Linked Life Data

2153197

Source:http://linkedlifedata.com/resource/pubmed/id/2153197

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1990-2-21
pubmed:abstractText
The silent corticotroph-cell adenoma (SCCA) is characterized by the presence of immunoreactive adrenocorticotropic hormone (ACTH) in the tumor tissue in patients without symptoms of Cushing's disease. To elucidate the pathophysiology of SCCA, the expression of pro-opiomelanocortin (a ACTH precursor) genes was studied in a patient with SCCA and in three patients with Cushing's disease. Pro-opiomelanocortin messenger ribonucleic acid (mRNA) was found in the SCCA tissue to a greater degree than in the adenomas of the patients with Cushing's disease. Northern blot analysis revealed that the size of pro-opiomelanocortin mRNA present in the SCCA tissue was indistinguishable from that in the adenomas associated with Cushing's disease. A ribonuclease mapping study indicated that there were no point mutations in the coding sequence of pro-opiomelanocortin mRNA present in the SCCA tissue. Because of the presence of pro-opiomelanocortin mRNA and immunoreactive ACTH in the adenoma tissue, it is proposed that translation of the mRNA and subsequent accumulation of ACTH precursor occurred in the SCCA. Thus, the absence of Cushing's disease symptoms in this SCCA could not be caused by abnormality in the coding sequence of the pro-opiomelanocortin gene or in ribonucleic acid processing. The occurrence of abnormality at or after the translational steps was strongly suggested.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-3085
pubmed:author
pubmed:issnType
Print
pubmed:volume
72
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
262-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Pro-opiomelanocortin gene expression in silent corticotroph-cell adenoma and Cushing's disease.
pubmed:affiliation
Department of Endocrinology and Metabolism, Nagoya University, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't