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T. Yusa



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    P2.09 - Mesothelioma (ID 710)

    • Event: WCLC 2017
    • Type: Poster Session with Presenters Present
    • Track: Mesothelioma
    • Presentations: 1
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      P2.09-006 - FISH Analysis of p16 and BAP1 Immunohistochemistry for the Diagnosis of Mesothelioma (ID 9144)

      09:30 - 09:30  |  Author(s): T. Yusa

      • Abstract
      • Slides

      Background:
      Distinction between mesothelioma and reactive mesothelial proliferation is difficult because of cytological and morphological overlap between these conditions. It is also difficult to differentiate sarcomatoid mesothelioma from fibrous pleuritis on biopsy. However, separation of reactive mesothelial proliferation from epithelioid mesothelioma and that of fibrous pleuritis from sarcomatoid mesothelioma is important because of therapeutic option and prognosis of the patients. There are some reports claiming that ancillary techniques such as fluorescence in situ hybridization (FISH) analysis of p16 and immunohistochemistry of BAP1 improve the diagnostic accuracy of mesothelioma. However, reported sensitivity of p16 FISH and BAP1 loss is different depending on the subtype of mesothelioma and on studies from various authors. The aim of this study was to elucidate the frequency of p16 deletion and BAP1 loss in mesotheliomas by multiple institutions in Japan.

      Method:
      We collected 262 malignant pleural mesotheliomas, 29 malignant peritoneal mesotheliomas, 23 cases with reactive mesothelial proliferation, and 37 cases with fibrous pleuritis from Tokyo Women’s Medical University, Chiba Rosai Hospital, Fukuoka University, Hyogo Medical University, Kagawa University, and Kanagawa Cancer Center. FISH analysis was performed with p16 probe. Immunostaining was performed with anti-BAP1 antibody.

      Result:
      We analyzed 262 pleural mesotheliomas (170 epithelioid, 38 biphasic, and 54 sarcomatoid) with p16 FISH, and 92 pleural mesotheliomas (58 epithelioid, 20 biphasic and 14 sarcomatoid) with BAP1 immunohistochemistry. Homozygous deletion (HD) of p16 was observed in 74% of epithelioid, 92% of biphasic, and 100% of sarcomatoid mesotheliomas. BAP1 loss was observed in 64% of epithelioid mesotheliomas and 55% of biphasic mesotheliomas, but not in sarcomatoid mesotheliomas. Concordance of HD of p16 and BAP1 loss between epithelioid and sarcomatoid components of 19 biphasic mesotheliomas was 100%. We analyzed 29 peritoneal mesotheliomas (25 epithelioid, 2 biphasic, and 2 sarcomatoid) with p16 FISH and 9 peritoneal epithelioid mesotheliomas with BAP1 loss. HD of p16 was observed in 52% of epithelioid mesotheliomas, 50% of biphasic mesotheliomas, and 50% of sarcomatoid mesotheliomas. BAP1 loss was observed in 56% of epithelioid mesotheliomas. No case with reactive mesothelial proliferation or fibrous pleuritis harbored HD of p16 and showed BAP1 loss.

      Conclusion:
      Separation of epithelioid or biphasic mesothelioma from reactive mesothelial proliferation may be possible with p16 FISH and/or BAP1 immunohistochemistry. Because all of the pleural sarcomatoid mesotheliomas but no cases with fibrous pleuritis harbor HD of p16, p16 FISH helps the separation of sarcomatoid mesothelioma from fibrous pleuritis, but BAP1 does not.

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