Linked Life Data

8370627

Source:http://linkedlifedata.com/resource/pubmed/id/8370627

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1993-10-8
pubmed:abstractText
Hereditary melanoma in Xiphophorus hybrids carrying the melanoma-inducing Tu-Sd locus is caused by transcriptional activation of the Xmrk gene that resides at the Tu-Sd locus and encodes a novel member of receptor tyrosine kinases (RTK). In this study, a total of 27 hereditary melanomas from various hybrid genotypes harbouring 7 different Tu alleles were also found to over-express the corresponding Xmrk alleles. The level of over-expression correlated with the degree of malignancy of the melanoma. In addition, Xsrc expression was high in many malignant melanomas. Expression patterns and levels of the Xiphophorus EGF-receptor gene (Xerb B), the c-myc (Xmyc), and the PDGF (Xsis) gene(s) were not intriguing. Transcription of the ras gene(s) may be correlated to secondary events of melanoma progression. Expression patterns of Xfms, the Xiphophorus CSF-I receptor homologue, can be explained by different contents of infiltrating macrophages in the tumors. In carcinogen-induced tumors including one melanoma no significant expression of the Xmrk oncogene could be detected. Xsrc expression, however, was strikingly high. This indicates that activation of oncogenes other than Xmrk is instrumental in tumorigenesis of neoplasia of non-hereditary origin.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0020-7136
pubmed:author
pubmed:issnType
Print
pubmed:day
9
pubmed:volume
55
pubmed:geneSymbol
Xerb B, Xfms, Xmrk, Xmyc, Xras, Xsis, Xsrc
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
288-96
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Different expression patterns of oncogenes and proto-oncogenes in hereditary and carcinogen-induced tumors of Xiphophorus.
pubmed:affiliation
Max-Planck-Institut für Biochemie, Martinsried bei München, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't