Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1992-9-3
pubmed:abstractText
The pathophysiological mechanism of pituitary ACTH oversecretion in Cushing's disease remains unclear. The question of whether a collection of corticotroph cells is a primary pituitary event or is driven by increased production of hypothalamic corticotropin releasing factor is still debated. Establishing whether or not there is a clonal nature of such pituitary lesions has important conceptual and practical implications. Clonal composition of corticotroph cell adenomas was determined by X chromosome inactivation analysis using a DNA probe, M27 beta, which detects a multiallelic polymorphism in 90% of females. A first digestion by PstI reveals the polymorphism. A second digestion by MspI or its methylation sensitive isoschizomer HpaII, distinguishes the active from the inactive copy. DNA was extracted from 11 corticotroph macroadenomas responsible for Cushing's disease or Nelson's syndrome. Eight of the 11 female patients were heterozygous for the locus and included in the study. Blood leukocytes were available for 5 females and were used as controls. All 8 tumors demonstrated a monoclonal pattern while the 5 leukocyte DNA were polyclonal. Ours results show that a somatic modification plays an important role in the pathogenesis of corticotroph macroadenomas allowing monoclonal expansion of a genetically aberrant cell.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0021-972X
pubmed:author
pubmed:issnType
Print
pubmed:volume
75
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
472-5
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Monoclonality of corticotroph macroadenomas in Cushing's disease.
pubmed:affiliation
Laboratoire d'Explorations Fonctionnelles Endocriniennes, Hôpital Trousseau, Paris, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't