with anaplastic lymphoma kinase immunoreactivity: A novel ALK fusion gene?
Author(s) -
Yamamoto Morio,
Takeuchi Kengo,
Shimoji Masaki,
Maniwa Tomohiro,
Isaka Mitsuhiro,
Nakagawa Kazuo,
Ohde Yasuhisa,
Kondo Haruhiko,
Nakajima Takashi
Publication year - 2012
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/j.1349-7006.2011.02136.x
Subject(s) - anaplastic lymphoma kinase , fusion gene , cancer research , mucinous carcinoma , pathology , anaplastic large cell lymphoma , anaplastic carcinoma , lymphoma , medicine , carcinoma , gene , biology , adenocarcinoma , lung cancer , cancer , genetics , malignant pleural effusion
Echinoderm microtubule‐associated protein‐like 4 and anaplastic lymphoma kinase ( EML4–ALK ) and kinesin family member 5B ( KIF5B ) –ALK are newly identified transforming fusion oncogenes causing non‐small‐cell lung cancers. These molecular abnormalities have become detectable using not only molecular biological methods, but also highly sensitive immunohistochemistry. During the immunohistochemical study of ALK expression in adenocarcinoma of the lung, we unexpectedly discovered that a small bronchioloalveolar carcinoma (BAC) showed strong ALK immunoreactivity. However, FISH studies failed to reveal EML4–ALK and KIF5B–ALK fusion genes in this BAC. These findings suggest the possibility that a novel or unknown ALK fusion gene plays a crucial role in BAC development. ( Cancer Sci 2012; 103: 390–392)