Linked Life Data

11576941

Source:http://linkedlifedata.com/resource/pubmed/id/11576941

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4 Suppl 1
pubmed:dateCreated
2001-9-28
pubmed:abstractText
In addition to the well-known uremia-related factors calcium, phosphate, and vitamin D, genetic polymorphisms and gene mutations appear to have a role as well in modulating parathyroid function. Allelic polymorphisms of the vitamin D receptor gene have been most often examined but to date their precise place is not yet certain in patients with chronic renal failure. The frequent transformation of parathyroid cell proliferation from polyclonal to monoclonal growth in patients with severe secondary hyperparathyroidism must be attributed to mutations or deletions of various tumor-suppressor genes, and probably more rarely also to an activation of tumor-enhancer genes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1523-6838
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
38
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S143-6
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Genetic aspects of secondary hyperparathyroidism in uremia.
pubmed:affiliation
Inserm Unit 507, Necker Hospital, Paris, France. drueke@necker.fr
pubmed:publicationType
Journal Article, Review