Fig 1: IGF-1 per cent reduction after SSAs treatment and SSTR2 score. (A) Comparison of IGF-1 per cent reduction after 3 months of SSAs treatment with the different SSTR2 IHC scores. (B) Comparison of IGF-1 per cent reduction after 6 months of SSAs treatment with the different SSTR2 IHC scores. Data points represent values for each individual patient. Mean and S.E.M. are also displayed. The Kruskal–Wallis test was used for comparison among the three scores and the Mann–Whitney test for post hoc comparisons. (C) Percentage of patients responsive to SSAs treatment after 3 months compared to SSTR2 IHC score. Chi-square test was used. (D) Percentage of patients responsive to SSAs treatment after 6 months compared to SSTR2 IHC score. The Chi-square test was used. *P < 0.05; **P < 0.01; ***P < 0.001.
Fig 2: IHC analyses of NEC913 patient sample: (A) Primary NEC tumor at the ampulla of Vater. Scale bar represents 3 mm. (B) H&E staining of primary NEC tumor. (C–I) Staining for Ki67, CgA, SYP, SSTR2, ASCL1, p53, and Rb. Scale bar represents 200 µm.
Fig 3: Correlation between SSTR2 immunoreactivity and Ki-67 labeling index (LI). (a–c) In the foregut NETs, SSTR2 was significantly inversely correlated with Ki-67 LI, especially when using the Volante scores and IRSs (p = 0.0049, ? = -0.3709 and p = 0.0099, ? = -0.3418, respectively). (d–f) In the midgut NETs, SSTR2 was positively correlated with Ki-67 LI, although not significantly. (g–i) In the hindgut NETs, SSTR2 was positively correlated with Ki-67 LI, especially when evaluated using the Volante scores and IRSs; the former correlation was significant (p = 0.0044, ? = 0.3339 and p = 0.0600, ? = 0.2244, respectively).
Fig 4: Detection of somatostatin receptor 2 (SST2) agonist extravasation after focused ultrasound-mediated (MRgFUS) disruption of the blood–brain barrier (BBB) in the mouse brain. Control T1-weighted MR images close to the dorsal surface (a) and in deep brain areas (b) obtained before microbubble injection. The gadolinium (Gd)-based contrast enhancement in the FUS-targeted area (c, d; red dotted lines) demonstrates opening of the BBB by microbubble sonication (arrows), which extends from dorsal (c) to ventral (d) brain areas. In the FUS-targeted right cerebral cortex, clear-cut area of agonist-induced SST2 internalization is detected 45 minutes after i.p. injection of SST2 agonist octreotide (shaded area on e). Magnified panels show somatodendritic SST2 immunoreactivity in the FUS-targeted cortex (f) as compared to the homogenous SST2 labelling in the surrounding cortex (g). At high magnification, agonist-induced SST2 internalization within the FUS-targeted area is evidenced by the bright immunofluorescent granules in the cytoplasm (arrows) dorsally in the cortex (Cx; h) and ventrally in the amygdala (A; i). On the control side, SST2 is located at the surface of neurons both in the Cx (j) and in the A (k) (arrowheads). Ro, rostral; L, lateral. Scale bars: a-d, 4 mm; e, 500 µm; f, g, 100 µm; h-k, 10 µm.
Fig 5: In situ detection of SST2/SST2 and SST5/SST5 homo-dimers. Representative in situ PLA experiment performed in GH3 (A), A7 cells (B), and M2 cells (C) showing SST2/SST2 (upper panels) and SST5/SST5 (lower panels) homo-dimers. For SST2/SST2 homo-dimers, mouse anti-HA and rabbit anti-SNAP antibodies were used. For SST5/SST5 homo-dimers, mouse and rabbit anti-SST5 antibodies were used. PLA puncta representing homo-dimers are shown as green dots and nuclei are stained with DAPI in blue. A deconvoluted image of PLA events merged with DAPI is shown. White arrows indicated the localization of PLA puncta. Scale bars: 10 µm.
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