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Article: New Insights into Pheochromocytoma Biology: the Role of the Insulin - Like Growth Factor 1 (IGF1) System.

Pennisi, Patricia A / Fernández, María Celia / Martin, Ayelen

2020 Volume 17, Issue 4, Page(s) 331–342

Abstract: Pheochromocytomas/paragangliomas (PCCs/PGLs) are rare neuroendocrine tumors, developed from chromaffin cells derived from the neural crest. From a genetic point of view PCCs/PGLs are divided as sporadic cases, and inherited cases as part of hereditary ( ... ...

Abstract	Pheochromocytomas/paragangliomas (PCCs/PGLs) are rare neuroendocrine tumors, developed from chromaffin cells derived from the neural crest. From a genetic point of view PCCs/PGLs are divided as sporadic cases, and inherited cases as part of hereditary (familial) syndromes. While the majority is benign, up to 26% of PCCs/PGLs will undergo malignant transformation. Validated prognostic pathological parameters for malignant PCCs/PGLs are still lacking. Signaling that follows the interactions between IGFs and their receptor/s in tumor cells received extensive attention when investigating the role of IGF1R in cancer. Increased IGF1R expression has been shown during progression to metastatic phenotypes and associated with worse prognosis in several types of cancer. In this review we provide evidence supporting a role for the IGFs system on PCC/PGL tumor biology and malignant behavior, endocrine actions to sustain tumor phenotype as well as heterotypic interaction´s regulation by IGF1, encouraging further research for targeted therapeutic options for these tumors.
MeSH term(s)	Adrenal Gland Neoplasms ; Growth Disorders ; Humans ; Insulins ; Pheochromocytoma
Chemical Substances	Insulins
Language	English
Publishing date	2020-08-11
Publishing country	Israel
Document type	Journal Article ; Review
ZDB-ID	2434390-0
ISSN	1565-4753
ISSN	1565-4753
DOI	10.17458/per.vol17.2020.kc.insightspheochromocytomabiology
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Article ; Online: Fibroblast deficiency of insulin-like growth factor 1 receptor type 1 (IGF1R) impairs initial steps of murine pheochromocytoma development.

Martin, Ayelen / Venara, Marcela / Mathó, Cecilia / Olea, Fernanda D / Fernández, María Celia / Pennisi, Patricia A

Biochimie

2019 Volume 163, Page(s) 108–116

Abstract: Insulin-like growth factor 1 (IGF1) has a critical role in maintaining tumor phenotype and survival of already transformed murine pheochromocytoma (pheo) cells (MPC4/30) and it is required for the initial establishment of these tumors. However, the role ... ...

Abstract	Insulin-like growth factor 1 (IGF1) has a critical role in maintaining tumor phenotype and survival of already transformed murine pheochromocytoma (pheo) cells (MPC4/30) and it is required for the initial establishment of these tumors. However, the role of local IGF1/IGF1R system in tumor microenvironment has not been fully understood. In vivo, by subcutaneous injection of pheo cells in heterozygous IGF1R knockout mice (L/n), we found that the time of noticeable tumor appearance was delayed, and incidence was decreased in L/n group compared to control (L/L) mice. Once established, tumor proliferation, vascularization or growth rate did not differ between groups. In vitro, fibroblast from L/n and L/L mice were cultured to generate conditioned media (CM) and differential matrixes on which pheo cells were seeded. Proliferation rate was higher when pheo cells were cultured with CM, or in differential matrix generated by L/L murine fibroblasts. A diminished fibronectin (FN) expression and secretion from L/n fibroblast was associated with decreased expression of integrin subunits in tumor cells. Also, soluble factors as IGF1 and insulin-like growth factor binding protein 2 (IGFBP2) were reduced. Our data suggest that IGF1 signaling through IGF1R may contribute to tumor cells anchorage and survival by interaction with both matrix and soluble factors produced by tumor microenvironment fibroblasts.
MeSH term(s)	Adrenal Gland Neoplasms/genetics ; Adrenal Gland Neoplasms/metabolism ; Adrenal Gland Neoplasms/physiopathology ; Animals ; Cell Proliferation ; Fibroblasts/metabolism ; Fibronectins/genetics ; Gene Expression Regulation, Neoplastic ; Haploinsufficiency ; Male ; Mice ; Neovascularization, Pathologic ; Pheochromocytoma/genetics ; Pheochromocytoma/metabolism ; Pheochromocytoma/physiopathology ; Receptor, IGF Type 1/genetics ; Tumor Microenvironment
Chemical Substances	Fibronectins ; Igf1r protein, mouse ; Receptor, IGF Type 1 (EC 2.7.10.1)
Language	English
Publishing date	2019-06-08
Publishing country	France
Document type	Journal Article
ZDB-ID	120345-9
ISSN	1638-6183 ; 0300-9084
ISSN (online)	1638-6183
ISSN	0300-9084
DOI	10.1016/j.biochi.2019.06.004
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Article: Fibroblast deficiency of insulin-like growth factor 1 receptor type 1 (IGF1R) impairs initial steps of murine pheochromocytoma development

Martin, Ayelen / Fernández, María Celia / Mathó, Cecilia / Olea, Fernanda D / Pennisi, Patricia A / Venara, Marcela

Biochimie. 2019 Aug., v. 163

2019

Abstract	Insulin-like growth factor 1 (IGF1) has a critical role in maintaining tumor phenotype and survival of already transformed murine pheochromocytoma (pheo) cells (MPC4/30) and it is required for the initial establishment of these tumors. However, the role of local IGF1/IGF1R system in tumor microenvironment has not been fully understood. In vivo, by subcutaneous injection of pheo cells in heterozygous IGF1R knockout mice (L/n), we found that the time of noticeable tumor appearance was delayed, and incidence was decreased in L/n group compared to control (L/L) mice. Once established, tumor proliferation, vascularization or growth rate did not differ between groups. In vitro, fibroblast from L/n and L/L mice were cultured to generate conditioned media (CM) and differential matrixes on which pheo cells were seeded. Proliferation rate was higher when pheo cells were cultured with CM, or in differential matrix generated by L/L murine fibroblasts. A diminished fibronectin (FN) expression and secretion from L/n fibroblast was associated with decreased expression of integrin subunits in tumor cells. Also, soluble factors as IGF1 and insulin-like growth factor binding protein 2 (IGFBP2) were reduced. Our data suggest that IGF1 signaling through IGF1R may contribute to tumor cells anchorage and survival by interaction with both matrix and soluble factors produced by tumor microenvironment fibroblasts.
Keywords	binding proteins ; fibroblasts ; fibronectins ; heterozygosity ; insulin-like growth factor I ; insulin-like growth factor I receptor ; integrins ; knockout mutants ; mice ; neoplasm cells ; neoplasms ; phenotype ; secretion ; subcutaneous injection
Language	English
Dates of publication	2019-08
Size	p. 108-116.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	120345-9
ISSN	0300-9084
ISSN	0300-9084
DOI	10.1016/j.biochi.2019.06.004
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Article: Type 1 Insulin-Like Growth Factor Receptor Nuclear Localization in High-Grade Glioma Cells Enhances Motility, Metabolism, and

Martin, Ayelen / Fernandez, María Celia / Cattaneo, Elizabeth R / Schuster, Claudio D / Venara, Marcela / Clément, Florencia / Berenstein, Ariel / Lombardi, Mercedes García / Bergadá, Ignacio / Gutierrez, Mariana / Martí, Marcelo A / Gonzalez-Baro, María R / Pennisi, Patricia A

Frontiers in endocrinology

2022 Volume 13, Page(s) 849279

Abstract: Gliomas are the most frequent solid tumors in children. Among these, high-grade gliomas are less common in children than in adults, though they are similar in their aggressive clinical behavior. In adults, glioblastoma is the most lethal tumor of the ... ...

Abstract	Gliomas are the most frequent solid tumors in children. Among these, high-grade gliomas are less common in children than in adults, though they are similar in their aggressive clinical behavior. In adults, glioblastoma is the most lethal tumor of the central nervous system. Insulin-like growth factor 1 receptor (IGF1R) plays an important role in cancer biology, and its nuclear localization has been described as an adverse prognostic factor in different tumors. Previously, we have demonstrated that, in pediatric gliomas, IGF1R nuclear localization is significantly associated with high-grade tumors, worst clinical outcome, and increased risk of death. Herein we explore the role of IGF1R intracellular localization by comparing two glioblastoma cell lines that differ only in their IGF1R capacity to translocate to the nucleus.
MeSH term(s)	Adult ; Carcinogenesis/metabolism ; Cell Nucleus/metabolism ; Child ; Glioblastoma/metabolism ; Glioma/metabolism ; Humans ; Receptors, Somatomedin/metabolism
Chemical Substances	Receptors, Somatomedin
Language	English
Publishing date	2022-04-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2022.849279
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Article ; Online: Novel Insulin-Like Growth Factor 1 Gene Mutation: Broadening of the Phenotype and Implications for Insulin Resistance.

Giacomozzi, Claudio / Martin, Ayelen / Fernández, María Celia / Gutiérrez, Mariana / Iascone, Maria / Domené, Horacio M / Dominici, Fernando P / Bergadá, Ignacio / Cangiano, Biagio / Persani, Luca / Pennisi, Patricia A

The Journal of clinical endocrinology and metabolism

2022 Volume 108, Issue 6, Page(s) 1355–1369

Abstract: Context: Insulin-like growth factor (IGF)1 gene mutations are extremely rare causes of pre- and postnatal growth retardation. Phenotype can be heterogenous with varying degrees of neurosensory deafness, cognitive defects, glucose metabolism impairment ... ...

Abstract	Context: Insulin-like growth factor (IGF)1 gene mutations are extremely rare causes of pre- and postnatal growth retardation. Phenotype can be heterogenous with varying degrees of neurosensory deafness, cognitive defects, glucose metabolism impairment and short stature. Objective: This study describes a 12.6-year-old girl presenting with severe short stature and insulin resistance, but with normal hearing and neurological development at the lower limit of normal. Methods: DNA was obtained from the proband and both parents for whole exome sequencing (WES). In silico analysis was performed to predict the impact of the IGF1 variant on IGF1 and insulin receptors (IGF1R and IR) signaling. Phosphorylation of the IGF1R at activating Tyr residues and cell proliferation analyses were used to assess the ability of each subject's IGF1 to bind and activate IGF1R. Results: The proband had low immunoreactive IGF1 in serum and WES revealed a novel homozygous IGF1 missense variant (c.247A>T), causing a change of serine 83 for cysteine (p.Ser83Cys; p.Ser35Cys in mature peptide). The proband's parents were heterozygous for this mutation. In silico analyses indicated the pathogenic potential of the variant with electrostatic variations with the potential of hampering the interaction with the IGF1R but strengthening the binding to IR. The mutant IGF1 protein had a significantly reduced activity on in vitro bioassays. Conclusion: We describe a novel IGF1 mutation leading to severe loss of circulating IGF1 immunoreactivity and bioactivity. In silico modeling predicts that the mutant IGF1 could interfere with IR signaling, providing a possible explanation for the severe insulin resistance observed in the patient. The absence of significant hearing and neurodevelopmental involvement in the present case is unusual and broadens the clinical spectrum of IGF1 mutations.
MeSH term(s)	Humans ; Insulin-Like Growth Factor I/genetics ; Insulin-Like Growth Factor I/metabolism ; Insulin Resistance/genetics ; Receptor, IGF Type 1/genetics ; Receptor, IGF Type 1/metabolism ; Mutation ; Mutation, Missense ; Dwarfism/genetics ; Phenotype
Chemical Substances	Insulin-Like Growth Factor I (67763-96-6) ; Receptor, IGF Type 1 (EC 2.7.10.1)
Language	English
Publishing date	2022-12-16
Publishing country	United States
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgac738
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Article ; Online: Insulin signaling in the heart is impaired by growth hormone: a direct and early event.

Muñoz, Marina C / Piazza, Verónica G / Burghi, Valeria / Giani, Jorge F / Martinez, Carolina S / Cicconi, Nadia S / Muia, Nadia V / Fang, Yimin / Lavandero, Sergio / Sotelo, Ana I / Bartke, Andrzej / Pennisi, Patricia A / Dominici, Fernando P / Miquet, Johanna G

Journal of molecular endocrinology

2022 Volume 69, Issue 2, Page(s) 357–376

Abstract: Growth hormone (GH) exerts major actions in cardiac growth and metabolism. Considering the important role of insulin in the heart and the well-established anti-insulin effects of GH, cardiac insulin resistance may play a role in the cardiopathology ... ...

Abstract	Growth hormone (GH) exerts major actions in cardiac growth and metabolism. Considering the important role of insulin in the heart and the well-established anti-insulin effects of GH, cardiac insulin resistance may play a role in the cardiopathology observed in acromegalic patients. As conditions of prolonged exposure to GH are associated with a concomitant increase of circulating GH, IGF1 and insulin levels, to dissect the direct effects of GH, in this study, we evaluated the activation of insulin signaling in the heart using four different models: (i) transgenic mice overexpressing GH, with chronically elevated GH, IGF1 and insulin circulating levels; (ii) liver IGF1-deficient mice, with chronically elevated GH and insulin but decreased IGF1 circulating levels; (iii) mice treated with GH for a short period of time; (iv) primary culture of rat cardiomyocytes incubated with GH. Despite the differences in the development of cardiomegaly and in the metabolic alterations among the three experimental mouse models analyzed, exposure to GH was consistently associated with a decreased response to acute insulin stimulation in the heart at the receptor level and through the PI3K/AKT pathway. Moreover, a blunted response to insulin stimulation of this signaling pathway was also observed in cultured cardiomyocytes of neonatal rats incubated with GH. Therefore, the key novel finding of this work is that impairment of insulin signaling in the heart is a direct and early event observed as a consequence of exposure to GH, which may play a major role in the development of cardiac pathology.
MeSH term(s)	Acromegaly ; Animals ; Growth Hormone/metabolism ; Human Growth Hormone ; Insulin/metabolism ; Insulin-Like Growth Factor I/metabolism ; Mice ; Myocytes, Cardiac/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Rats ; Signal Transduction
Chemical Substances	Insulin ; Human Growth Hormone (12629-01-5) ; Insulin-Like Growth Factor I (67763-96-6) ; Growth Hormone (9002-72-6)
Language	English
Publishing date	2022-06-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	645012-x
ISSN	1479-6813 ; 0952-5041
ISSN (online)	1479-6813
ISSN	0952-5041
DOI	10.1530/JME-21-0242
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Article ; Online: VHL Germline Mutations in Argentinian Patients with Clinical Diagnoses or Single Typical Manifestations of Type 1 von Hippel-Lindau Disease.

Mathó, Cecilia / Sansó, Gabriela / Diez, Blanca / Barontini, Marta / Pennisi, Patricia A

Genetic testing and molecular biomarkers

2016 Volume 20, Issue 12, Page(s) 771–776

Abstract: Aims: von Hippel-Lindau (VHL) disease is caused by mutations in the VHL tumor suppressor gene. As tumors that develop in the context of VHL also occur in a sporadic context, the frequency of this syndrome may be underestimated. Our aim was to identify ... ...

Abstract	Aims: von Hippel-Lindau (VHL) disease is caused by mutations in the VHL tumor suppressor gene. As tumors that develop in the context of VHL also occur in a sporadic context, the frequency of this syndrome may be underestimated. Our aim was to identify VHL gene mutations in Argentinian patients who fulfilled the clinical criteria for type 1 VHL disease and in patients with VHL-associated manifestations that did not meet these criteria. Methods: We performed a retrospective cohort study, including patients who met current diagnostic criteria for type 1 VHL (Group 1, n = 19) and patients with VHL-associated manifestations that did not meet these criteria (Group 2, n = 21). Genomic DNA was extracted from peripheral blood leukocytes. Mutation analysis involved DNA sequencing, while large deletions were determined by universal primer quantitative fluorescent multiplex polymerase chain reaction (UPQFM-PCR) and multiplex ligation-dependent probe amplification (MLPA) analysis. Results: VHL mutations were detected in 16/19 (84.2%) patients in Group 1 and included: gross deletions (4/16); nonsense mutations (6/16); frameshift mutations (4/16); missense mutations (1/16); and splicing mutations (1/16). Three of these mutations were novel. No alterations were found in 3 of 19 VHL patients. In Group 2, one nonsense VHL mutation was detected in a young patient with a solitary central nervous system hemangioblastoma without familial history. A study of 30 first-degree relatives revealed four carriers with VHL mutations. Conclusions: We found three novel mutations in the VHL gene in our population. Our results emphasize the importance of a complete genetic study of VHL to confirm type 1 VHL disease, not only in patients with clinical diagnostic criteria but also in those presenting a single typical manifestation.
MeSH term(s)	Adolescent ; Adult ; Aged ; Argentina ; Asian Continental Ancestry Group/genetics ; Child ; Child, Preschool ; Codon, Nonsense/genetics ; Cohort Studies ; DNA Mutational Analysis ; Female ; Frameshift Mutation/genetics ; Germ-Line Mutation ; Hemangioblastoma/genetics ; Humans ; Male ; Middle Aged ; Multiplex Polymerase Chain Reaction ; Mutation, Missense/genetics ; Pedigree ; Retrospective Studies ; Sequence Deletion ; Von Hippel-Lindau Tumor Suppressor Protein/blood ; Von Hippel-Lindau Tumor Suppressor Protein/genetics ; Von Hippel-Lindau Tumor Suppressor Protein/metabolism ; von Hippel-Lindau Disease/genetics
Chemical Substances	Codon, Nonsense ; Von Hippel-Lindau Tumor Suppressor Protein (EC 2.3.2.27) ; VHL protein, human (EC 6.3.2.-)
Language	English
Publishing date	2016-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	2486664-7
ISSN	1945-0257 ; 1945-0265
ISSN (online)	1945-0257
ISSN	1945-0265
DOI	10.1089/gtmb.2016.0204
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Article ; Online: Type 1 IGF Receptor Localization in Paediatric Gliomas: Significant Association with WHO Grading and Clinical Outcome.

Clément, Florencia / Martin, Ayelen / Venara, Marcela / de Luján Calcagno, Maria / Mathó, Cecilia / Maglio, Silvana / Lombardi, Mercedes García / Bergadá, Ignacio / Pennisi, Patricia A

Hormones & cancer

2018 Volume 9, Issue 3, Page(s) 205–214

Abstract: Nuclear localization of insulin-like growth factor receptor type 1 (IGF-1R) has been described as adverse prognostic factor in some cancers. We studied the expression and localization of IGF-1R in paediatric patients with gliomas, as well as its ... ...

Abstract	Nuclear localization of insulin-like growth factor receptor type 1 (IGF-1R) has been described as adverse prognostic factor in some cancers. We studied the expression and localization of IGF-1R in paediatric patients with gliomas, as well as its association with World Health Organization (WHO) grading and survival. We conducted a single cohort, prospective study of paediatric patients with gliomas. Samples were taken at the time of the initial surgery; IGF-1R expression and localization were characterized by immunohistochemistry (IHC), subcellular fractionation and western blotting. Tumours (47/53) showed positive staining for IGF-1R by IHC. IGF-1R nuclear labelling was observed in 10/47 cases. IGF-1R staining was mostly non-nuclear in low-grade tumours, while IGF-1R nuclear labelling was predominant in high-grade gliomas (p = 0.0001). Survival was significantly longer in patients with gliomas having non-nuclear IGF-1R localization than in patients with nuclear IGF-1R tumours (p = 0.016). In gliomas, IGF-1R nuclear localization was significantly associated with both high-grade tumours and increased risk of death. Based on a prospective design, we provide evidence of a potential usefulness of intracellular localization of IGF-1R as prognostic factor in paediatric patients with gliomas.
MeSH term(s)	Active Transport, Cell Nucleus ; Adolescent ; Biomarkers, Tumor/metabolism ; Brain Neoplasms/diagnosis ; Brain Neoplasms/metabolism ; Brain Neoplasms/mortality ; Cell Nucleus/metabolism ; Child ; Child, Preschool ; Cohort Studies ; Female ; Glioma/diagnosis ; Glioma/metabolism ; Glioma/mortality ; Humans ; Immunohistochemistry ; Infant ; Male ; Neoplasm Staging ; Prognosis ; Prospective Studies ; Receptor, IGF Type 1/genetics ; Receptor, IGF Type 1/metabolism ; Survival Analysis ; World Health Organization
Chemical Substances	Biomarkers, Tumor ; Receptor, IGF Type 1 (EC 2.7.10.1)
Language	English
Publishing date	2018-03-09
Publishing country	United States
Document type	Journal Article ; Observational Study ; Research Support, Non-U.S. Gov't
ZDB-ID	2543318-0
ISSN	1868-8500 ; 1868-8500
ISSN (online)	1868-8500
ISSN	1868-8500
DOI	10.1007/s12672-018-0328-7
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Article ; Online: Igf-I regulates pheochromocytoma cell proliferation and survival in vitro and in vivo.

Fernández, María Celia / Venara, Marcela / Nowicki, Susana / Chemes, Héctor E / Barontini, Marta / Pennisi, Patricia A

Endocrinology

2012 Volume 153, Issue 8, Page(s) 3724–3734

Abstract: IGFs are involved in malignant transformation and growth of several tissues, including the adrenal medulla. The present study was designed to evaluate the impact of IGF-I on pheochromocytoma development. We used a murine pheochromocytoma (MPC) cell line ( ...

Abstract	IGFs are involved in malignant transformation and growth of several tissues, including the adrenal medulla. The present study was designed to evaluate the impact of IGF-I on pheochromocytoma development. We used a murine pheochromocytoma (MPC) cell line (MPC4/30) and an animal model with a reduction of 75% in circulating IGF-I levels [liver-IGF-I-deficient (LID) mice] to perform studies in vitro and in vivo. We found that, in culture, IGF-I stimulation increases proliferation, migration, and anchorage-independent growth, whereas it inhibits apoptosis of MPC cells. When injected to control and to LID mice, MPC cells grow and form tumors with features of pheochromocytoma. Six weeks after cell inoculation, all control mice developed sc tumors. In contrast, in 73% of LID mice, tumor development was delayed to 7-12 wk, and the remaining 27% did not develop tumors up to 12 wk after inoculation. LID mice harboring MPC cells and treated with recombinant human IGF-I (LID+) developed tumors as controls. Tumors developed in control, LID, and LID+ mice had similar histology and were similarly positive for IGF-I receptor expression. The apoptotic index was higher in tumors from LID mice compared with those from control mice, whereas vascular density was decreased. In summary, our work demonstrates that IGF-I has a critical role in maintaining tumor phenotype and survival of already transformed pheochromocytoma cells and is required for the initial establishment of these tumors, providing encouragement to carry on research studies to address the IGF-I/IGF-I receptor system as a target of therapeutic strategies for pheochromocytoma treatment in the future.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Blotting, Western ; Cell Line, Tumor ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Disease Models, Animal ; Female ; Humans ; Immunohistochemistry ; Immunoprecipitation ; Insulin-Like Growth Factor I/pharmacology ; Male ; Mice ; PC12 Cells ; Pheochromocytoma/metabolism ; Rats ; Receptor, IGF Type 1/metabolism
Chemical Substances	Insulin-Like Growth Factor I (67763-96-6) ; Receptor, IGF Type 1 (EC 2.7.10.1)
Language	English
Publishing date	2012-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2012-1107
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Article ; Online: Safety of growth hormone replacement in survivors of cancer and intracranial and pituitary tumours: a consensus statement.

Boguszewski, Margaret C S / Boguszewski, Cesar L / Chemaitilly, Wassim / Cohen, Laurie E / Gebauer, Judith / Higham, Claire / Hoffman, Andrew R / Polak, Michel / Yuen, Kevin C J / Alos, Nathalie / Antal, Zoltan / Bidlingmaier, Martin / Biller, Beverley M K / Brabant, George / Choong, Catherine S Y / Cianfarani, Stefano / Clayton, Peter E / Coutant, Regis / Cardoso-Demartini, Adriane A /

Fernandez, Alberto / Grimberg, Adda / Guðmundsson, Kolbeinn / Guevara-Aguirre, Jaime / Ho, Ken K Y / Horikawa, Reiko / Isidori, Andrea M / Jørgensen, Jens Otto Lunde / Kamenicky, Peter / Karavitaki, Niki / Kopchick, John J / Lodish, Maya / Luo, Xiaoping / McCormack, Ann I / Meacham, Lillian / Melmed, Shlomo / Mostoufi Moab, Sogol / Müller, Hermann L / Neggers, Sebastian J C M M / Aguiar Oliveira, Manoel H / Ozono, Keiichi / Pennisi, Patricia A / Popovic, Vera / Radovick, Sally / Savendahl, Lars / Touraine, Philippe / van Santen, Hanneke M / Johannsson, Gudmundur

European journal of endocrinology

2022 Volume 186, Issue 6, Page(s) P35–P52

Abstract: Growth hormone (GH) has been used for over 35 years, and its safety and efficacy has been studied extensively. Experimental studies showing the permissive role of GH/insulin-like growth factor 1 (IGF-I) in carcinogenesis have raised concerns regarding ... ...

Abstract	Growth hormone (GH) has been used for over 35 years, and its safety and efficacy has been studied extensively. Experimental studies showing the permissive role of GH/insulin-like growth factor 1 (IGF-I) in carcinogenesis have raised concerns regarding the safety of GH replacement in children and adults who have received treatment for cancer and those with intracranial and pituitary tumours. A consensus statement was produced to guide decision-making on GH replacement in children and adult survivors of cancer, in those treated for intracranial and pituitary tumours and in patients with increased cancer risk. With the support of the European Society of Endocrinology, the Growth Hormone Research Society convened a Workshop, where 55 international key opinion leaders representing 10 professional societies were invited to participate. This consensus statement utilized: (1) a critical review paper produced before the Workshop, (2) five plenary talks, (3) evidence-based comments from four breakout groups, and (4) discussions during report-back sessions. Current evidence reviewed from the proceedings from the Workshop does not support an association between GH replacement and primary tumour or cancer recurrence. The effect of GH replacement on secondary neoplasia risk is minor compared to host- and tumour treatment-related factors. There is no evidence for an association between GH replacement and increased mortality from cancer amongst GH-deficient childhood cancer survivors. Patients with pituitary tumour or craniopharyngioma remnants receiving GH replacement do not need to be treated or monitored differently than those not receiving GH. GH replacement might be considered in GH-deficient adult cancer survivors in remission after careful individual risk/benefit analysis. In children with cancer predisposition syndromes, GH treatment is generally contraindicated but may be considered cautiously in select patients.
MeSH term(s)	Adult ; Child ; Growth Hormone ; Human Growth Hormone/adverse effects ; Humans ; Insulin-Like Growth Factor I ; Neoplasm Recurrence, Local/chemically induced ; Pituitary Neoplasms/drug therapy ; Survivors
Chemical Substances	Human Growth Hormone (12629-01-5) ; Insulin-Like Growth Factor I (67763-96-6) ; Growth Hormone (9002-72-6)
Language	English
Publishing date	2022-04-21
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1183856-5
ISSN	1479-683X ; 0804-4643
ISSN (online)	1479-683X
ISSN	0804-4643
DOI	10.1530/EJE-21-1186
Database	MEDical Literature Analysis and Retrieval System OnLINE

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