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Michael C. Riddell - One of the best experts on this subject based on the ideXlab platform.
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12-LB: Subcutaneous Administration of the Novel Somatostatin Receptor 2 Antagonist ZT-01 Restores the Glucagon Response to Hypoglycemia in STZ-Diabetic Rats to Normal Levels
Diabetes, 2020Co-Authors: Rawad Farhat, Michael C. Riddell, Eric Simonson, Richard Liggins, Owen ChanAbstract:Restoration of the lost glucagon response to hypoglycemia may be an effective means to prevent the onset of hypoglycemia in patients with type 1 diabetes (T1D). Elevation of the inhibitory hormone Somatostatin in T1D may act on alpha cells, via the Somatostatin Receptor 2 (SSTR2), to suppress glucagon release during hypoglycemia. We previously demonstrated that a novel SSTR2 antagonist, ZT-01, exhibited superior efficacy at restoring the glucagon response to hypoglycemia compared to an established SSTR2 antagonist, PRL-2903, when given intraperitoneally at a dose of 10 mg/kg. In this study, we first evaluated the pharmacokinetics of ZT-01 in healthy Sprague-Dawley rats. Within one hour after intraperitoneal administration of a 10 mg/kg dose, ZT-01 achieved 10-fold higher plasma Cmax compared to PRL-2903; however, pancreas concentration at 6 h post-dose was almost 4-fold higher for PRL-2903 compared to ZT-01 and plasma concentrations were similar for both 24 h post-dose. We subsequently conducted a dose de-escalation study to identify the lowest dose of ZT-01 that could improve glucagon secretion in poorly controlled insulin-treated streptozotocin (STZ)-diabetic Sprague Dawley rats, under hypoglycemic clamp conditions. ZT-01 was administered subcutaneously one hour prior to the induction of hypoglycemia (blood glucose Disclosure R. Farhat: None. E. Simonson: None. M. Riddell: Advisory Panel; Self; Zucara Therapeutics Inc. Consultant; Self; Lilly Diabetes. Research Support; Self; Dexcom, Inc., Insulet Corporation. Speaker’s Bureau; Self; Medtronic, Novo Nordisk A/S. R. Liggins: Advisory Panel; Self; Zucara Therapeutics Inc. Stock/Shareholder; Self; Zucara Therapeutics Inc. O. Chan: None. Funding JDRF; The Leona M. and Harry B. Helmsley Charitable Trust
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9-LB: Novel Somatostatin Receptor 2 Antagonist ZT-01 Prevents Hypoglycemia Onset in STZ-Diabetic Rats by Improving Glucagon Secretion
Diabetes, 2020Co-Authors: Julian Aiken, Ninoschka C. D’souza, Eric Simonson, Rawad Farhat, Owen Chan, Richard Liggins, Michael C. RiddellAbstract:Iatrogenic hypoglycemia remains one of the most serious risks for people with type 1 diabetes (T1D) undergoing intensive insulin therapy. Development of counterregulatory failure, occurring in the early stages of diabetes, highlighted by loss of the ability to secrete glucagon in response to hypoglycemia, is one of the main contributing factors. While the reason for this loss is still uncertain, it has been suggested that enhanced secretion of the pancreatic hormone, Somatostatin, in T1D may play a role. Previously, it was reported that antagonism of Somatostatin Receptor 2 (SSTR2) with the peptide PRL-2903 successfully improved the glucagon response to insulin-induced hypoglycemia in streptozotocin (STZ)-diabetic rats. In the current study, we assessed the effectiveness of a new SSTR2 antagonist, ZT-01, to prevent hypoglycemia during an insulin bolus challenge and evaluated the effect of both ZT-01 and PRL-2903 under stepped hyperinsulinemic-euglycemic-hypoglycemic clamp conditions. In both studies, STZ-diabetic rats maintained with daily insulin were administered either vehicle, PRL-2903 (10 mg/kg) or ZT-01 (10 mg/kg) intraperitoneally, one hour prior to the induction of hypoglycemia. ZT-01 was more effective than PRL-2903 in preventing the onset of hypoglycemia in response to the insulin bolus challenge. Median time of hypoglycemia onset (BG ≤54 mg/dL) was 60 min in controls, 70 min with PRL-2903 administration, and 125 min with ZT-01 administration. Furthermore, all control and PRL-2903 dosed rats experienced, while 28% of rats receiving ZT-01, avoided hypoglycemia. During the hypoglycemic clamp, ZT-01 was more effective than PRL-2903 at improving glucagon responses in hypoglycemia. ZT-01 administration increased glucagon peak by 4-fold over the response to PRL-2903 (P Disclosure J. Aiken: None. N.C. D’Souza: None. E. Simonson: None. R. Farhat: None. O. Chan: None. R. Liggins: Advisory Panel; Self; Zucara Therapeutics Inc. Stock/Shareholder; Self; Zucara Therapeutics Inc. M. Riddell: Advisory Panel; Self; Zucara Therapeutics Inc. Consultant; Self; Lilly Diabetes. Research Support; Self; Dexcom, Inc., Insulet Corporation. Speaker’s Bureau; Self; Medtronic, Novo Nordisk A/S. Funding JDRF; The Leona M. and Harry B. Helmsley Charitable Trust
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14-LB: Somatostatin Receptor 2 Antagonism Enhances Plasma Glucagon Levels during Insulin-Induced Hypoglycemia in a Rodent Model of Type 2 Diabetes Mellitus
Diabetes, 2019Co-Authors: Mehran Nejad-mansouri, Parinaz Zaree Bavani, Julian Aiken, Ninoschka C. D’souza, Emily G. Hoffman, Richard T. Liggins, Michael C. RiddellAbstract:Somatostatin Receptor 2 antagonists (SSTR2a) increase glucagon counter-regulation to hypoglycemia in various rodent models of type-1 diabetes mellitus. Here we investigated the efficacy of SSTR2a in improving glucagon counter-regulation in a rat model of type-2 diabetes mellitus (T2DM). For this, male Sprague Dawley rats (n=18) were given a high fat diet for 3 weeks, followed by low-dose streptozotocin exposure (35 mg/kg, IP) to induce T2DM. Rats were then divided into SSTR2a treatment (PRL-2903, 10 mg/kg) or vehicle (n=9 for each) 1-hour before insulin-induced hypoglycemia (3 IU/kg NovoRapid). This process was repeated 1 week later in a cross-over design, with the data pooled over SSTR2a and vehicle treatments. A group of normal-chow-fed rats (n=3) served as nondiabetic controls. Mean blood glucose levels were higher at 20, 30, 40, and 50 minutes post insulin administration in the T2DM rats treated with PRL-2903, as compared to vehicle (p ≤ 0.05). The number of T2DM rats that developed biochemical hypoglycemia (blood glucose ≤ 3.5 mmol/L) tended to be less with PRL-2903 (5/18) vs. vehicle (9/18). Compared with vehicle treatment, PRL-2903 promoted higher plasma glucagon counter-regulation, as indicated by area under curve (AUC) analysis (p Disclosure M. Nejad-Mansouri: None. P. Zaree Bavani: None. J. Aiken: None. N.C. DSouza: None. E.G. Hoffman: None. R. Liggins: None. M. Riddell: Advisory Panel; Self; Xeris Pharmaceuticals, Inc. Research Support; Self; Dexcom, Inc. Speaker’s Bureau; Self; Insulet Corporation, Medtronic MiniMed, Inc. Stock/Shareholder; Self; Zucara Therapeutics Inc. Funding National Research Council Canada; Zucara Therapeutics
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Glucagon responses to exercise-induced hypoglycaemia are improved by Somatostatin Receptor type 2 antagonism in a rat model of diabetes
Diabetologia, 2016Co-Authors: Erwan Leclair, Richard T. Liggins, Ashley J. Peckett, Trevor Teich, David H. Coy, Mladen Vranic, Michael C. RiddellAbstract:Aims/hypothesis Regular exercise is at the cornerstone of care in type 1 diabetes. However, relative hyperinsulinaemia and a blunted glucagon response to exercise promote hypoglycaemia. Recently, a selective antagonist of Somatostatin Receptor 2, PRL-2903, was shown to improve glucagon counterregulation to hypoglycaemia in resting streptozotocin-induced diabetic rats. The aim of this study was to test the efficacy of PRL-2903 in enhancing glucagon counterregulation during repeated hyperinsulinaemic exercise.
Heidi Chen - One of the best experts on this subject based on the ideXlab platform.
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Somatostatin Receptor 2 signaling promotes growth and tumor survival in small cell lung cancer
International Journal of Cancer, 2019Co-Authors: Jonathan M. Lehman, Megan D. Hoeksema, Jeremy Staub, Jun Qian, Bradford K. Harris, Jennifer Miao, Chanjuan Shi, Rosana Eisenberg, Clay J Callison, Heidi ChenAbstract:Somatostatin Receptor 2 (SSTR2) is overexpressed in a majority of neuroendocrine neoplasms, including small-cell lung carcinomas (SCLCs). SSTR2 was previously considered an inhibitory Receptor on cell growth, but its agonists had poor clinical responses in multiple clinical trials. The role of this Receptor as a potential therapeutic target in lung cancer merits further investigation. We evaluated the expression of SSTR2 in a cohort of 96 primary tumors from patients with SCLC and found 48% expressed SSTR2. Correlation analysis in both CCLE and an SCLC RNAseq cohort confirmed high-level expression and identified an association between NEUROD1 and SSTR2. There was a significant association with SSTR2 expression profile and poor clinical outcome. We tested whether SSTR2 expression might contribute to tumor progression through activation of downstream signaling pathways, using in vitro and in vivo systems and downregulated SSTR2 expression in lung cancer cells by shRNA. SSTR2 downregulation led to increased apoptosis and dramatically decreased tumor growth in vitro and in vivo in multiple cell lines with decreased AMPKα phosphorylation and increased oxidative metabolism. These results demonstrate a role for SSTR2 signaling in SCLC and suggest that SSTR2 is a poor prognostic biomarker in SCLC and potential future therapeutic signaling target.
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Somatostatin Receptor 2 signaling promotes growth and tumor survival in small‐cell lung cancer
International journal of cancer, 2018Co-Authors: Jonathan M. Lehman, Megan D. Hoeksema, Jeremy Staub, Jun Qian, Bradford K. Harris, J. Clay Callison, Jennifer Miao, Chanjuan Shi, Rosana Eisenberg, Heidi ChenAbstract:Somatostatin Receptor 2 (SSTR2) is overexpressed in a majority of neuroendocrine neoplasms, including small-cell lung carcinomas (SCLCs). SSTR2 was previously considered an inhibitory Receptor on cell growth, but its agonists had poor clinical responses in multiple clinical trials. The role of this Receptor as a potential therapeutic target in lung cancer merits further investigation. We evaluated the expression of SSTR2 in a cohort of 96 primary tumors from patients with SCLC and found 48% expressed SSTR2. Correlation analysis in both CCLE and an SCLC RNAseq cohort confirmed high-level expression and identified an association between NEUROD1 and SSTR2. There was a significant association with SSTR2 expression profile and poor clinical outcome. We tested whether SSTR2 expression might contribute to tumor progression through activation of downstream signaling pathways, using in vitro and in vivo systems and downregulated SSTR2 expression in lung cancer cells by shRNA. SSTR2 downregulation led to increased apoptosis and dramatically decreased tumor growth in vitro and in vivo in multiple cell lines with decreased AMPKα phosphorylation and increased oxidative metabolism. These results demonstrate a role for SSTR2 signaling in SCLC and suggest that SSTR2 is a poor prognostic biomarker in SCLC and potential future therapeutic signaling target.
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Loss of Somatostatin Receptor 2 expression and cellular metabolism and survival in small cell lung cancer.
Journal of Clinical Oncology, 2016Co-Authors: Jonathan M. Lehman, Megan D. Hoeksema, Jun Qian, Chanjuan Shi, Rosana Eisenberg, Heidi Chen, Pierre P. MassionAbstract:e20090Background: Small cell lung cancer (SCLC) is a high grade poorly differentiated neuroendocrine carcinoma responsible for ~15% of diagnosed lung cancers and up to 25% of lung cancer deaths. Tr...
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Loss of Somatostatin Receptor 2 expression and lung cancer growth.
Journal of Clinical Oncology, 2015Co-Authors: Jonathan M. Lehman, Megan D. Hoeksema, Chanjuan Shi, Rosana Eisenberg, Heidi Chen, Pierre P. MassionAbstract:7569 Background: Small cell lung cancer (SCLC) is a neuroendocrine cancer of the lung responsible for up to 25% of lung cancer deaths. Targeted therapies for SCLC are sorely needed. Somatostatin re...
Jonathan M. Lehman - One of the best experts on this subject based on the ideXlab platform.
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Somatostatin Receptor 2 targeting in small cell lung carcinoma: perspectives.
Oncotarget, 2019Co-Authors: Jonathan M. Lehman, Pierre P. AmassionAbstract:// Jonathan M. Lehman 1 , 2 , 3 and Pierre P. aMassion 1 , 2 , 3 1 Division of Medical Oncology, Thoracic Program, Vanderbilt Ingram Cancer Center, Nashville, TN, USA 2 Thoracic Program, Vanderbilt Ingram Cancer Center, Nashville, TN, USA 3 Veterans Affairs, Tennessee Valley Healthcare System, Nashville Campus, Nashville, TN, USA Correspondence to: Jonathan M. Lehman, email: jonathan.m.lehman@vanderbilt.edu Keywords: small cell lung cancer; Somatostatin Receptor 2; antibody-drug conjugate; peptide drug conjugate; perspectives Received: June 18, 2019 Accepted: June 29, 2019 Published: July 30, 2019 ABSTRACT Small Cell lung carcinoma (SCLC) is the most lethal and aggressive subtype of lung cancer. Novel targeting approaches and agents are desperately needed. In this perspectives, we briefly explore recent data published in the International Journal of Cancer suggesting Somatostatin Receptor 2 (SSTR2) as a viable target for SCLC, summarize the current clinical trial space, and describe promising new research and clinical directions for Somatostatin Receptor 2 targeting in SCLC.
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Somatostatin Receptor 2 signaling promotes growth and tumor survival in small cell lung cancer
International Journal of Cancer, 2019Co-Authors: Jonathan M. Lehman, Megan D. Hoeksema, Jeremy Staub, Jun Qian, Bradford K. Harris, Jennifer Miao, Chanjuan Shi, Rosana Eisenberg, Clay J Callison, Heidi ChenAbstract:Somatostatin Receptor 2 (SSTR2) is overexpressed in a majority of neuroendocrine neoplasms, including small-cell lung carcinomas (SCLCs). SSTR2 was previously considered an inhibitory Receptor on cell growth, but its agonists had poor clinical responses in multiple clinical trials. The role of this Receptor as a potential therapeutic target in lung cancer merits further investigation. We evaluated the expression of SSTR2 in a cohort of 96 primary tumors from patients with SCLC and found 48% expressed SSTR2. Correlation analysis in both CCLE and an SCLC RNAseq cohort confirmed high-level expression and identified an association between NEUROD1 and SSTR2. There was a significant association with SSTR2 expression profile and poor clinical outcome. We tested whether SSTR2 expression might contribute to tumor progression through activation of downstream signaling pathways, using in vitro and in vivo systems and downregulated SSTR2 expression in lung cancer cells by shRNA. SSTR2 downregulation led to increased apoptosis and dramatically decreased tumor growth in vitro and in vivo in multiple cell lines with decreased AMPKα phosphorylation and increased oxidative metabolism. These results demonstrate a role for SSTR2 signaling in SCLC and suggest that SSTR2 is a poor prognostic biomarker in SCLC and potential future therapeutic signaling target.
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Somatostatin Receptor 2 signaling promotes growth and tumor survival in small‐cell lung cancer
International journal of cancer, 2018Co-Authors: Jonathan M. Lehman, Megan D. Hoeksema, Jeremy Staub, Jun Qian, Bradford K. Harris, J. Clay Callison, Jennifer Miao, Chanjuan Shi, Rosana Eisenberg, Heidi ChenAbstract:Somatostatin Receptor 2 (SSTR2) is overexpressed in a majority of neuroendocrine neoplasms, including small-cell lung carcinomas (SCLCs). SSTR2 was previously considered an inhibitory Receptor on cell growth, but its agonists had poor clinical responses in multiple clinical trials. The role of this Receptor as a potential therapeutic target in lung cancer merits further investigation. We evaluated the expression of SSTR2 in a cohort of 96 primary tumors from patients with SCLC and found 48% expressed SSTR2. Correlation analysis in both CCLE and an SCLC RNAseq cohort confirmed high-level expression and identified an association between NEUROD1 and SSTR2. There was a significant association with SSTR2 expression profile and poor clinical outcome. We tested whether SSTR2 expression might contribute to tumor progression through activation of downstream signaling pathways, using in vitro and in vivo systems and downregulated SSTR2 expression in lung cancer cells by shRNA. SSTR2 downregulation led to increased apoptosis and dramatically decreased tumor growth in vitro and in vivo in multiple cell lines with decreased AMPKα phosphorylation and increased oxidative metabolism. These results demonstrate a role for SSTR2 signaling in SCLC and suggest that SSTR2 is a poor prognostic biomarker in SCLC and potential future therapeutic signaling target.
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Loss of Somatostatin Receptor 2 expression and cellular metabolism and survival in small cell lung cancer.
Journal of Clinical Oncology, 2016Co-Authors: Jonathan M. Lehman, Megan D. Hoeksema, Jun Qian, Chanjuan Shi, Rosana Eisenberg, Heidi Chen, Pierre P. MassionAbstract:e20090Background: Small cell lung cancer (SCLC) is a high grade poorly differentiated neuroendocrine carcinoma responsible for ~15% of diagnosed lung cancers and up to 25% of lung cancer deaths. Tr...
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Loss of Somatostatin Receptor 2 expression and lung cancer growth.
Journal of Clinical Oncology, 2015Co-Authors: Jonathan M. Lehman, Megan D. Hoeksema, Chanjuan Shi, Rosana Eisenberg, Heidi Chen, Pierre P. MassionAbstract:7569 Background: Small cell lung cancer (SCLC) is a neuroendocrine cancer of the lung responsible for up to 25% of lung cancer deaths. Targeted therapies for SCLC are sorely needed. Somatostatin re...
Owen Chan - One of the best experts on this subject based on the ideXlab platform.
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9-LB: Novel Somatostatin Receptor 2 Antagonist ZT-01 Prevents Hypoglycemia Onset in STZ-Diabetic Rats by Improving Glucagon Secretion
Diabetes, 2020Co-Authors: Julian Aiken, Ninoschka C. D’souza, Eric Simonson, Rawad Farhat, Owen Chan, Richard Liggins, Michael C. RiddellAbstract:Iatrogenic hypoglycemia remains one of the most serious risks for people with type 1 diabetes (T1D) undergoing intensive insulin therapy. Development of counterregulatory failure, occurring in the early stages of diabetes, highlighted by loss of the ability to secrete glucagon in response to hypoglycemia, is one of the main contributing factors. While the reason for this loss is still uncertain, it has been suggested that enhanced secretion of the pancreatic hormone, Somatostatin, in T1D may play a role. Previously, it was reported that antagonism of Somatostatin Receptor 2 (SSTR2) with the peptide PRL-2903 successfully improved the glucagon response to insulin-induced hypoglycemia in streptozotocin (STZ)-diabetic rats. In the current study, we assessed the effectiveness of a new SSTR2 antagonist, ZT-01, to prevent hypoglycemia during an insulin bolus challenge and evaluated the effect of both ZT-01 and PRL-2903 under stepped hyperinsulinemic-euglycemic-hypoglycemic clamp conditions. In both studies, STZ-diabetic rats maintained with daily insulin were administered either vehicle, PRL-2903 (10 mg/kg) or ZT-01 (10 mg/kg) intraperitoneally, one hour prior to the induction of hypoglycemia. ZT-01 was more effective than PRL-2903 in preventing the onset of hypoglycemia in response to the insulin bolus challenge. Median time of hypoglycemia onset (BG ≤54 mg/dL) was 60 min in controls, 70 min with PRL-2903 administration, and 125 min with ZT-01 administration. Furthermore, all control and PRL-2903 dosed rats experienced, while 28% of rats receiving ZT-01, avoided hypoglycemia. During the hypoglycemic clamp, ZT-01 was more effective than PRL-2903 at improving glucagon responses in hypoglycemia. ZT-01 administration increased glucagon peak by 4-fold over the response to PRL-2903 (P Disclosure J. Aiken: None. N.C. D’Souza: None. E. Simonson: None. R. Farhat: None. O. Chan: None. R. Liggins: Advisory Panel; Self; Zucara Therapeutics Inc. Stock/Shareholder; Self; Zucara Therapeutics Inc. M. Riddell: Advisory Panel; Self; Zucara Therapeutics Inc. Consultant; Self; Lilly Diabetes. Research Support; Self; Dexcom, Inc., Insulet Corporation. Speaker’s Bureau; Self; Medtronic, Novo Nordisk A/S. Funding JDRF; The Leona M. and Harry B. Helmsley Charitable Trust
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12-LB: Subcutaneous Administration of the Novel Somatostatin Receptor 2 Antagonist ZT-01 Restores the Glucagon Response to Hypoglycemia in STZ-Diabetic Rats to Normal Levels
Diabetes, 2020Co-Authors: Rawad Farhat, Michael C. Riddell, Eric Simonson, Richard Liggins, Owen ChanAbstract:Restoration of the lost glucagon response to hypoglycemia may be an effective means to prevent the onset of hypoglycemia in patients with type 1 diabetes (T1D). Elevation of the inhibitory hormone Somatostatin in T1D may act on alpha cells, via the Somatostatin Receptor 2 (SSTR2), to suppress glucagon release during hypoglycemia. We previously demonstrated that a novel SSTR2 antagonist, ZT-01, exhibited superior efficacy at restoring the glucagon response to hypoglycemia compared to an established SSTR2 antagonist, PRL-2903, when given intraperitoneally at a dose of 10 mg/kg. In this study, we first evaluated the pharmacokinetics of ZT-01 in healthy Sprague-Dawley rats. Within one hour after intraperitoneal administration of a 10 mg/kg dose, ZT-01 achieved 10-fold higher plasma Cmax compared to PRL-2903; however, pancreas concentration at 6 h post-dose was almost 4-fold higher for PRL-2903 compared to ZT-01 and plasma concentrations were similar for both 24 h post-dose. We subsequently conducted a dose de-escalation study to identify the lowest dose of ZT-01 that could improve glucagon secretion in poorly controlled insulin-treated streptozotocin (STZ)-diabetic Sprague Dawley rats, under hypoglycemic clamp conditions. ZT-01 was administered subcutaneously one hour prior to the induction of hypoglycemia (blood glucose Disclosure R. Farhat: None. E. Simonson: None. M. Riddell: Advisory Panel; Self; Zucara Therapeutics Inc. Consultant; Self; Lilly Diabetes. Research Support; Self; Dexcom, Inc., Insulet Corporation. Speaker’s Bureau; Self; Medtronic, Novo Nordisk A/S. R. Liggins: Advisory Panel; Self; Zucara Therapeutics Inc. Stock/Shareholder; Self; Zucara Therapeutics Inc. O. Chan: None. Funding JDRF; The Leona M. and Harry B. Helmsley Charitable Trust
Antonio Tito Fojo - One of the best experts on this subject based on the ideXlab platform.
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first in human phase 1 2a study of pen 221 Somatostatin analog ssa dm1 conjugate for patients pts with advanced neuroendocrine tumor net or small cell lung cancer sclc phase 1 results
Journal of Clinical Oncology, 2018Co-Authors: Melissa Lynne Johnson, Antonio Tito Fojo, Kristina Kriksciukaite, Tim Meyer, Daniel M Halperin, Natalie Cook, Lawrence S Blaszkowsky, Benjamin L Schlechter, Yannis Jemiai, Marsha JonesAbstract:4097Background: Somatostatin Receptor 2 (SSTR2) is highly expressed in NET and SCLC. PEN-221, a SSA-DM1 conjugate that targets SSTR2, results in complete tumor regressions in SSTR2+ SCLC xenograft ...
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pet ct comparing 68ga dotatate and other radiopharmaceuticals and in comparison with ct mri for the localization of sporadic metastatic pheochromocytoma and paraganglioma
European Journal of Nuclear Medicine and Molecular Imaging, 2016Co-Authors: Ingo Janssen, Clara C Chen, Corina Millo, Alexander Ling, David Taieb, Frank I Lin, Karen T Adams, Katherine I Wolf, Peter Herscovitch, Antonio Tito FojoAbstract:Purpose Pheochromocytomas/paragangliomas (PPGLs) and their metastases are tumors that predominantly express Somatostatin Receptor 2 (SSR2). 68Ga-DOTA(0)-Tyr(3)-octreotate (68Ga-DOTATATE) is a PET radiopharmaceutical with both high and selective affinity for SSRs. The purpose of this study was to evaluate the utility of 68Ga-DOTATATE in comparison with other specific and nonspecific radiopharmaceuticals recommended in the current guidelines for the localization of metastatic sporadic PPGL by PET/CT.
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PET/CT comparing 68Ga-DOTATATE and other radiopharmaceuticals and in comparison with CT/MRI for the localization of sporadic metastatic pheochromocytoma and paraganglioma
European journal of nuclear medicine and molecular imaging, 2016Co-Authors: Ingo Janssen, Clara C Chen, Corina Millo, Alexander Ling, David Taieb, Frank I Lin, Karen T Adams, Katherine I Wolf, Peter Herscovitch, Antonio Tito FojoAbstract:Purpose Pheochromocytomas/paragangliomas (PPGLs) and their metastases are tumors that predominantly express Somatostatin Receptor 2 (SSR2). 68Ga-DOTA(0)-Tyr(3)-octreotate (68Ga-DOTATATE) is a PET radiopharmaceutical with both high and selective affinity for SSRs. The purpose of this study was to evaluate the utility of 68Ga-DOTATATE in comparison with other specific and nonspecific radiopharmaceuticals recommended in the current guidelines for the localization of metastatic sporadic PPGL by PET/CT.