Effect of SOM230 (Pasireotide) on corticotropic cells: Action in dogs with Cushing's disease

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SOM230 (pasireotide) is a multiligand somatostatin (SRIF) analog able to bind to somatostatin receptor (SSTR) subtypes 1, 2, 3 and 5, and trigger antisecretory and antiproliferative signaling cascades. Canines have become in vivo models to test the pharmacological treatment of corticotropinomas beca...

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Autor principal: Castillo, V.
Otros Autores: Theodoropoulou, M., Stalla, J., Gallelli, M.F, Cabrera-Blatter, M.F, Haedo, M.R, Labeur, M., Schmid, H.A, Stalla, G.K, Arzt, E.
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: 2011
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som 230, Novartis, Switzerland
Acceso en línea:Registro en Scopus
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Biblioteca Central Dr. Luis F. Leloir (FCEN) de Universidad de Buenos Aires
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100 1 |a Castillo, V. 
245 1 0 |a Effect of SOM230 (Pasireotide) on corticotropic cells: Action in dogs with Cushing's disease 
260 |c 2011 
270 1 0 |m Castillo, V.; Unidad de Endocrinología, Facultad de Ciencias Veterinarias, Universidad de Buenos Aires, Buenos Aires, Argentina 
506 |2 openaire  |e Política editorial 
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520 3 |a SOM230 (pasireotide) is a multiligand somatostatin (SRIF) analog able to bind to somatostatin receptor (SSTR) subtypes 1, 2, 3 and 5, and trigger antisecretory and antiproliferative signaling cascades. Canines have become in vivo models to test the pharmacological treatment of corticotropinomas because they frequently develop Cushing's disease in a spontaneous manner, due to adrenocorticotropic hormone (ACTH)-producing pituitary adenomas. Different levels of expression of SSTR2 and SSTR5 have been shown in both mouse AtT20 cells and canine tumoral corticotropinoma cells. The objective of this study was to evaluate whether SOM230 controls both tumor cell growth and hormone synthesis, therefore controlling the disease. SOM230 was tested in dogs suffering from Cushing's disease (10 animals were treated continuously during 6 months, and another 10 were treated with 3 cycles consisting of 2 months of treatment followed by a 2-month rest period). A significant decrease in ACTH, urinary cortisol creatinine ratio, adenoma size (magnetic nuclear resonance) and improvement of clinical signs were obtained, without side effects. AtT20 cells treated with SOM230 suppressed pro-opiomelanocortin (POMC) promoter activity through SSTR2, via the G i α-subunit, and reduced Nur77/Nurr1 transcriptional activity. We conclude that SOM230, in addition to its well-described antisecretory effects, inhibits, as shown in AtT20 cells, ACTH synthesis at the POMC transcriptional level, an effect mediated mainly through SSTR2, and limits tumor growth. The controlled Cushing's disease in the dogs that received the treatment indicates that SOM230 has a potential therapeutic use in humans suffering from Cushing's disease. Copyright © 2011 S. Karger AG, Basel.  |l eng 
593 |a Unidad de Endocrinología, Facultad de Ciencias Veterinarias, Universidad de Buenos Aires, Buenos Aires, Argentina 
593 |a Max Planck Institute of Psychiatry, Munich, Germany 
593 |a Laboratorio de Fisiología y Biología Molecular, Depto. de Fisiología, Biología Molecular y Celular, Universidad de Buenos Aires, Aires Ciudad Universitaria, Pabellon II, Buenos Aires 1428, Argentina 
593 |a Argentine National Research Council, Buenos Aires, Argentina 
593 |a Novartis Institutes for Biomedical Research, Basel, Switzerland 
690 1 0 |a CORTICOTROPES 
690 1 0 |a CUSHING'S DISEASE 
690 1 0 |a PITUITARY ADENOMA 
690 1 0 |a SOM231 
690 1 0 |a CORTICOTROPIN 
690 1 0 |a CREATININE 
690 1 0 |a HYDROCORTISONE 
690 1 0 |a PASIREOTIDE 
690 1 0 |a PROOPIOMELANOCORTIN 
690 1 0 |a SOMATOSTATIN RECEPTOR 2 
690 1 0 |a SOMATOSTATIN RECEPTOR 5 
690 1 0 |a ACTH SECRETING ADENOMA 
690 1 0 |a ACTH SECRETING CELL 
690 1 0 |a ANIMAL CELL 
690 1 0 |a ANIMAL EXPERIMENT 
690 1 0 |a ANIMAL MODEL 
690 1 0 |a ARTICLE 
690 1 0 |a CONTROLLED STUDY 
690 1 0 |a CUSHING DISEASE 
690 1 0 |a DOG 
690 1 0 |a DRUG MECHANISM 
690 1 0 |a DRUG RECEPTOR BINDING 
690 1 0 |a FEMALE 
690 1 0 |a HORMONE SYNTHESIS 
690 1 0 |a MALE 
690 1 0 |a NONHUMAN 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a PROTEIN EXPRESSION 
690 1 0 |a TUMOR GROWTH 
690 1 0 |a TUMOR VOLUME 
690 1 0 |a ADRENOCORTICOTROPIC HORMONE 
690 1 0 |a ALANINE TRANSAMINASE 
690 1 0 |a ALKALINE PHOSPHATASE 
690 1 0 |a ALPHA-MSH 
690 1 0 |a ANIMALS 
690 1 0 |a ASPARTATE AMINOTRANSFERASES 
690 1 0 |a BLOOD GLUCOSE 
690 1 0 |a CELL LINE, TUMOR 
690 1 0 |a CHOLESTEROL 
690 1 0 |a CORTICOTROPHS 
690 1 0 |a CREATININE 
690 1 0 |a DOGS 
690 1 0 |a FEMALE 
690 1 0 |a HYDROCORTISONE 
690 1 0 |a LIVER FUNCTION TESTS 
690 1 0 |a MAGNETIC RESONANCE IMAGING 
690 1 0 |a MALE 
690 1 0 |a PITUITARY ACTH HYPERSECRETION 
690 1 0 |a SOMATOSTATIN 
690 1 0 |a TRIGLYCERIDES 
653 0 0 |a som 230, Novartis, Switzerland 
700 1 |a Theodoropoulou, M. 
700 1 |a Stalla, J. 
700 1 |a Gallelli, M.F. 
700 1 |a Cabrera-Blatter, M.F. 
700 1 |a Haedo, M.R. 
700 1 |a Labeur, M. 
700 1 |a Schmid, H.A. 
700 1 |a Stalla, G.K. 
700 1 |a Arzt, E. 
773 0 |d 2011  |g v. 94  |h pp. 124-136  |k n. 2  |p Neuroendocrinology  |x 00283835  |w (AR-BaUEN)CENRE-6253  |t Neuroendocrinology 
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856 4 0 |u https://doi.org/10.1159/000327429  |y DOI 
856 4 0 |u https://hdl.handle.net/20.500.12110/paper_00283835_v94_n2_p124_Castillo  |y Handle 
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