You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


ABOUT JAMA
Advanced Search

Welcome   | My Account | E-mail Alerts | Access Rights | Sign In


  Vol. 285 No. 16, April 25, 2001 TABLE OF CONTENTS
  JAMA
  •  Online Features
  Medical News & Perspectives
 This Article
 •Full text
 •PDF
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citing articles on HighWire
 •Citing articles on Web of Science (5)
 •Contact me when this article is cited
 Related Content
 •Similar articles in JAMA
 Social Bookmarking
  Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit Add to Technorati Add to Twitter What's this?

Antibiotics Show Promise as Therapy for Genetic Disorders

Joan Stephenson, PhD

JAMA. 2001;285:2067-2068.

Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

New research findings involving a tried-and-true antibiotic developed decades ago are pointing the way toward a novel approach for treating genetic disorders in the 21st century, researchers suggest.

In one recent study, investigators at the University of Alabama at Birmingham (UAB) found evidence that gentamicin treatment enabled cells from patients with Hurler syndrome to override the effects of the mutation underlying the disease (Hum Mol Genet. 2001:10:291-299).

Furthermore, a growing body of research by the UAB group and others indicates that drugs such as gentamicin may one day be used to treat a subset of patients with a variety of genetic disorders, such as cystic fibrosis and muscular dystrophy. Although clinical trials testing gentamicin or agents with similar properties are at least a few years off, researchers say that laboratory and animal studies, as well as some pilot studies in human subjects, suggest that the . . . [Full Text of this Article]



Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter     What's this?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Translational readthrough by the aminoglycoside geneticin (G418) modulates SMN stability in vitro and improves motor function in SMA mice in vivo
Heier and DiDonato
Hum Mol Genet 2009;18:1310-1322.
ABSTRACT | FULL TEXT  





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 2001 American Medical Association. All Rights Reserved.