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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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during postnatal life. Congenital IGF1 deficiency is characterized by low to undetectable serum IGF1 levels, but normal to elevated GH production. These conditions may result from the following: (1) GH-releasing hormone-receptor ( GHRH-R ) gene defect, (2
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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
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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
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Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Verona, Italy
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Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Verona, Italy
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symptoms, including osteoarticular manifestations: acromegaly is considered as a cause of secondary osteoporosis. The GH/IGF1 axis represents in fact a major signaling system, among others, for bone development and remodeling. It is known that GH/IGF1
Institute for Molecular Bioscience, Department of Dermatology, University of Queensland, 360 Carmody Road, St Lucia, Brisbane, Queensland 4072, Australia
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/lox mice are associated with systemic Igf1 deficiency. GH levels (A) do not differ between controls and K14-Cre:Ptch1 lox/lox mice and GH induces JAK2 (B) and STAT5 (C) in K14-Cre:Ptch1 lox/lox mice similar to controls. Igf hormone levels
Instituto de Endocrinología IEMYR, Quito, Ecuador
Maastricht University, Maastricht, The Netherlands
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Research 17 54 – 57 . ( https://doi.org/10.1016/j.ghir.2006.10.007 ) Steuerman R Shevah O & Laron Z 2011 Congenital IGF1 deficiency tends to confer protection against post-natal development of malignancies . European Journal of Endocrinology 164
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Department of Nutritional Sciences, Department of Molecular Carcinogenesis, Dell Pediatric Research Institute, University of Texas, 1400 Barbara Jordan Boulevard, DPRI 2.834, Austin, Texas 78722, USA
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(in LC mice) partially mimics liver IGF1 deficiency on Met1 tumor growth, systemic IGF1 levels, tumoral Akt pathway signaling, and EMT and chemokine gene expression. In addition, the inhibitory effects of CR on tumor growth are repressed in LID mice
The Liggins Institute, Hefei National Laboratory for Physical Sciences at Microscale and School of Life Sciences, Cancer Science Institute of Singapore and Department of Pharmacology, University of Auckland, 2-6 Park Avenue, Private Bag 92019, Auckland 1023, New Zealand
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The Liggins Institute, Hefei National Laboratory for Physical Sciences at Microscale and School of Life Sciences, Cancer Science Institute of Singapore and Department of Pharmacology, University of Auckland, 2-6 Park Avenue, Private Bag 92019, Auckland 1023, New Zealand
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M Fairbairn LJ 2006 Radioprotective gene therapy through retroviral expression of manganese superoxide dismutase . Journal of Gene Medicine 8 557 – 565 . ( doi:10.1002/jgm.890 ). Steuerman R Shevah O Laron Z 2011 Congenital IGF1
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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described as a critical regulator of the capacity to respond to DNA damage. The study showed that developmental GH–IGF-1 deficiency is characterized by resistance to damaging agents, such as γ-radiation, due to a very efficient DNA repair capacity. This