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Previous Volume 349:1110-1112 September 18, 2003 Number 12 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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In this issue of the Journal, Kofoed et al. (pages 1139–1147) describe a novel mechanism for impaired growth in the form of a mutation in the gene for the intracytoplasmic protein signal transducer and activator of transcription 5b (STAT5b). The mutation disrupts the intracellular signaling that promulgates the physiologic effects of growth hormone. This finding illuminates an important arena of molecular genetic abnormalities involving the growth hormone–insulin-like growth factor I (IGF-I) axis.

The most striking feature of the patient described by Kofoed et al. is profound growth failure, manifested by a height at a chronologic age of 16.5 years that . . . [Full Text of this Article]

Source Information

From the Section of Pediatric Endocrinology and Diabetology, Department of Pediatrics, Riley Hospital for Children, Indiana University School of Medicine, Indianapolis.

This article has been cited by other articles:

• Camacho-Hubner, C., Rose, S., Preece, M. A., Sleevi, M., Storr, H. L., Miraki-Moud, F., Minuto, F., Frystyk, J., Rogol, A., Allan, G., Sommer, A., Savage, M. O. (2006). Pharmacokinetic Studies of Recombinant Human Insulin-Like Growth Factor I (rhIGF-I)/rhIGF-Binding Protein-3 Complex Administered to Patients with Growth Hormone Insensitivity Syndrome. J. Clin. Endocrinol. Metab. 91: 1246-1253 [Abstract] [Full Text]