FREE NEJM E-TOC    HOME   |   SUBSCRIBE   |   CURRENT ISSUE   |   PAST ISSUES   |   COLLECTIONS   |   Search Term  Advanced Search

Sign in | Get NEJM's E-Mail Table of Contents — Free | Subscribe

Previous Volume 343:880-882 September 21, 2000 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.

	Full Text Purchase this article Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited

Clinical disorders that arise as a result of resistance to the intracellular action of a hormone are being characterized with increasing frequency. Perhaps the most notable example is the testicular feminization syndrome, now referred to as the complete androgen-insensitivity syndrome, which is characterized by a completely female appearance, a 46,XY karyotype, and serum testosterone concentrations that are normal for men. The change in terms is not just a matter of semantics but came about because several syndromes associated with partial insensitivity to androgens give rise to a range of phenotypes due to undermasculinization.

In a 46,XY fetus, androgens normally mediate . . . [Full Text of this Article]

References

This article has been cited by other articles:

• Chen, H., Hewison, M., Hu, B., Adams, J. S. (2003). Heterogeneous nuclear ribonucleoprotein (hnRNP) binding to hormone response elements: A cause of vitamin D resistance. Proc. Natl. Acad. Sci. USA 100: 6109-6114 [Abstract] [Full Text]  
• Thin, T. H., Kim, E., Yeh, S., Sampson, E. R., Chen, Y.-T., Collins, L. L., Basavappa, R., Chang, C. (2002). Mutations in the Helix 3 Region of the Androgen Receptor Abrogate ARA70 Promotion of 17beta -Estradiol-induced Androgen Receptor Transactivation. J. Biol. Chem. 277: 36499-36508 [Abstract] [Full Text]