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Instituto de Endocrinología IEMYR, Quito, Ecuador
Maastricht University, Maastricht, The Netherlands
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Background The Ecuadorian cohort of subjects with Laron syndrome (ELS) is the world’s most numerous and genetically homogenous group of individuals with this condition. The ELS clinical phenotype is one of severe short stature and obesity, and
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of Laron syndrome (LS) patients, a prototypical case of congenital IGF-1 deficiency. The identification of novel GH–IGF-1 downstream targets reflects the key role of this axis in cancer as well as the complexity of the mechanisms responsible for
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Yoran Institute for Human Genome Research, Tel Aviv University, Tel Aviv, Israel
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Yoran Institute for Human Genome Research, Tel Aviv University, Tel Aviv, Israel
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) GH gene deletion (isolated GH deficiency, IGHD), (3) GH receptor ( GH-R ) gene defects (Laron syndrome, LS), and (4) IGF1 gene deletion. Additional conditions leading to congenital IGF1 deficiency are defects of post-GH-R signaling (e.g. STAT5
Instituto de Endocrinología IEMYR, Quito, Ecuador
Maastricht University, Maastricht, The Netherlands
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. 2011 , Marinho et al. 2018 ). Cancer protective pathways in Laron syndrome There are various reports on the negative association of Laron syndrome (LS) and cancer, and, in general, these studies show that cancer incidence is diminished in
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rates in individuals with Laron syndrome (LS) who lack GH-induced signaling and an association between elevated circulating IGF-1 and increased cancer risk (reviewed by accompanying articles in this collection). This review focuses on experiments in mice
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compared with their normal siblings ( Ikeno et al. 2003 ). Moreover, GH -/- and GHR -/- mice (Laron Syndrome, LS), both display severe IGF-1 deficiency, smaller body size, in both length and weight ( Zhou et al. 1997 ), and reduced incidence of
Departamento de Tecnología Médica, Facultad de Medicina, Universidad de Chile, Santiago, Chile
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Department of Chemistry and Biochemistry, Ohio University, Athens, Ohio, USA
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syndrome, known today as Laron syndrome (LS), is characterized by the inability of producing IGF-1 in response to GH due to genetic alterations of the GHR, leading then to GH resistance. Interestingly, the epidemiological analysis of LS individuals
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et al. 1997 , Junnila et al. 2013 , Basu et al. 2018 ) similar to Laron syndrome patients harboring inactivating GHR mutations ( Guevara-Aguirre et al. 2011 , Laron 2015 , Bartke et al. 2016 ), while in acromegaly, unrepaired lymphocyte
Maurice Wilkins Centre for Molecular Biodiscovery, Auckland, New Zealand
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Auckland Cancer Society Research Centre, University of Auckland, Auckland, New Zealand
Department of Pharmacology and Clinical Pharmacology, University of Auckland, Auckland, New Zealand
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Maurice Wilkins Centre for Molecular Biodiscovery, Auckland, New Zealand
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. 2016 , Aguiar-Oliveira & Bartke 2019 , Lu et al. 2019 , Duran-Ortiz et al. 2021 , Bartke 2022 , Brown-Borg 2022 ). Supporting this, humans born with Laron syndrome have remarkably reduced incidence of cancer, increased insulin sensitivity and
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examples of human disorders associated with congenital isolated or combined GHD or GH resistance with severe IGF1 deficiency (Laron syndrome) have found lower incidences or even absence of cancer in these groups of patients ( Aguiar-Oliveira & Bartke 2019
