1.Ovarian Clear Cell Carcinoma Sub-Typing by ARID1A Expression.
Jae Yoon CHOI ; Hyun Ho HAN ; Young Tae KIM ; Joo Hyun LEE ; Baek Gil KIM ; Suki KANG ; Nam Hoon CHO
Yonsei Medical Journal 2017;58(1):59-66
PURPOSE: Loss of AT-rich DNA-interacting domain 1A (ARID1A) has been identified as a driving mutation of ovarian clear cell carcinoma (O-CCC), a triple-negative ovarian cancer that is intermediary between serous and endometrioid subtypes, in regards to molecular and clinical behaviors. However, about half of O-CCCs still express BAF250a, the protein encoded by ARID1A. Herein, we aimed to identify signatures of ARID1A-positive O-CCC in comparison with its ARID1A-negative counterpart. MATERIALS AND METHODS: Seventy cases of O-CCC were included in this study. Histologic grades and patterns of primary tumor, molecular marker immunohistochemistry profiles, and clinical outcomes were analyzed. RESULTS: Forty-eight (69%) O-CCCs did not express BAF250a, which were designated as "ARID1A-negative." The other 22 (31%) O-CCCs were designated as "ARID1A-positive." ARID1A-positive tumors were more likely to be histologically of high grades (41% vs. 10%, p=0.003), ERβ-positive (45% vs. 17%, p=0.011), and less likely to be HNF1β-positive (77% vs. 96%, p=0.016) and E-cadherin-positive (59% vs. 83%, p=0.028) than ARID1A-negative tumors. Patient age, parity, tumor stage were not significantly different in between the two groups. Cancer-specific survival was not significantly different either. CONCLUSION: We classified O-CCCs according to ARID1A expression status. ARID1A-positive O-CCCs exhibited distinct immunohistochemical features from ARID1A-negative tumors, suggesting a different underlying molecular event during carcinogenesis.
Adenocarcinoma, Clear Cell/*metabolism/mortality/pathology
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Adult
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Aged
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Biomarkers, Tumor/metabolism
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Cadherins/metabolism
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Estrogen Receptor beta/metabolism
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Female
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Humans
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Immunohistochemistry
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Middle Aged
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Mutation
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Neoplasm Proteins/*metabolism
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Nuclear Proteins/*metabolism
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Ovarian Neoplasms/*metabolism/mortality/pathology
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Transcription Factors/*metabolism