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. 2023 Mar 22;108(10):2676–2685. doi: 10.1210/clinem/dgad166

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© The Author(s) 2023. Published by Oxford University Press on behalf of the Endocrine Society.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 2. — (A) Mean SSTR2 staining intensity in SDHx-related PPGLs compared with PPGLs without SDHx mutations. SSTR2 IHC staining intensity was scored semiquantitatively according to the Volante score (0 = absence of staining, 3 = strong staining). Statistical significance is denoted with stars (*P < .05). Error bars show standard error of the mean (SEM). (B) Mean SSTR2 staining intensity according to cluster. SSTR2 IHC staining intensity was scored semiquantitatively according to the Volante score (0 = absence of staining, 3 = strong staining). According to their mutation profile, PPGLs are divided into 3 main molecular clusters: (1) pseudohypoxia cluster (1A and 1B), (2) kinase-signaling cluster 2, and (3) Wnt signaling cluster 3. Cluster 1 is further divided into cluster 1A (mutations in the Krebs cycle associated genes) and 1B (mutations in the hypoxia-signaling pathway). Statistical significance is denoted with stars (***P < .001). Error bars show standard error of the mean (SEM).