sstr2 Search Results


90
Novus Biologicals sstr2 alexa fluor 594 antibody
Figure 4. SCLC subtypes possess unique therapeutic vulnerabilities (A) Comparison between each SCLC cell line subtype of mean relative in vitro IC50 values for PARP inhibitors, nucleoside analogues, anti-folates, AURK inhibitors, and BCL2 inhibitors (A). (B and C) Comparison if IC50 values for cisplatin (B) and the PARPi olaparib (C) among SCLC-A cell lines separated into high and low SLFN11 expression. (D) IHC analysis of tumors representing each subtype (representative images for SCLC-A and -N; and n = 1 each for SCLC-P and -I) for expression of BCL2, with associated H-score noted (D). (E) Western blot showing expression of E-cadherin and Vimentin in H-841 cell line with addition of TGFb (EMT inducer) and mocetinostat (E). (F) Murine H841 flank cell line xenograft growth curves with vehicle or mocetinostat treatment (F). (G–J) Mean expression of the cell surface protein encoding gene <t>SSTR2</t> in multiple datasets (G-I) along with flow cytometry analysis of proportion of analyzed cells that express SSTR2 protein in subtyped cell lines (J). Sample sizes: n = 62 cell lines (A, H), n = 38 cell lines (B-C), n = 8 mouse tumors per treatment arm 81 tumors (G), n = 23 tumors (I), and n = 18 cell lines (J). p values are the result of one-way two-sided t test (B-C) or one-way ANOVA (A, G-J). Error bars: ± 1.5x interquartile range (B, C, G–J) or ± SEM (F).
Sstr2 Alexa Fluor 594 Antibody, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sstr2/pm33482121-333-14-19?v=Novus+Biologicals
Average 90 stars, based on 1 article reviews
sstr2 alexa fluor 594 antibody - by Bioz Stars, 2026-08
90/100 stars
  Buy from Supplier

94
R&D Systems sstr5
Figure 1 Expression of SSTR2 and <t>SSTR5</t> by NET cell lines. (A) WB of membrane extracts from CM, BON1, QGP1, H727 and CNDT2.5 cell lines. Na+/K+ATPase membrane expression was used as loading control. (B) Representative flow cytometry analysis of SSTR2 and SSTR5 expression in CM and BON1 cells as well as in HAP1 cells as negative control. (C) Representative confocal microscopy evaluation of SSTR2 and SSTR5 expression in CM and BON1 cells. For both flow cytometry and confocal microscopy experiments permeabilization procedures were omitted to allow detection of membrane SSTRs only. SSTRs, somatostatin receptors; WB, Western blot.
Sstr5, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sstr2/pm35764366-64-6-11?v=R%26D+Systems
Average 94 stars, based on 1 article reviews
sstr5 - by Bioz Stars, 2026-08
94/100 stars
  Buy from Supplier

93
R&D Systems antibody against sstr2
(A) Representative images showing increased expression of <t>SSTR2</t> in TC compared with normal thyroid documented by immunostaining (Supplemental Table 1). PNET – positive control-pancreatic neuroendocrine tumor; No SSTR2 Antibodies (Ab) – negative control; FTC- follicular thyroid cancer, PTC- papillary thyroid cancer, PDTC – poorly differentiated thyroid cancer, MTC – medullary thyroid cancer, HTC – Hürthle cell thyroid cancer
Antibody Against Sstr2, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sstr2/pmc09531406-102-12-16?v=R%26D+Systems
Average 93 stars, based on 1 article reviews
antibody against sstr2 - by Bioz Stars, 2026-08
93/100 stars
  Buy from Supplier

85
R&D Systems anti human sstr2
(A) Representative images showing increased expression of <t>SSTR2</t> in TC compared with normal thyroid documented by immunostaining (Supplemental Table 1). PNET – positive control-pancreatic neuroendocrine tumor; No SSTR2 Antibodies (Ab) – negative control; FTC- follicular thyroid cancer, PTC- papillary thyroid cancer, PDTC – poorly differentiated thyroid cancer, MTC – medullary thyroid cancer, HTC – Hürthle cell thyroid cancer
Anti Human Sstr2, supplied by R&D Systems, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sstr2/pmc05111513-438-31-33?v=R%26D+Systems
Average 85 stars, based on 1 article reviews
anti human sstr2 - by Bioz Stars, 2026-08
85/100 stars
  Buy from Supplier

91
R&D Systems alexa fluor 488 conjugated anti sstr2
(A) Representative images showing increased expression of <t>SSTR2</t> in TC compared with normal thyroid documented by immunostaining (Supplemental Table 1). PNET – positive control-pancreatic neuroendocrine tumor; No SSTR2 Antibodies (Ab) – negative control; FTC- follicular thyroid cancer, PTC- papillary thyroid cancer, PDTC – poorly differentiated thyroid cancer, MTC – medullary thyroid cancer, HTC – Hürthle cell thyroid cancer
Alexa Fluor 488 Conjugated Anti Sstr2, supplied by R&D Systems, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sstr2/10__1158_slash_1535___7163__mct___22___0798-105-11-20?v=R%26D+Systems
Average 91 stars, based on 1 article reviews
alexa fluor 488 conjugated anti sstr2 - by Bioz Stars, 2026-08
91/100 stars
  Buy from Supplier

92
R&D Systems anti sstr2
(A) Representative images showing increased expression of <t>SSTR2</t> in TC compared with normal thyroid documented by immunostaining (Supplemental Table 1). PNET – positive control-pancreatic neuroendocrine tumor; No SSTR2 Antibodies (Ab) – negative control; FTC- follicular thyroid cancer, PTC- papillary thyroid cancer, PDTC – poorly differentiated thyroid cancer, MTC – medullary thyroid cancer, HTC – Hürthle cell thyroid cancer
Anti Sstr2, supplied by R&D Systems, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sstr2/bio_rxiv__2022__04__25__489401-64-20-25?v=R%26D+Systems
Average 92 stars, based on 1 article reviews
anti sstr2 - by Bioz Stars, 2026-08
92/100 stars
  Buy from Supplier

93
OriGene sstr2
Fig. 1. Baseline <t>SSTR2</t> expression varies in mouse mammary carcinoma cell lines. (a) Representative Western blot showing mouse mammary carcinoma cell lines basal expression of SSTR2 (~ 76 kDa) relative to β-actin (42 kDa). ThermoFisher MagicMark XP ladder is in the left lane and H727 pulmonary NET cells are used as a positive control. (b) Immunohistochemical data showing somatostatin expression in untreated syngeneic EO771 (top) and 4T1 (bottom) mouse breast cancer tumors with matched hematoxylin and eosin slides. Scale bar represents 50 µm. (c) Quantification of SSTR2 IHC staining in untreated EO771 and 4T1 tumors via MATLAB code (n = 7). (d) Cellular uptake of [52Mn]Mn-DOTATATE shows EO771 cells have significantly higher uptake compared to 4T1 cells (p = 0.0003 for 0.001, p = 0.0004 for 0.01, p = 0.0087 for 0.1). Uptake was normalized to milligram of protein and represented as % cell uptake/mg of protein (n = 4 per group).
Sstr2, supplied by OriGene, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sstr2/pm40121305-64-14-65?v=OriGene
Average 93 stars, based on 1 article reviews
sstr2 - by Bioz Stars, 2026-08
93/100 stars
  Buy from Supplier

93
R&D Systems sstr2
Comparison of Prodigy manufactured CAR T cells for cell expansion, viability, transduction, VCN, and subsets. ( A ) A schematic of the insert sequence of AIC100 lentiviral vector. SS = signal sequence; TM = transmembrane; Cyt = cytosolic domain; hSSTR2 = human <t>SSTR2.</t> DNA ruler is shown above features. ( B , C ) Cell expansion and viability were quantified manually by hemocytometer. CD3 and CD4/CD8 subsets, and CAR positive cells were analyzed by flow cytometer. VCN was determined by ddPCR. ( D ) CAR expression was determined by dual labeling of cells by anti-Myc and anti-SSTR2 antibodies for CD4/CD8 sorted cells (day 0) and T cells harvested from Prodigy (day 9, 10, or 11).
Sstr2, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sstr2/pmc06650612-265-13-15?v=R%26D+Systems
Average 93 stars, based on 1 article reviews
sstr2 - by Bioz Stars, 2026-08
93/100 stars
  Buy from Supplier

91
Novus Biologicals rabbit polyclonal antibody to sstr2
Immunostaining of IHCC tumor tissue for <t>SSTR2</t> and Bcl2. a Expression of SSTR2 was only observed in the cell membrane of the cancer cells (× 200 magnification). b Expression of Bcl2 was observed in the cytoplasm of the cancer cells (× 200 magnification). c Expression of SSTR2 was observed in the normal large bile duct (× 200 magnification). d Expression of Bcl2 was observed in the normal small bile duct including bile ductule (× 200 magnification). IHCC: intrahepatic cholangiocarcinoma, SSTR2: <t>somatostatin</t> <t>receptor</t> <t>2,</t> Bcl2: b cell leukemia/lymphoma 2
Rabbit Polyclonal Antibody To Sstr2, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sstr2/pmc08106133-102-7-17?v=Novus+Biologicals
Average 91 stars, based on 1 article reviews
rabbit polyclonal antibody to sstr2 - by Bioz Stars, 2026-08
91/100 stars
  Buy from Supplier

90
Novus Biologicals phosphorylation independent sst2a antibody
Immunostaining of IHCC tumor tissue for <t>SSTR2</t> and Bcl2. a Expression of SSTR2 was only observed in the cell membrane of the cancer cells (× 200 magnification). b Expression of Bcl2 was observed in the cytoplasm of the cancer cells (× 200 magnification). c Expression of SSTR2 was observed in the normal large bile duct (× 200 magnification). d Expression of Bcl2 was observed in the normal small bile duct including bile ductule (× 200 magnification). IHCC: intrahepatic cholangiocarcinoma, SSTR2: <t>somatostatin</t> <t>receptor</t> <t>2,</t> Bcl2: b cell leukemia/lymphoma 2
Phosphorylation Independent Sst2a Antibody, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sstr2/pmc03349840-55-9-13?v=Novus+Biologicals
Average 90 stars, based on 1 article reviews
phosphorylation independent sst2a antibody - by Bioz Stars, 2026-08
90/100 stars
  Buy from Supplier

93
Santa Cruz Biotechnology antibodies against sstr2
Figure 5. The effects of Notch1 active form ICN1 or the combination of VPA and <t>SSTR2-targeted</t> peptide–drug conjugate CPT-SST on BON cell growth. As shown, ICN1 overexpression by transient transfection-induced cell proliferation suppression (A). The in vitro assay showed that VPA and the conjugate CPT-SST suppressed cell proliferation in a dose-dependent manner, with VPA at 2.5 mM significantly enhanced CPT-SST’s suppressive effects (B). The in vivo assay showed that the combination at lower doses (50 mg/kg (VPA) + 0.5 mg/kg (CPT-SST)) significantly suppressed tumor growth compared to each alone. The suppressive rates are 66.02% (the combination), 16.78% (VPA: 200 mg/kg) and 41.48% (CPT-SST: 1 mg/kg).
Antibodies Against Sstr2, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sstr2/10__3109_slash_1061186x__2015__1066794-53-0-36?v=Santa+Cruz+Biotechnology
Average 93 stars, based on 1 article reviews
antibodies against sstr2 - by Bioz Stars, 2026-08
93/100 stars
  Buy from Supplier

Image Search Results


Figure 4. SCLC subtypes possess unique therapeutic vulnerabilities (A) Comparison between each SCLC cell line subtype of mean relative in vitro IC50 values for PARP inhibitors, nucleoside analogues, anti-folates, AURK inhibitors, and BCL2 inhibitors (A). (B and C) Comparison if IC50 values for cisplatin (B) and the PARPi olaparib (C) among SCLC-A cell lines separated into high and low SLFN11 expression. (D) IHC analysis of tumors representing each subtype (representative images for SCLC-A and -N; and n = 1 each for SCLC-P and -I) for expression of BCL2, with associated H-score noted (D). (E) Western blot showing expression of E-cadherin and Vimentin in H-841 cell line with addition of TGFb (EMT inducer) and mocetinostat (E). (F) Murine H841 flank cell line xenograft growth curves with vehicle or mocetinostat treatment (F). (G–J) Mean expression of the cell surface protein encoding gene SSTR2 in multiple datasets (G-I) along with flow cytometry analysis of proportion of analyzed cells that express SSTR2 protein in subtyped cell lines (J). Sample sizes: n = 62 cell lines (A, H), n = 38 cell lines (B-C), n = 8 mouse tumors per treatment arm 81 tumors (G), n = 23 tumors (I), and n = 18 cell lines (J). p values are the result of one-way two-sided t test (B-C) or one-way ANOVA (A, G-J). Error bars: ± 1.5x interquartile range (B, C, G–J) or ± SEM (F).

Journal: Cancer cell

Article Title: Patterns of transcription factor programs and immune pathway activation define four major subtypes of SCLC with distinct therapeutic vulnerabilities.

doi: 10.1016/j.ccell.2020.12.014

Figure Lengend Snippet: Figure 4. SCLC subtypes possess unique therapeutic vulnerabilities (A) Comparison between each SCLC cell line subtype of mean relative in vitro IC50 values for PARP inhibitors, nucleoside analogues, anti-folates, AURK inhibitors, and BCL2 inhibitors (A). (B and C) Comparison if IC50 values for cisplatin (B) and the PARPi olaparib (C) among SCLC-A cell lines separated into high and low SLFN11 expression. (D) IHC analysis of tumors representing each subtype (representative images for SCLC-A and -N; and n = 1 each for SCLC-P and -I) for expression of BCL2, with associated H-score noted (D). (E) Western blot showing expression of E-cadherin and Vimentin in H-841 cell line with addition of TGFb (EMT inducer) and mocetinostat (E). (F) Murine H841 flank cell line xenograft growth curves with vehicle or mocetinostat treatment (F). (G–J) Mean expression of the cell surface protein encoding gene SSTR2 in multiple datasets (G-I) along with flow cytometry analysis of proportion of analyzed cells that express SSTR2 protein in subtyped cell lines (J). Sample sizes: n = 62 cell lines (A, H), n = 38 cell lines (B-C), n = 8 mouse tumors per treatment arm 81 tumors (G), n = 23 tumors (I), and n = 18 cell lines (J). p values are the result of one-way two-sided t test (B-C) or one-way ANOVA (A, G-J). Error bars: ± 1.5x interquartile range (B, C, G–J) or ± SEM (F).

Article Snippet: Cells were harvested after 72 hr and surface stained against Somatostatin R2 using the SSTR2 Alexa Fluor 594 antibody (Novus Biologicals; IC4224T).

Techniques: Comparison, In Vitro, Analogues, Expressing, Western Blot, Cytometry

Figure 1 Expression of SSTR2 and SSTR5 by NET cell lines. (A) WB of membrane extracts from CM, BON1, QGP1, H727 and CNDT2.5 cell lines. Na+/K+ATPase membrane expression was used as loading control. (B) Representative flow cytometry analysis of SSTR2 and SSTR5 expression in CM and BON1 cells as well as in HAP1 cells as negative control. (C) Representative confocal microscopy evaluation of SSTR2 and SSTR5 expression in CM and BON1 cells. For both flow cytometry and confocal microscopy experiments permeabilization procedures were omitted to allow detection of membrane SSTRs only. SSTRs, somatostatin receptors; WB, Western blot.

Journal: Journal for immunotherapy of cancer

Article Title: Development of anti-somatostatin receptors CAR T cells for treatment of neuroendocrine tumors.

doi: 10.1136/jitc-2022-004854

Figure Lengend Snippet: Figure 1 Expression of SSTR2 and SSTR5 by NET cell lines. (A) WB of membrane extracts from CM, BON1, QGP1, H727 and CNDT2.5 cell lines. Na+/K+ATPase membrane expression was used as loading control. (B) Representative flow cytometry analysis of SSTR2 and SSTR5 expression in CM and BON1 cells as well as in HAP1 cells as negative control. (C) Representative confocal microscopy evaluation of SSTR2 and SSTR5 expression in CM and BON1 cells. For both flow cytometry and confocal microscopy experiments permeabilization procedures were omitted to allow detection of membrane SSTRs only. SSTRs, somatostatin receptors; WB, Western blot.

Article Snippet: The membrane expression of SSTR2 and SSTR5 was evaluated using human- (R&D Systems, cat#FAB4224A; R&D Systems, cat#IC4448G) or mouse- reactive (Novus Biologicals, cat#NB300- 157SS; Novus Biologicals, cat#NB100- 74540) Abs targeting extracellular epitopes of these receptors after omission of cell permeabilization procedures.

Techniques: Expressing, Membrane, Control, Flow Cytometry, Negative Control, Confocal Microscopy, Western Blot

Figure 3 Anti-SSTR CAR T cells exhibit antigen-specific tumoricidal activity. (A) Anti-SSTR CARs endow human T lymphocytes with reactivity against SSTR-expressing targets. By in vitro BLI assay, CAR T cells induced cell death in up to 58% of Luc+ NET cell lines as compared with UT T cells at an E:T ratio of 1:1. The percentage of specific tumor cell lysis was calculated as the ratio between CAR T cell and UT T cell antitumor activity using the formula: % lysis=1-(mean BLI signal in the presence of anti-SSTR CAR T cells/mean BLI signal in the presence of UT cells) x 100%. (B) In vitro BLI assay to evaluate the cytolytic activity of CAR T cells as compared with UT T cells according to increasing E:T ratios after 24 hours of coculture with NET cells. The degree of cytotoxicity induced by CAR T cells increased when the number of effector cells increased. (C) IFN-γ and (D) TNF-α release on 24 hours coculture of NET cells with CAR T cells or UT T cells at an E:T ratio of 1:1. Cytokine production was measured in culture supernatants by ELISA. CD3/CD28 T cell stimulation through TransAct was used for positive control experiments. (E) In vitro BLI assay to investigate the cytolytic activity of CAR T cells as compared with UT T cells against mutant CM cells and parental cells at an E:T ratio of 1:1. (F) Evaluation of the cytotoxic potential of CAR T cells against CM cells harboring wild-type or mutated SSTR2 and/or SSTR5 according to increasing E:T ratios after 24 hours of coculture. (G) IFN-γ and (H) TNF-α release on 24 hours coculture of CAR T cells or UT T cells with mutated or parental CM cells at an E:T ratio of 1:1. All experiments were carried out in technical triplicate using lymphocytes from three healthy donors. Mean values and standard errors are represented in figure. *P<0.05, **p<0.01. CAR, chimeric antigen receptor; E:T, effector:target; NET, neuroendocrine tumor; SSTR, somatostatin receptor; UT, untransduced.

Journal: Journal for immunotherapy of cancer

Article Title: Development of anti-somatostatin receptors CAR T cells for treatment of neuroendocrine tumors.

doi: 10.1136/jitc-2022-004854

Figure Lengend Snippet: Figure 3 Anti-SSTR CAR T cells exhibit antigen-specific tumoricidal activity. (A) Anti-SSTR CARs endow human T lymphocytes with reactivity against SSTR-expressing targets. By in vitro BLI assay, CAR T cells induced cell death in up to 58% of Luc+ NET cell lines as compared with UT T cells at an E:T ratio of 1:1. The percentage of specific tumor cell lysis was calculated as the ratio between CAR T cell and UT T cell antitumor activity using the formula: % lysis=1-(mean BLI signal in the presence of anti-SSTR CAR T cells/mean BLI signal in the presence of UT cells) x 100%. (B) In vitro BLI assay to evaluate the cytolytic activity of CAR T cells as compared with UT T cells according to increasing E:T ratios after 24 hours of coculture with NET cells. The degree of cytotoxicity induced by CAR T cells increased when the number of effector cells increased. (C) IFN-γ and (D) TNF-α release on 24 hours coculture of NET cells with CAR T cells or UT T cells at an E:T ratio of 1:1. Cytokine production was measured in culture supernatants by ELISA. CD3/CD28 T cell stimulation through TransAct was used for positive control experiments. (E) In vitro BLI assay to investigate the cytolytic activity of CAR T cells as compared with UT T cells against mutant CM cells and parental cells at an E:T ratio of 1:1. (F) Evaluation of the cytotoxic potential of CAR T cells against CM cells harboring wild-type or mutated SSTR2 and/or SSTR5 according to increasing E:T ratios after 24 hours of coculture. (G) IFN-γ and (H) TNF-α release on 24 hours coculture of CAR T cells or UT T cells with mutated or parental CM cells at an E:T ratio of 1:1. All experiments were carried out in technical triplicate using lymphocytes from three healthy donors. Mean values and standard errors are represented in figure. *P<0.05, **p<0.01. CAR, chimeric antigen receptor; E:T, effector:target; NET, neuroendocrine tumor; SSTR, somatostatin receptor; UT, untransduced.

Article Snippet: The membrane expression of SSTR2 and SSTR5 was evaluated using human- (R&D Systems, cat#FAB4224A; R&D Systems, cat#IC4448G) or mouse- reactive (Novus Biologicals, cat#NB300- 157SS; Novus Biologicals, cat#NB100- 74540) Abs targeting extracellular epitopes of these receptors after omission of cell permeabilization procedures.

Techniques: Activity Assay, Expressing, In Vitro, Lysis, Enzyme-linked Immunosorbent Assay, Cell Stimulation, Positive Control, Mutagenesis

Figure 5 Anti-SSTR CAR T cells infiltrate human xenografts and murine SSTR-expressing organs. (A) Visualization of SSTR2 (UMB1 mAb) and SSTR5 (UMB5 mAb) within tumor xenografts by IHC. Magnification: ×20. Scale bar: 100 µm. (B) Explanted CM tumor xenografts as well as SSTR-expressing organs such as murine spleen, pancreas and brain were lysed and subjected to DNA extraction. The infiltration of CAR T cells was demonstrated by PCR using primers specific for the anti-SSTR CAR sequence. The purified CAR construct DNA was used for positive control experiments. Distilled water was used in negative control experiments. (C) FAM-labeled and HEX-labeled probes against the CAR sequence and the MKL2 reference gene, respectively, were employed in ddPCR experiments to quantify the infiltration of CM (blue dots) and BON1 xenografts (red dots) by anti-SSTR CAR T cells. An inverse correlation can be observed between CAR T cell infiltration and tumor bioluminescence increase relative to baseline. (D) Anti-SSTR CAR T cells recognize and kill the MIN6 cells, a murine NET cell line expressing SSTR2/5. By in vitro BLI, CAR T cells induced cell death in the 48% of Luc+ MIN6 cells as compared with UT T cells at an E:T ratio of 1:1 after 72 hours of coculture. (E) IFN-γ release on 24 hours coculture of NET cells with CAR T cells or UT T cells at an E:T ratio of 1:1. (F) Histopathological analysis of human NET xenografts and murine pancreas and brain by H&E staining. Extensive necrosis foci could be identified within tumors (arrowhead). Representative microphotographs show the absence of necrosis or other tissue damages in the context of the murine pancreas and brain. Magnification: x20. Scale bar: 100 µm. **P<0.01. CAR, chimeric antigen receptor; ddPCR, droplet digital PCR; E:T, effector:target; IHC, immunohistochemistry; NET, neuroendocrine tumor; SSTR, somatostatin receptor; UT, untransduced.

Journal: Journal for immunotherapy of cancer

Article Title: Development of anti-somatostatin receptors CAR T cells for treatment of neuroendocrine tumors.

doi: 10.1136/jitc-2022-004854

Figure Lengend Snippet: Figure 5 Anti-SSTR CAR T cells infiltrate human xenografts and murine SSTR-expressing organs. (A) Visualization of SSTR2 (UMB1 mAb) and SSTR5 (UMB5 mAb) within tumor xenografts by IHC. Magnification: ×20. Scale bar: 100 µm. (B) Explanted CM tumor xenografts as well as SSTR-expressing organs such as murine spleen, pancreas and brain were lysed and subjected to DNA extraction. The infiltration of CAR T cells was demonstrated by PCR using primers specific for the anti-SSTR CAR sequence. The purified CAR construct DNA was used for positive control experiments. Distilled water was used in negative control experiments. (C) FAM-labeled and HEX-labeled probes against the CAR sequence and the MKL2 reference gene, respectively, were employed in ddPCR experiments to quantify the infiltration of CM (blue dots) and BON1 xenografts (red dots) by anti-SSTR CAR T cells. An inverse correlation can be observed between CAR T cell infiltration and tumor bioluminescence increase relative to baseline. (D) Anti-SSTR CAR T cells recognize and kill the MIN6 cells, a murine NET cell line expressing SSTR2/5. By in vitro BLI, CAR T cells induced cell death in the 48% of Luc+ MIN6 cells as compared with UT T cells at an E:T ratio of 1:1 after 72 hours of coculture. (E) IFN-γ release on 24 hours coculture of NET cells with CAR T cells or UT T cells at an E:T ratio of 1:1. (F) Histopathological analysis of human NET xenografts and murine pancreas and brain by H&E staining. Extensive necrosis foci could be identified within tumors (arrowhead). Representative microphotographs show the absence of necrosis or other tissue damages in the context of the murine pancreas and brain. Magnification: x20. Scale bar: 100 µm. **P<0.01. CAR, chimeric antigen receptor; ddPCR, droplet digital PCR; E:T, effector:target; IHC, immunohistochemistry; NET, neuroendocrine tumor; SSTR, somatostatin receptor; UT, untransduced.

Article Snippet: The membrane expression of SSTR2 and SSTR5 was evaluated using human- (R&D Systems, cat#FAB4224A; R&D Systems, cat#IC4448G) or mouse- reactive (Novus Biologicals, cat#NB300- 157SS; Novus Biologicals, cat#NB100- 74540) Abs targeting extracellular epitopes of these receptors after omission of cell permeabilization procedures.

Techniques: Expressing, DNA Extraction, Sequencing, Purification, Construct, Positive Control, Negative Control, Labeling, In Vitro, Staining, Digital PCR, Immunohistochemistry

(A) Representative images showing increased expression of SSTR2 in TC compared with normal thyroid documented by immunostaining (Supplemental Table 1). PNET – positive control-pancreatic neuroendocrine tumor; No SSTR2 Antibodies (Ab) – negative control; FTC- follicular thyroid cancer, PTC- papillary thyroid cancer, PDTC – poorly differentiated thyroid cancer, MTC – medullary thyroid cancer, HTC – Hürthle cell thyroid cancer

Journal: Clinical cancer research : an official journal of the American Association for Cancer Research

Article Title: 177 Lu-DOTA-EB-TATE, A Radiolabeled Analog of Somatostatin Receptor Type 2, for the Imaging and Treatment of Thyroid Cancer

doi: 10.1158/1078-0432.CCR-20-3453

Figure Lengend Snippet: (A) Representative images showing increased expression of SSTR2 in TC compared with normal thyroid documented by immunostaining (Supplemental Table 1). PNET – positive control-pancreatic neuroendocrine tumor; No SSTR2 Antibodies (Ab) – negative control; FTC- follicular thyroid cancer, PTC- papillary thyroid cancer, PDTC – poorly differentiated thyroid cancer, MTC – medullary thyroid cancer, HTC – Hürthle cell thyroid cancer

Article Snippet: The membranes were incubated overnight at 4 o C with a primary antibody against SSTR2 (1:400, R&D systems, MAB4224), acetylated histone 3 (1:500, Millipore, 06–599) or acetylated histone 4 (1:500, Millipore, 06–598), GAPDH (1:1000; Invitrogen; MA5–15738) and β-actin (1:1000, Santa Cruz Biotechnology, sc-47778).

Techniques: Expressing, Immunostaining, Positive Control, Negative Control

(A, F, K) An increase in SSTR2 mRNA expression in FTC133 (n=4), BCPAP (n=4), and AR42J cells (n=4) upon VAC treatment (2mM and 4Mm; 72h). ***p<0.001, **p<0.01, *p<0.05. C-control; VAC-valproic acid.

Journal: Clinical cancer research : an official journal of the American Association for Cancer Research

Article Title: 177 Lu-DOTA-EB-TATE, A Radiolabeled Analog of Somatostatin Receptor Type 2, for the Imaging and Treatment of Thyroid Cancer

doi: 10.1158/1078-0432.CCR-20-3453

Figure Lengend Snippet: (A, F, K) An increase in SSTR2 mRNA expression in FTC133 (n=4), BCPAP (n=4), and AR42J cells (n=4) upon VAC treatment (2mM and 4Mm; 72h). ***p<0.001, **p<0.01, *p<0.05. C-control; VAC-valproic acid.

Article Snippet: The membranes were incubated overnight at 4 o C with a primary antibody against SSTR2 (1:400, R&D systems, MAB4224), acetylated histone 3 (1:500, Millipore, 06–599) or acetylated histone 4 (1:500, Millipore, 06–598), GAPDH (1:1000; Invitrogen; MA5–15738) and β-actin (1:1000, Santa Cruz Biotechnology, sc-47778).

Techniques: Expressing, Control

Fig. 1. Baseline SSTR2 expression varies in mouse mammary carcinoma cell lines. (a) Representative Western blot showing mouse mammary carcinoma cell lines basal expression of SSTR2 (~ 76 kDa) relative to β-actin (42 kDa). ThermoFisher MagicMark XP ladder is in the left lane and H727 pulmonary NET cells are used as a positive control. (b) Immunohistochemical data showing somatostatin expression in untreated syngeneic EO771 (top) and 4T1 (bottom) mouse breast cancer tumors with matched hematoxylin and eosin slides. Scale bar represents 50 µm. (c) Quantification of SSTR2 IHC staining in untreated EO771 and 4T1 tumors via MATLAB code (n = 7). (d) Cellular uptake of [52Mn]Mn-DOTATATE shows EO771 cells have significantly higher uptake compared to 4T1 cells (p = 0.0003 for 0.001, p = 0.0004 for 0.01, p = 0.0087 for 0.1). Uptake was normalized to milligram of protein and represented as % cell uptake/mg of protein (n = 4 per group).

Journal: Scientific reports

Article Title: Characterizing SSTR2 expression and modulation for targeted imaging and therapy in preclinical models of triple-negative breast cancer.

doi: 10.1038/s41598-025-94578-x

Figure Lengend Snippet: Fig. 1. Baseline SSTR2 expression varies in mouse mammary carcinoma cell lines. (a) Representative Western blot showing mouse mammary carcinoma cell lines basal expression of SSTR2 (~ 76 kDa) relative to β-actin (42 kDa). ThermoFisher MagicMark XP ladder is in the left lane and H727 pulmonary NET cells are used as a positive control. (b) Immunohistochemical data showing somatostatin expression in untreated syngeneic EO771 (top) and 4T1 (bottom) mouse breast cancer tumors with matched hematoxylin and eosin slides. Scale bar represents 50 µm. (c) Quantification of SSTR2 IHC staining in untreated EO771 and 4T1 tumors via MATLAB code (n = 7). (d) Cellular uptake of [52Mn]Mn-DOTATATE shows EO771 cells have significantly higher uptake compared to 4T1 cells (p = 0.0003 for 0.001, p = 0.0004 for 0.01, p = 0.0087 for 0.1). Uptake was normalized to milligram of protein and represented as % cell uptake/mg of protein (n = 4 per group).

Article Snippet: The sequences of the PCR primers used for the analysis of mRNA expression of SSTR2 in this experiment are forward: C A A G C A A T G G C T C C A A C C A G A C, reverse: C T T G G C A T A G C G G A G G A T G A C A (Origene MP215984).

Techniques: Expressing, Western Blot, Positive Control, Immunohistochemical staining, Immunohistochemistry

Fig. 2. PET imaging reveals model-dependent differences in SSTR2 expression. (a) Representative images from EO771 and 4T1 tumor-bearing mice taken 60-min post-injection of 100 ± 20 µCi [68Ga]Ga-DOTATATE on day 0. ROIs encircling tumors are represented by grey dotted circles. (b) Frequency histogram distributions for [68Ga]Ga-DOTATATE uptake in EO771 and 4T1 tumors are represented as the average ± standard deviation, comparison of the two models, and individual animals from each model. (c) SUV values are significantly higher for EO771 tumors compared to 4T1 tumors in the top 10% (p = 0.0014) of frequency distributions (n = 12 for EO771, n = 17 for 4T1).

Journal: Scientific reports

Article Title: Characterizing SSTR2 expression and modulation for targeted imaging and therapy in preclinical models of triple-negative breast cancer.

doi: 10.1038/s41598-025-94578-x

Figure Lengend Snippet: Fig. 2. PET imaging reveals model-dependent differences in SSTR2 expression. (a) Representative images from EO771 and 4T1 tumor-bearing mice taken 60-min post-injection of 100 ± 20 µCi [68Ga]Ga-DOTATATE on day 0. ROIs encircling tumors are represented by grey dotted circles. (b) Frequency histogram distributions for [68Ga]Ga-DOTATATE uptake in EO771 and 4T1 tumors are represented as the average ± standard deviation, comparison of the two models, and individual animals from each model. (c) SUV values are significantly higher for EO771 tumors compared to 4T1 tumors in the top 10% (p = 0.0014) of frequency distributions (n = 12 for EO771, n = 17 for 4T1).

Article Snippet: The sequences of the PCR primers used for the analysis of mRNA expression of SSTR2 in this experiment are forward: C A A G C A A T G G C T C C A A C C A G A C, reverse: C T T G G C A T A G C G G A G G A T G A C A (Origene MP215984).

Techniques: Imaging, Expressing, Injection, Standard Deviation, Comparison

Fig. 3. SAHA increases expression of SSTR2 at the transcriptional, translational, and functional levels of two TNBC cell lines. (a) qRT-PCR shows 4 × increase (p < 0.0001 for 1.7 µM and 3.3 µM) in mRNA expression of Sstr2 expression in EO771 cells treated with SAHA compared to control. (b) qRT-PCR shows 2 × change (p = 0.001 for 3 µM) and almost 8 × increase (p = 0.0009 for 5 µM) in Sstr2 mRNA in 4T1 cells treated with SAHA compared to control. Flow cytometry demonstrates increased cell surface expression of SSTR2 for EO771 (p < 0.0001 for 1.7 µM and 3.3 µM) and 4T1 (p = 0.0001 for 3 µM, p = 0.0006 for 5 µM) cells following SAHA treatment compared to DMSO control (c, d). Cell binding assay with [52n]Mn-DOTATATE shows increased uptake of somatostatin analogue in 4T1 (p < 0.0001 for 3 µM and 5 µM) and EO771 (p = 0.002 for 1.7 µM, p < 0.0001 for 3.3 µM) cells compared to DMSO control after HDACi for 48 h (e, f).

Journal: Scientific reports

Article Title: Characterizing SSTR2 expression and modulation for targeted imaging and therapy in preclinical models of triple-negative breast cancer.

doi: 10.1038/s41598-025-94578-x

Figure Lengend Snippet: Fig. 3. SAHA increases expression of SSTR2 at the transcriptional, translational, and functional levels of two TNBC cell lines. (a) qRT-PCR shows 4 × increase (p < 0.0001 for 1.7 µM and 3.3 µM) in mRNA expression of Sstr2 expression in EO771 cells treated with SAHA compared to control. (b) qRT-PCR shows 2 × change (p = 0.001 for 3 µM) and almost 8 × increase (p = 0.0009 for 5 µM) in Sstr2 mRNA in 4T1 cells treated with SAHA compared to control. Flow cytometry demonstrates increased cell surface expression of SSTR2 for EO771 (p < 0.0001 for 1.7 µM and 3.3 µM) and 4T1 (p = 0.0001 for 3 µM, p = 0.0006 for 5 µM) cells following SAHA treatment compared to DMSO control (c, d). Cell binding assay with [52n]Mn-DOTATATE shows increased uptake of somatostatin analogue in 4T1 (p < 0.0001 for 3 µM and 5 µM) and EO771 (p = 0.002 for 1.7 µM, p < 0.0001 for 3.3 µM) cells compared to DMSO control after HDACi for 48 h (e, f).

Article Snippet: The sequences of the PCR primers used for the analysis of mRNA expression of SSTR2 in this experiment are forward: C A A G C A A T G G C T C C A A C C A G A C, reverse: C T T G G C A T A G C G G A G G A T G A C A (Origene MP215984).

Techniques: Expressing, Functional Assay, Quantitative RT-PCR, Control, Flow Cytometry, Cell Binding Assay

Fig. 4. HDAC inhibition increases SSTR2 expression and overall survival in vivo. (a) Representative images from EO771 and 4T1 tumor-bearing mice at day 0 and 7 of treatment with SAHA (n = 12 EO771, n = 17 4T1) or saline for control animals (n = 4) taken 60-min post-injection of 100 ± 20 µCi [68Ga]Ga-DOTATATE. (b) Quantification of the highest voxel, SUVmax, of [68Ga]Ga-DOTATATE uptake normalized to muscle is significantly increased in EO771 tumors following treatment with SAHA (p = 0.0583). (c) Quantification of SUV shows that radiotracer uptake is significantly higher after treatment with SAHA in the top 10% (right, p = 0.0113) of the frequency distribution for EO771 tumors. (e) [68Ga]Ga-DOTATATE SUVmax normalized to heart and muscle is significantly increased in 4T1 tumors following treatment with SAHA (p = 0.014). (f) SUV uptake in the top 10% (p = 0.0448) of the distribution is significantly increased after SAHA treatment in 4T1 tumors. Overall survival is significantly increased for animals with EO771 tumors (d, p = 0.0043) and 4T1 tumors (g, p = 0.023) treated with SAHA.

Journal: Scientific reports

Article Title: Characterizing SSTR2 expression and modulation for targeted imaging and therapy in preclinical models of triple-negative breast cancer.

doi: 10.1038/s41598-025-94578-x

Figure Lengend Snippet: Fig. 4. HDAC inhibition increases SSTR2 expression and overall survival in vivo. (a) Representative images from EO771 and 4T1 tumor-bearing mice at day 0 and 7 of treatment with SAHA (n = 12 EO771, n = 17 4T1) or saline for control animals (n = 4) taken 60-min post-injection of 100 ± 20 µCi [68Ga]Ga-DOTATATE. (b) Quantification of the highest voxel, SUVmax, of [68Ga]Ga-DOTATATE uptake normalized to muscle is significantly increased in EO771 tumors following treatment with SAHA (p = 0.0583). (c) Quantification of SUV shows that radiotracer uptake is significantly higher after treatment with SAHA in the top 10% (right, p = 0.0113) of the frequency distribution for EO771 tumors. (e) [68Ga]Ga-DOTATATE SUVmax normalized to heart and muscle is significantly increased in 4T1 tumors following treatment with SAHA (p = 0.014). (f) SUV uptake in the top 10% (p = 0.0448) of the distribution is significantly increased after SAHA treatment in 4T1 tumors. Overall survival is significantly increased for animals with EO771 tumors (d, p = 0.0043) and 4T1 tumors (g, p = 0.023) treated with SAHA.

Article Snippet: The sequences of the PCR primers used for the analysis of mRNA expression of SSTR2 in this experiment are forward: C A A G C A A T G G C T C C A A C C A G A C, reverse: C T T G G C A T A G C G G A G G A T G A C A (Origene MP215984).

Techniques: Inhibition, Expressing, In Vivo, Saline, Control, Injection

Comparison of Prodigy manufactured CAR T cells for cell expansion, viability, transduction, VCN, and subsets. ( A ) A schematic of the insert sequence of AIC100 lentiviral vector. SS = signal sequence; TM = transmembrane; Cyt = cytosolic domain; hSSTR2 = human SSTR2. DNA ruler is shown above features. ( B , C ) Cell expansion and viability were quantified manually by hemocytometer. CD3 and CD4/CD8 subsets, and CAR positive cells were analyzed by flow cytometer. VCN was determined by ddPCR. ( D ) CAR expression was determined by dual labeling of cells by anti-Myc and anti-SSTR2 antibodies for CD4/CD8 sorted cells (day 0) and T cells harvested from Prodigy (day 9, 10, or 11).

Journal: Scientific Reports

Article Title: Manufacturing and preclinical validation of CAR T cells targeting ICAM-1 for advanced thyroid cancer therapy

doi: 10.1038/s41598-019-46938-7

Figure Lengend Snippet: Comparison of Prodigy manufactured CAR T cells for cell expansion, viability, transduction, VCN, and subsets. ( A ) A schematic of the insert sequence of AIC100 lentiviral vector. SS = signal sequence; TM = transmembrane; Cyt = cytosolic domain; hSSTR2 = human SSTR2. DNA ruler is shown above features. ( B , C ) Cell expansion and viability were quantified manually by hemocytometer. CD3 and CD4/CD8 subsets, and CAR positive cells were analyzed by flow cytometer. VCN was determined by ddPCR. ( D ) CAR expression was determined by dual labeling of cells by anti-Myc and anti-SSTR2 antibodies for CD4/CD8 sorted cells (day 0) and T cells harvested from Prodigy (day 9, 10, or 11).

Article Snippet: CAR expression was confirmed by antibodies against Myc (Cat #: 130-092-472, Miltenyi) and SSTR2 (FAB4224A, R&D Systems).

Techniques: Comparison, Transduction, Sequencing, Plasmid Preparation, Flow Cytometry, Expressing, Labeling

Effect of SSTR2 expression and activation on CAR T cell activity in vitro and in vivo . ( A ) The level of antibody binding to SSTR2 was measured to assess SSTR2 internalization induced by SSTR2 agonist (lanreotide). ( B ) E to T assay of AIC100 cells with or without 1 μM of lanreotide against 293T and 8505C cells. The ratio of T cells to target cells was 2.5:1 (n = 3 each for P2 and P3). ( C ) A weekly measurement of whole body luminescence to detect tumor growth or killing by AIC100 (P2 and P2b) at MTD doses with or without lanreotide. Lanreotide was administered to mice by intraperitoneal injection at days of 9, 19, 23, 34, and 40 post tumor xenograft. n = 5 for AIC100/Lanreotide; n = 3 for AIC100; n = 4 for No T. Significant difference (p = 0.01) for No T vs. AIC100 or AIC100/Lanreotide; no significance for AIC100 vs. AIC100/Lanreotide by one-way ANOVA with Tukey’s multiple comparisons test.

Journal: Scientific Reports

Article Title: Manufacturing and preclinical validation of CAR T cells targeting ICAM-1 for advanced thyroid cancer therapy

doi: 10.1038/s41598-019-46938-7

Figure Lengend Snippet: Effect of SSTR2 expression and activation on CAR T cell activity in vitro and in vivo . ( A ) The level of antibody binding to SSTR2 was measured to assess SSTR2 internalization induced by SSTR2 agonist (lanreotide). ( B ) E to T assay of AIC100 cells with or without 1 μM of lanreotide against 293T and 8505C cells. The ratio of T cells to target cells was 2.5:1 (n = 3 each for P2 and P3). ( C ) A weekly measurement of whole body luminescence to detect tumor growth or killing by AIC100 (P2 and P2b) at MTD doses with or without lanreotide. Lanreotide was administered to mice by intraperitoneal injection at days of 9, 19, 23, 34, and 40 post tumor xenograft. n = 5 for AIC100/Lanreotide; n = 3 for AIC100; n = 4 for No T. Significant difference (p = 0.01) for No T vs. AIC100 or AIC100/Lanreotide; no significance for AIC100 vs. AIC100/Lanreotide by one-way ANOVA with Tukey’s multiple comparisons test.

Article Snippet: CAR expression was confirmed by antibodies against Myc (Cat #: 130-092-472, Miltenyi) and SSTR2 (FAB4224A, R&D Systems).

Techniques: Expressing, Activation Assay, Activity Assay, In Vitro, In Vivo, Binding Assay, Injection

Immunostaining of IHCC tumor tissue for SSTR2 and Bcl2. a Expression of SSTR2 was only observed in the cell membrane of the cancer cells (× 200 magnification). b Expression of Bcl2 was observed in the cytoplasm of the cancer cells (× 200 magnification). c Expression of SSTR2 was observed in the normal large bile duct (× 200 magnification). d Expression of Bcl2 was observed in the normal small bile duct including bile ductule (× 200 magnification). IHCC: intrahepatic cholangiocarcinoma, SSTR2: somatostatin receptor 2, Bcl2: b cell leukemia/lymphoma 2

Journal: World Journal of Surgical Oncology

Article Title: A new pathological classification of intrahepatic cholangiocarcinoma according to protein expression of SSTR2 and Bcl2

doi: 10.1186/s12957-021-02216-3

Figure Lengend Snippet: Immunostaining of IHCC tumor tissue for SSTR2 and Bcl2. a Expression of SSTR2 was only observed in the cell membrane of the cancer cells (× 200 magnification). b Expression of Bcl2 was observed in the cytoplasm of the cancer cells (× 200 magnification). c Expression of SSTR2 was observed in the normal large bile duct (× 200 magnification). d Expression of Bcl2 was observed in the normal small bile duct including bile ductule (× 200 magnification). IHCC: intrahepatic cholangiocarcinoma, SSTR2: somatostatin receptor 2, Bcl2: b cell leukemia/lymphoma 2

Article Snippet: The sections were incubated with a primary rabbit polyclonal antibody to SSTR2 (NB300-157, diluted 1:200 in PBS; NOVUS Biologicals LLC, Centennial, CO, USA) and a primary mouse monoclonal antibody to Bcl2 (M088701, diluted 1:40 in PBS; Dako, Santa Clara, CA, USA) overnight at 4 °C, respectively.

Techniques: Immunostaining, Expressing, Membrane

Comparison of various factors among three groups of IHCC patients classified by  SSTR2  and Bcl2 expression

Journal: World Journal of Surgical Oncology

Article Title: A new pathological classification of intrahepatic cholangiocarcinoma according to protein expression of SSTR2 and Bcl2

doi: 10.1186/s12957-021-02216-3

Figure Lengend Snippet: Comparison of various factors among three groups of IHCC patients classified by SSTR2 and Bcl2 expression

Article Snippet: The sections were incubated with a primary rabbit polyclonal antibody to SSTR2 (NB300-157, diluted 1:200 in PBS; NOVUS Biologicals LLC, Centennial, CO, USA) and a primary mouse monoclonal antibody to Bcl2 (M088701, diluted 1:40 in PBS; Dako, Santa Clara, CA, USA) overnight at 4 °C, respectively.

Techniques: Comparison, Virus, Infection

Overall survival and disease-free survival of IHCC patients classified by histological type. a Overall survival curves of IHCC patients. The survival of patients in the p-Group P was better than that of those in both the p-Group H and the p-Group U ( p = 0.098, p < 0.05, respectively). b Disease-free survival curves of IHCC patients. The survival of patients in the p-Group P was significantly better than that of those in both the p-Group H and the p-Group U ( p < 0.05). IHCC: intrahepatic cholangiocarcinoma, p-Group P: SSTR2 negative and Bcl2 positive, p-Group H: SSTR2 positive and Bcl2 negative, p-Group U: SSTR2 positive and Bcl2 positive or SSTR2 negative and Bcl2 negative

Journal: World Journal of Surgical Oncology

Article Title: A new pathological classification of intrahepatic cholangiocarcinoma according to protein expression of SSTR2 and Bcl2

doi: 10.1186/s12957-021-02216-3

Figure Lengend Snippet: Overall survival and disease-free survival of IHCC patients classified by histological type. a Overall survival curves of IHCC patients. The survival of patients in the p-Group P was better than that of those in both the p-Group H and the p-Group U ( p = 0.098, p < 0.05, respectively). b Disease-free survival curves of IHCC patients. The survival of patients in the p-Group P was significantly better than that of those in both the p-Group H and the p-Group U ( p < 0.05). IHCC: intrahepatic cholangiocarcinoma, p-Group P: SSTR2 negative and Bcl2 positive, p-Group H: SSTR2 positive and Bcl2 negative, p-Group U: SSTR2 positive and Bcl2 positive or SSTR2 negative and Bcl2 negative

Article Snippet: The sections were incubated with a primary rabbit polyclonal antibody to SSTR2 (NB300-157, diluted 1:200 in PBS; NOVUS Biologicals LLC, Centennial, CO, USA) and a primary mouse monoclonal antibody to Bcl2 (M088701, diluted 1:40 in PBS; Dako, Santa Clara, CA, USA) overnight at 4 °C, respectively.

Techniques:

Comparison of various factors among two groups of grossly peripheral IHCC patients classified by  SSTR2  and Bcl2 expression

Journal: World Journal of Surgical Oncology

Article Title: A new pathological classification of intrahepatic cholangiocarcinoma according to protein expression of SSTR2 and Bcl2

doi: 10.1186/s12957-021-02216-3

Figure Lengend Snippet: Comparison of various factors among two groups of grossly peripheral IHCC patients classified by SSTR2 and Bcl2 expression

Article Snippet: The sections were incubated with a primary rabbit polyclonal antibody to SSTR2 (NB300-157, diluted 1:200 in PBS; NOVUS Biologicals LLC, Centennial, CO, USA) and a primary mouse monoclonal antibody to Bcl2 (M088701, diluted 1:40 in PBS; Dako, Santa Clara, CA, USA) overnight at 4 °C, respectively.

Techniques: Comparison, Virus, Infection

Overall survival and disease-free survival of grossly peripheral IHCC patients classified by histological type. a Overall survival curves of grossly peripheral IHCC patients. The survival of patients in the p-Group P was better than that of those in the p-Group H ( p = 0.150). b Disease-free survival curves of grossly peripheral IHCC patients. The survival of patients in the p-Group P was significantly better than that of those in the p-Group H ( p < 0.05). IHCC: intrahepatic cholangiocarcinoma, p-Group P: SSTR2 negative and Bcl2 positive, p-Group H; SSTR2 positive and Bcl2 negative

Journal: World Journal of Surgical Oncology

Article Title: A new pathological classification of intrahepatic cholangiocarcinoma according to protein expression of SSTR2 and Bcl2

doi: 10.1186/s12957-021-02216-3

Figure Lengend Snippet: Overall survival and disease-free survival of grossly peripheral IHCC patients classified by histological type. a Overall survival curves of grossly peripheral IHCC patients. The survival of patients in the p-Group P was better than that of those in the p-Group H ( p = 0.150). b Disease-free survival curves of grossly peripheral IHCC patients. The survival of patients in the p-Group P was significantly better than that of those in the p-Group H ( p < 0.05). IHCC: intrahepatic cholangiocarcinoma, p-Group P: SSTR2 negative and Bcl2 positive, p-Group H; SSTR2 positive and Bcl2 negative

Article Snippet: The sections were incubated with a primary rabbit polyclonal antibody to SSTR2 (NB300-157, diluted 1:200 in PBS; NOVUS Biologicals LLC, Centennial, CO, USA) and a primary mouse monoclonal antibody to Bcl2 (M088701, diluted 1:40 in PBS; Dako, Santa Clara, CA, USA) overnight at 4 °C, respectively.

Techniques:

Representative images of gross and histological findings in IHCC tumors. a – c CT images showed the presence of a 5.5 cm, low density mass in the S3 segment of the liver in all phases. d The resected specimen showed the presence of a nodular tumor in the S3 segment of the liver. This tumor was consistent with the mass-forming type. e Histologic findings (× 100 magnification) revealed that the tumor consisted of duct-forming, abundant fibrotic stroma. The cancer cells had a clear cytoplasm. f SSTR2 expression can be seen in the cell membrane of IHCC tumor cells (× 100 magnification). g IHCC cancer cells were negative for Bcl2 (× 100 magnification). IHCC: intrahepatic cholangiocarcinoma, CT: computed tomography. SSTR2: somatostatin receptor 2, Bcl2: b-cell leukemia/lymphoma 2

Journal: World Journal of Surgical Oncology

Article Title: A new pathological classification of intrahepatic cholangiocarcinoma according to protein expression of SSTR2 and Bcl2

doi: 10.1186/s12957-021-02216-3

Figure Lengend Snippet: Representative images of gross and histological findings in IHCC tumors. a – c CT images showed the presence of a 5.5 cm, low density mass in the S3 segment of the liver in all phases. d The resected specimen showed the presence of a nodular tumor in the S3 segment of the liver. This tumor was consistent with the mass-forming type. e Histologic findings (× 100 magnification) revealed that the tumor consisted of duct-forming, abundant fibrotic stroma. The cancer cells had a clear cytoplasm. f SSTR2 expression can be seen in the cell membrane of IHCC tumor cells (× 100 magnification). g IHCC cancer cells were negative for Bcl2 (× 100 magnification). IHCC: intrahepatic cholangiocarcinoma, CT: computed tomography. SSTR2: somatostatin receptor 2, Bcl2: b-cell leukemia/lymphoma 2

Article Snippet: The sections were incubated with a primary rabbit polyclonal antibody to SSTR2 (NB300-157, diluted 1:200 in PBS; NOVUS Biologicals LLC, Centennial, CO, USA) and a primary mouse monoclonal antibody to Bcl2 (M088701, diluted 1:40 in PBS; Dako, Santa Clara, CA, USA) overnight at 4 °C, respectively.

Techniques: Expressing, Membrane, Computed Tomography

Analysis of overall survival in IHCC patients

Journal: World Journal of Surgical Oncology

Article Title: A new pathological classification of intrahepatic cholangiocarcinoma according to protein expression of SSTR2 and Bcl2

doi: 10.1186/s12957-021-02216-3

Figure Lengend Snippet: Analysis of overall survival in IHCC patients

Article Snippet: The sections were incubated with a primary rabbit polyclonal antibody to SSTR2 (NB300-157, diluted 1:200 in PBS; NOVUS Biologicals LLC, Centennial, CO, USA) and a primary mouse monoclonal antibody to Bcl2 (M088701, diluted 1:40 in PBS; Dako, Santa Clara, CA, USA) overnight at 4 °C, respectively.

Techniques: Expressing

Figure 5. The effects of Notch1 active form ICN1 or the combination of VPA and SSTR2-targeted peptide–drug conjugate CPT-SST on BON cell growth. As shown, ICN1 overexpression by transient transfection-induced cell proliferation suppression (A). The in vitro assay showed that VPA and the conjugate CPT-SST suppressed cell proliferation in a dose-dependent manner, with VPA at 2.5 mM significantly enhanced CPT-SST’s suppressive effects (B). The in vivo assay showed that the combination at lower doses (50 mg/kg (VPA) + 0.5 mg/kg (CPT-SST)) significantly suppressed tumor growth compared to each alone. The suppressive rates are 66.02% (the combination), 16.78% (VPA: 200 mg/kg) and 41.48% (CPT-SST: 1 mg/kg).

Journal: Journal of Drug Targeting

Article Title: Valproic acid induces NET cell growth arrest and enhances tumor suppression of the receptor-targeted peptide–drug conjugate via activating somatostatin receptor type II

doi: 10.3109/1061186x.2015.1066794

Figure Lengend Snippet: Figure 5. The effects of Notch1 active form ICN1 or the combination of VPA and SSTR2-targeted peptide–drug conjugate CPT-SST on BON cell growth. As shown, ICN1 overexpression by transient transfection-induced cell proliferation suppression (A). The in vitro assay showed that VPA and the conjugate CPT-SST suppressed cell proliferation in a dose-dependent manner, with VPA at 2.5 mM significantly enhanced CPT-SST’s suppressive effects (B). The in vivo assay showed that the combination at lower doses (50 mg/kg (VPA) + 0.5 mg/kg (CPT-SST)) significantly suppressed tumor growth compared to each alone. The suppressive rates are 66.02% (the combination), 16.78% (VPA: 200 mg/kg) and 41.48% (CPT-SST: 1 mg/kg).

Article Snippet: Antibodies against SSTR2 (Cat. No.: sc-11609), p21 (sc-756), p63 (sc-8343), COX2 (sc-7951), Chromogranin A (CgA, sc-13090), Histone 4 (H4, sc-10810), Histone deacetylase 4 (HDAC4, sc-11418), Acetylated histone 4 (AcH4, sc8660-R) and b-actin (sc-1616-HRP) were purchased from Santa Cruz Biotechnology (Santa Cruz, CA), with Notch1 (Cat. No.: 4380) from Cell Signaling Technology (Danvers, MA).

Techniques: Over Expression, Transfection, In Vitro, In Vivo