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

Naka T, Hatanaka Y, Marukawa K, Okada H, Hatanaka KC, Sakakibara-Konishi J, Oizumi S, Hida Y, Kaga K, Mitsuhashi T, Matsuno Y - Diagn Pathol (2016)

Bottom Line: 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.PAC did not harbor CNAs that have been identified in asbestos-associated lung cancer, but did harbor some of the CNAs associated with smoking.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Surgical Pathology, Hokkaido University Hospital, Kita 14, Nishi 5, Kita-ku, Sapporo, Hokkaido, 060-8648, Japan.

ABSTRACT

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.

No MeSH data available.


Related in: MedlinePlus

Macroscopic appearance of the synchronous collision tumor. A cross-section of the resected specimen shows diffuse pleural thickening confluent with the multinodular grayish-white solid tumor (red arrow), and an intrapulmonary tumor showing an irregular and ill-defined border and a gray-white cut surface (blue arrow) colliding within the left lower lobe of the lung
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Fig1: Macroscopic appearance of the synchronous collision tumor. A cross-section of the resected specimen shows diffuse pleural thickening confluent with the multinodular grayish-white solid tumor (red arrow), and an intrapulmonary tumor showing an irregular and ill-defined border and a gray-white cut surface (blue arrow) colliding within the left lower lobe of the lung

Mentions: Cross-sectional examination of the resected specimen showed that the left lung was widely covered by diffuse pleural thickening confluent with the multinodular grayish-white solid tumor (Fig. 1). The tumor involved both the parietal and visceral pleurae, invading the diaphragm and mediastinal tissues surrounding the thoracic aorta. In the close vicinity of this major pleural tumor described above, an intrapulmonary tumor was found in the lower lobe (Fig. 1). This latter tumor had an ill-defined border and a gray-white cut surface. This intrapulmonary tumor had not been demonstrated in the preoperative imaging work-up.Fig. 1


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

Naka T, Hatanaka Y, Marukawa K, Okada H, Hatanaka KC, Sakakibara-Konishi J, Oizumi S, Hida Y, Kaga K, Mitsuhashi T, Matsuno Y - Diagn Pathol (2016)

Macroscopic appearance of the synchronous collision tumor. A cross-section of the resected specimen shows diffuse pleural thickening confluent with the multinodular grayish-white solid tumor (red arrow), and an intrapulmonary tumor showing an irregular and ill-defined border and a gray-white cut surface (blue arrow) colliding within the left lower lobe of the lung
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4836188&req=5

Fig1: Macroscopic appearance of the synchronous collision tumor. A cross-section of the resected specimen shows diffuse pleural thickening confluent with the multinodular grayish-white solid tumor (red arrow), and an intrapulmonary tumor showing an irregular and ill-defined border and a gray-white cut surface (blue arrow) colliding within the left lower lobe of the lung
Mentions: Cross-sectional examination of the resected specimen showed that the left lung was widely covered by diffuse pleural thickening confluent with the multinodular grayish-white solid tumor (Fig. 1). The tumor involved both the parietal and visceral pleurae, invading the diaphragm and mediastinal tissues surrounding the thoracic aorta. In the close vicinity of this major pleural tumor described above, an intrapulmonary tumor was found in the lower lobe (Fig. 1). This latter tumor had an ill-defined border and a gray-white cut surface. This intrapulmonary tumor had not been demonstrated in the preoperative imaging work-up.Fig. 1

Bottom Line: 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.PAC did not harbor CNAs that have been identified in asbestos-associated lung cancer, but did harbor some of the CNAs associated with smoking.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Surgical Pathology, Hokkaido University Hospital, Kita 14, Nishi 5, Kita-ku, Sapporo, Hokkaido, 060-8648, Japan.

ABSTRACT

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.

No MeSH data available.


Related in: MedlinePlus