Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1997-9-16
pubmed:abstractText
Loss of heterozygosity on chromosome 10 is considered to be associated with the progression of glioblastomas. Two closely related regions have recently been proposed to contain the glioblastoma suppressor locus on chromosome 10q25-26; a 1 cM region between the polymorphic (CA)n-repeat markers D10S587 and D10S216, and an area of 5 cM between the markers D10S221 and D10S209. To confirm and further delineate this region, we analyzed 51 glioblastomas and 11 intermediate and low-grade gliomas for loss of heterozygosity on chromosome 10. 47/62 mostly malignant gliomas displayed complete loss of chromosome 10 and nine tumors were unaltered, whereas four glioblastomas and two low-grade oligodendrogliomas had partial loss on distal 10q. With these six tumors, we constructed a deletion map with increased marker density at 10q25-26 which shows two centromeric breakpoints at the markers D10S587 and D10S216, thus only confirming the distal, but not the proximal candidate glioblastoma suppressor locus. Two out of four low-grade oligodendrogliomas displayed partial deletions on 10q25-26. This suggests that deletion on chromosome 10 is not merely a late event in the progression of glioblastomas, but could play a role earlier in the development of gliomas.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
18
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
997-1000
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
New deletion in low-grade oligodendroglioma at the glioblastoma suppressor locus on chromosome 10q25-26.
pubmed:affiliation
Molecular Neuro-Oncology, Department of Research, University Hospital, Basel, Switzerland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't