Linked Life Data

8649865

Source:http://linkedlifedata.com/resource/pubmed/id/8649865

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1996-7-22
pubmed:abstractText
Although soft tissue sarcoma has a high incidence of p53 mutations, it is not clear if such alterations facilitate tumor growth and metastasis. In this study, fresh autologous normal lymphocytes, normal muscle, primary and metastatic sarcoma tissues from a single synovial sarcoma patient were examined for p53-related alterations that potentially associated with sarcoma tumor development and metastasis. Normal tissues contain two wild-type p53 alleles. Primary sarcoma had one chromosome 17p p53 allelic deletion without apparent p53 mutation in the other allele. However, metastatic tumor had deletion of one p53 allele with an exon 5 codon 135 missense mutation in the other allele. This p53 gene point mutation in the metastasis was associated with the production of mutated p53 protein. A small clone of cells harboring the identical p53 gene point mutation was identified in the primary tumor using mutant allele specific PCR amplification, albeit at levels much less than in the metastatic sarcoma. This single patient example indicate that soft tissue sarcoma metastasis can develop from clonal expansion of primary tumor cells bearing p53 mutations.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
2
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2035-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Soft tissue sarcoma metastasis from clonal expansion of p53 mutated tumor cells.
pubmed:affiliation
The University of Texas MD Anderson Cancer Center, Department of Surgical Oncology, Houston 77030, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.