Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1999-3-2
pubmed:databankReference
pubmed:abstractText
Gliomas constantly overexpress the receptor subtype SST2 for the inhibitory peptide somatostatin. Since somatostatin or metabolically stable agonists like octreotide have an antiproliferative and antisecretory potential for the treatment of SST2-expressing tumors, we evaluated the molecular integrity of SST2 in gliomas on the DNA, mRNA and protein levels. Sequencing of about 1800 bases from the SST2 gene in nine gliomas and five control samples revealed no mutations, but polymorphisms were detected in the 5'-region irrespective of the malignancy of the sample. Gliomas and the human glioma cell line U343 expressed mRNA for the receptor splice variant SST2A with a size of about 4.2 kb. A novel antibody generated against an extracellular part of the SST2 amino acid sequence strongly reacted with an 75-kDa protein in membranes from glioma or meningioma cells and-much weaker-normal rat astrocytes. The receptor could be immunostained on the surface of intact glioma cells or (weaker) astrocytes at the light and electron microscopic level. These results show that the somatostatin receptor SST2 is non-mutated in gliomas and has similar molecular properties as in non-malignant cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0169-328X
pubmed:author
pubmed:copyrightInfo
Copyright 1999 Elsevier Science B.V.
pubmed:issnType
Print
pubmed:day
22
pubmed:volume
64
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
101-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Molecular analysis of the somatostatin receptor subtype 2 in human glioma cells.
pubmed:affiliation
Department of Anatomy, University of Kiel, Olshausenstrasse 40 D-24098, Kiel, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't