Linked Life Data

12952224

Source:http://linkedlifedata.com/resource/pubmed/id/12952224

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2003-9-3
pubmed:abstractText
The FAS antigen (CD95/APO-1) is suggested to be a tumor suppressor gene since mice and patients with congenital FAS mutations are prone to B cell lymphomas and somatic FAS mutations are described in hematological and solid tumors. Indeed, mutations of the FAS antigen have been found in 13% of multiple myelomas, 6% of follicle center lymphomas (FCL) and 21% of diffuse large B-cell lymphomas (DLBCL). To assess the possible role of FAS mutations in higher-grade transformation of FCL, biopsy specimens from 16 FCL patients were analyzed by denaturing high performance liquid chromatography and direct sequencing. Overall, 17 biopsy specimens obtained at the time of FCL diagnosis (2 biopsy specimens from one patient), 4 sequential biopsies obtained at the time of FCL relapse and 14 sequential biopsies from the time of morphologic transformation to DLBCL were evaluated. Ten polymorphisms were detected, only 4 of which have been reported previously. Nine of the polymorphisms occurred in non-translated regions, while one silent mutation was located in exon 7. Neither loss of heterozygosity nor occurrence of new mutations was observed upon higher-grade transformation of FCL to DLBCL.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1042-8194
pubmed:author
pubmed:issnType
Print
pubmed:volume
44
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1317-23
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Analysis of FAS (CD95) gene mutations in higher-grade transformation of follicle center lymphoma.
pubmed:affiliation
Stanford Genome Technology Center, 855 California Avenue, Palo Alto, CA 94304, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.