Growth and Growth Factors

SOCS2 inactivation, which leads to growth hormone hypersensitivity and overgrowth, is selected as the mechanism of the year in this chapter. The second paper shows that PPAR plays a role in the growth of male mice. Under new paradigms, we learn that the disruption of a paternally expressed gene from the Gnas locus, XL s, is associated with poor postnatal growth, and we also discover a new molecular mechanism for Beckwith-Wiedemann syndrome. The effect of growth hormone treatment on the intelligence of subjects born small for gestational age is described in the new hopes section, whereas the associations between fetal growth and later suicidal behavior or breast cancer risk are reported in the new concerns section. Concept revised is represented by one paper showing that height does not influence quality of life in adult women with Turner syndrome previously treated by GH. Under clinical trials, we learn from two studies that early treatment with GH may be beneficial to body composition and motor function of infants with Prader-Willi. Two other papers in this section report the final height of GH-treated children with idiopathic short stature. Under new genes, we discover that TGF receptor-2 mutation is a cause of Marfan syndrome. We then learn that the testicular orphan nuclear receptor TR4, for which a ligand remains to be found, plays an important role in growth. Finally, in the food for thought section GH signaling is further described in 2 papers, one demonstrating a mutant biologically inactive GH, and the other dissecting SOCS2 action on the GH-receptor (GHR) pathway.