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JCI online early table of contents: July 1, 2008
Date:7/1/2008

by failed sexual maturation and infertility due to a deficiency in the small protein gonadotropin-releasing hormone (GnRH).

Six different mutations in FGF8 were identified in individuals with IHH and were associated with slightly different symptoms and varying degrees of GnRH deficiency. When mice expressing markedly reduced levels of FGF8 (approximately 55% less than normal) were analyzed they were found to lack nerve cells producing GnRH in a region of the brain known as the hypothalamus. By contrast, mice expressing slightly more FGF8 did have nerve cells producing GnRH in the hypothalamus, although fewer than normal mice. These data led the authors to conclude that FGF8 is important for the development of nerve cells producing GnRH in both mice and humans and that mutations in FGF8 can lead to GnRH deficiency and disease in humans.

TITLE: Decreased FGF8 signaling causes deficiency of gonadotropin-releasing hormone in humans and mice

AUTHOR CONTACT:
Nelly Pitteloud
Massachusetts General Hospital, Boston, Massachusetts, USA.
Phone: (617) 724-1830; Fax: (617) 726-3537; E-mail: npitteloud@partners.org.

View the PDF of this article at: https://www.the-jci.org/article.php?id=34538


ONCOLOGY: New way to predict prostate cancer spreading

For men, one of the leading causes of death from cancer is prostate cancer that has spread to a second site (something known as metastatic prostate cancer). Defining the molecular mechanisms by which the initial tumor becomes able to spread to a new site (a process known as metastasis) is likely to help clinicians predict an individual's chance of survival and help researchers develop new therapies. New data, generated by John Martignetti and colleagues, at Mount Sinai School of Medicine, New York, has identified a specific form of the protein KL
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Contact: Karen Honey
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Journal of Clinical Investigation
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