Comparative genetic analysis of a rare synchronous collision tumor composed of malignant pleural mesothelioma and primary pulmonary adenocarcinoma

Naka, Tomoaki; Hatanaka, Yutaka; Marukawa, Katsuji; Okada, Hiromi; Hatanaka, Kanako C.; Sakakibara-Konishi, Jun; Oizumi, Satoshi; Hida, Yasuhiro; Kaga, Kichizo; Mitsuhashi, Tomoko; Matsuno, Yoshihiro

Comparative genetic analysis of a rare synchronous collision tumor composed of malignant pleural mesothelioma and primary pulmonary adenocarcinoma

Naka, Tomoaki; Hatanaka, Yutaka; Marukawa, Katsuji et al.

Diagnostic pathology, 2016, 11, 38

Permalink : https://hdl.handle.net/2115/62282

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アクセス権	open access
URI	https://hdl.handle.net/2115/62282
タイトル	Comparative genetic analysis of a rare synchronous collision tumor composed of malignant pleural mesothelioma and primary pulmonary adenocarcinoma
著者	Naka, Tomoaki ; Hatanaka, Yutaka ; Marukawa, Katsuji ; Okada, Hiromi ; Hatanaka, Kanako C. ; Sakakibara-Konishi, Jun ; Oizumi, Satoshi ; Hida, Yasuhiro ; Kaga, Kichizo ; Mitsuhashi, Tomoko ; Matsuno, Yoshihiro
著者名 Naka, Tomoaki
e-Rad_Researcher 30589924 著者名 Hatanaka, Yutaka
著者名 Marukawa, Katsuji
著者名 Okada, Hiromi
著者名 Hatanaka, Kanako C.
e-Rad_Researcher 50374278 著者名 Sakakibara-Konishi, Jun
e-Rad_Researcher 10421968 著者名 Oizumi, Satoshi
e-Rad_Researcher 30399919 著者名 Hida, Yasuhiro
e-Rad_Researcher 80224335 著者名 Kaga, Kichizo
e-Rad_Researcher 60348208 著者名 Mitsuhashi, Tomoko
e-Rad_Researcher 00199829 著者名 Matsuno, Yoshihiro
言語	英語
キーワード	Copy number alteration
	Collision tumor
	Malignant pleural mesothelioma
発行日	2016-04-18
出版者	BioMed Central
収録物名	Diagnostic pathology
巻(号)	11
ページ	38
抄録	Background: Although asbestos acts as a potent carcinogen in pleural mesothelial and pulmonary epithelial cells, it still remains unclear whether asbestos causes specific and characteristic gene alterations in these different kinds of target cells, because direct comparison in an identical patient is not feasible. We experienced a rare synchronous collision tumor composed of malignant pleural mesothelioma (MPM) and primary pulmonary adenocarcinoma (PAC) in a 77-year-old man with a history of long-term smoking and asbestos exposure, and compared the DNA copy number alteration (CNA) and somatic mutation in these two independent tumors. Methods: Formalin-fixed paraffin-embedded (FFPE) tissues of MPM and PAC lesions from the surgically resected specimen were used. Each of these MPM and PAC lesions exhibited a typical histology and immunophenotype. CNA analysis using SNP array was performed using the Illumina Human Omni Express-12_FFPE (Illumina, San Diego, CA, USA) with DNA extracts from each lesion. Somatic mutation analysis using next-generation sequencing was performed using the TruSeq Amplicon Cancer Panel (Illumina). Results: The CNA analysis demonstrated a marked difference in the frequency of gain and loss between MPM and PAC. In PAC, copy number (CN) gain was detected more frequently and widely than CN loss, whereas in MPM there was no such obvious difference. PAC did not harbor CNAs that have been identified in asbestos-associated lung cancer, but did harbor some of the CNAs associated with smoking. MPM exhibited CN loss at 9p21.2-3, which is the most common genetic alteration in mesothelioma. Conclusion: In this particular case, asbestos exposure may not have played a primary role in PAC carcinogenesis, but cigarette smoking may have contributed more to the occurrence of CN gains in PAC. This comparative genetic analysis of two different lesions with same amount of asbestos exposure and cigarette smoke exposure has provided information on differences in the cancer genome related to carcinogenesis.
資源タイプ	学術雑誌論文
出版タイプ	Version of Record
権利情報	Creative Commons Attribution 4.0 International
PISSN	1746-1596
関連情報	PMID 27091358
関連情報 (isIdenticalTo)	出版社版DOI https://doi.org/10.1186/s13000-016-0488-0