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. Author manuscript; available in PMC: 2015 Oct 21.
Published in final edited form as: Mod Pathol. 2013 Jul 26;27(2):231–237. doi: 10.1038/modpathol.2013.142

Figure 1.

Figure 1

Representative images of histological appearance (hematoxylin–eosin, HE), p16 immunostaining, and fluorescence in-situ hybridization for CDKN2A of benign Brenner tumor (BT) and atypical proliferative Brenner tumor (APBT). Benign BT shows intense and diffuse epithelial p16 positivity, both cytoplasmic and nuclear, and normal copy number (either 1 or 2) for CDKN2A (red) as compared with centromere region (CEP9, green) in both epithelial cells (filled arrow) and stromal cells (empty arrow). APBT is consistently negative for p16 and shows complete loss of CDKN2A (red) and retention of centromere 9 (CEP9, green) in the majority of epithelial cells (filled arrow) as compared with stromal cells, where both signals are identified in normal number (empty arrow). Higher magnification in the insets.