Peutz-Jeghers syndrome pathophysiology: Difference between revisions
No edit summary |
No edit summary |
||
Line 3: | Line 3: | ||
{{CMG}} | {{CMG}} | ||
==Overview== | ==Overview== |
Revision as of 16:04, 18 August 2015
Peutz-Jeghers syndrome Microchapters |
Diagnosis |
---|
Treatment |
Case Studies |
Peutz-Jeghers syndrome pathophysiology On the Web |
American Roentgen Ray Society Images of Peutz-Jeghers syndrome pathophysiology |
Risk calculators and risk factors for Peutz-Jeghers syndrome pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Genetics
In 1998, a gene was found to be associated with the mutation. On chromosome 19, the gene known as STK11 (LKB1)[1] is a possible tumor suppressor gene. It is inherited in an Autosomal Dominant pattern (see Mendelian inheritance) which means that anyone who has PJS has a 50% chance of passing it onto their children.
References
- ↑ "UniProtKB/Swiss-Prot entry Q15831 [STK11_HUMAN] Serine/threonine-protein kinase 11". Retrieved 2007-07-21.
Template:Digestive system neoplasia
de:Peutz-Jeghers-Syndrom
it:Sindrome di Peutz-Jeghers
nl:Syndroom van Peutz-Jeghers