Noonan syndrome 5

Common Name(s)

Noonan syndrome 5

Noonan syndrome is a genetic disorder that causes abnormal development of multiple parts of the body. Characteristics of the syndrome include a distinctive facial appearance, short stature, a broad or webbed neck, congenital heart defects, bleeding problems, skeletal malformations, and developmental delay. Noonan syndrome may be caused by mutations in any one of several genes including the PTPN11, KRAS, RAF1, SOS1, NRAS and BRAF genes.  It is sometimes referred to as a specific subtype based on the specific, mutated gene that causes the syndrome in an affected individual. It is typically inherited in an autosomal dominant manner, although in many individuals with Noonan syndrome, the mutation occurs for the first time and neither of the parents has the condition.
 

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Advocacy and Support Organizations

 

Condition Specific Organizations

Following organizations serve the condition "Noonan syndrome 5" for support, advocacy or research.

There are currently no organizations listed in Disease InfoSearch that support this condition. Create a listing.

 

 

General Support Organizations

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Scientific Literature

Articles from the PubMed Database

Research articles describe the outcome of a single study. They are the published results of original research.
The terms "Noonan syndrome 5" returned 0 free, full-text research articles on human participants.

Reviews from the PubMed Database

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The terms "Noonan syndrome 5" returned 0 free, full-text review articles on human participants.

 
 
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Clinical Trial Information This information is provided by ClinicalTrials.gov

TD-6450 SAD and MAD in Healthy Subjects
 

Status: Recruiting

Condition Summary: Hepatitis C

 

Last Updated: 18 Aug 2014

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TD-6450 MAD Study in HCV Infected Subjects
 

Status: Recruiting

Condition Summary: Hepatitis C; HCV

 

Last Updated: 18 Aug 2014

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A Phase 1a/1b Study of PPI-383 in Healthy Adults and Hepatitis C Patients
 

Status: Recruiting

Condition Summary: Hepatitis C, Chronic

 

Last Updated: 20 Aug 2013

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