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

Table 2.

Characteristics of SSTR2 IHC-positive vs SSTR2 IHC-negative tumors

SSTR IHC-positive PPGLs (n = 101) SSTR IHC-negative PPGLs (n = 101)
Tumor location
 Pheochromocytoma 79 (78.2%) 87 (86.1%)
 Paraganglioma (not head and neck) 10 (9.9%) 8 (7.9%)
 Head and neck paraganglioma 11 (10.9%) 5 (5.0%)
 Not available 1 (1%) 1 (1%)
Tumor size
 >5 cm 22 (21.8%) 35 (34.7)
 <5 cm 56 (55.4%) 61 (60.4%)
 Not available 23 (22.7%) 5 (5.0%)
Clustera
 1A 17 (16.8%) 1 (1%)
 1B 2 (2.0%) 15 (14.9%)
 2 30 (29.7%) 18 (17.8%)
 No mutation 22 (21.8%) 19 (18.8%)
 Incomplete sequencing 30 (29.7%) 48 (47.5%)
Ki-67
 Ki-67 ≥ 3% 19 (18.8%) 20 (19.8%)
 Ki-67 < 3% 73 (72.3%) 67 (66.3%)
 Not available 9 (9.0%) 14 (13.9%)
SDHB IHC positive
 yes 82 (81.2%) 95 (94.1%)
 No 14 (13.9%) 6 (5.9%)
 Not available 5 (5.0%)

Abbreviations: IHC, immunohistochemistry; PPGL, pheochromocytoma and paraganglioma; SDHB, succinate dehydrogenase subunit B; SSTR, somatostatin receptor.

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).