Virtual Library
Start Your Search
K. Kuribayashi
Author of
-
+
P3.03 - Poster Session with Presenters Present (ID 473)
- Event: WCLC 2016
- Type: Poster Presenters Present
- Track: Mesothelioma/Thymic Malignancies/Esophageal Cancer/Other Thoracic Malignancies
- Presentations: 1
- Moderators:
- Coordinates: 12/07/2016, 14:30 - 15:45, Hall B (Poster Area)
-
+
P3.03-003 - Mesothelium Covering Pleural Plaque Is Not Primarily Involved in Asbestos-Induced Mesothelial Carcinogenesis in Human (ID 5638)
14:30 - 14:30 | Author(s): K. Kuribayashi
- Abstract
Background:
Malignant pleural mesothelioma (MPM) initially arises not from the visceral pleura but parietal pleural mesothelial cells in the thoracic cavity. MPM has a close relationship to asbestos exposure in etiology. The carcinogenic potential of asbestos fibers has been linked to their geometry, size, and chemical composition. Long respirable fibers(length>5μm, diameter<3μm) have an increased potential to cause mesothelioma. Asbestos also induces non-neoplastic diseases of the pleura. Pleural plaques are thought to be formed by lymphatic transport of short asbestos fibers from lung parenchyma to lymphatic stomata in the parietal pleura, with the fibers undergoing phagocytosis by macrophages in the submesothelial layer to synthesize collagen. Long fibers are lodged and retained at these stomata orifices to lead to asbestos carcinogenesis. Plaques, almost always, are produced in the parietal pleura, of which surface is covered with a single mesothelial cell layer. In this study, we evaluated whether mesothelium covering pleural plaque was primarily involved in asbestos-induced mesothelial carcinogenesis in human.
Methods:
40 patients with MPM were received a medical thoracoscopy with narrow band imaging(NBI) and autofluorescence imaging(AFI), in addition to white light under local anaesthesia. 10 patients were T1, and 8 were T2 clinical stage. All patients had a free thoracic cavity with pleural effusion. 40/32（80％）patients had a history of asbestos exposure(ex. 20 occupational exposure, 7 environmental exposure, 5 none).
Results:
Small nodules of mesothelioma and plaques were present simultaneously on the parietal pleura in 15 MPM patients. NBI could depict the blood vessels on parietal pleural surface more clearly than white light. T1 tumors changed in color to Brown with NBI, and to magenta with AFI. Plaques were usually sharply demarcated from surrounding the parietal pleura, and were avascular and raised hard yellow to white lesions. Individual plaques were smooth surfaced or composed of small rounded knobs. Small nodules of T1 tumors were visualized on the parietal pleura except for the surface of pleural plaques, where neo-vascularization was clearly demonstrated with NBI. With progress of the clinical stage of MPM(T1⇒T2), implanted small nodule came to be seen on the surface of pleural plaque with AFI and NBI.
Conclusion:
Thoracoscopical examination for early clinical stage of MPM shows that the origin of MPM is the mesothelial cells in the parietal pleura, and that mesothelium covering on the surface of pleural plaque was not primarily involved in asbestos-induced mesothelial carcinogenesis in human.
