@article{JTD16765,
author = {Katsuhiro Okuda and Takuya Watanabe and Risa Oda and Tadashi Sakane and Osamu Kawano and Hiroshi Haneda and Satoru Moriyama and Ryoichi Nakanishi},
title = {Pulmonary inflammatory myofibroblastic tumor with TPM4-ALK translocation},
journal = {Journal of Thoracic Disease},
volume = {9},
number = {11},
year = {2017},
keywords = {},
abstract = {A 35-year-old woman with shortness of breath and cough was referred to our hospital and agreed to receive therapy for lung tumor in our hospital. Based on the findings from a bronchoscopic biopsy, she was suspected of having pulmonary inflammatory myofibroblastic tumor (IMT), but a correct diagnosis was not indicated. Right upper wedge lobectomy was performed. The findings of a pathological examination of the permanent surgical resected tissue, the ultimate diagnosis was pulmonary IMT. The immunohistochemistry of ALK using the intercalated antibody-enhanced polymer (iAEP) method was positive. We extracted the RNA from frozen surgical resected tumor tissue and proved the tropomyosin alpha-4 chain (TPM4)-ALK by 5' rapid amplification of cDNA end (5' RACE) and reverse transcription polymerase chain reaction. The preoperative bronchial biopsy specimen was also found to be positive for anti-ALK immunohistochemistry with the iAEP method. A molecular therapeutic drug may be useful as personalized therapy for tumors with ALK translocation as oncogenic drivers. We should examine the ALK protein expression and translocation in cases of lung cancer and IMT using an adequate ALK immunohistochemistry system. We experienced a case of pulmonary IMT with TPM4-ALK translocation.},
issn = {2077-6624}, url = {https://jtd.amegroups.org/article/view/16765}
}