rdf:type |
|
lifeskim:mentions |
umls-concept:C0008633,
umls-concept:C0040715,
umls-concept:C0332281,
umls-concept:C0441712,
umls-concept:C0599718,
umls-concept:C0599813,
umls-concept:C0599893,
umls-concept:C1326912,
umls-concept:C1378703,
umls-concept:C1511487,
umls-concept:C1522702
|
pubmed:issue |
3
|
pubmed:dateCreated |
2006-9-25
|
pubmed:abstractText |
Members of a family carrying a constitutional balanced translocation [t(3;8) (p14;q24)] have a high risk of developing multiple, bilateral clear-cell renal carcinomas. Two genetic mechanisms of carcinogenesis for this malignancy have been proposed: (1) disruption of a gene at the translocation breakpoint and (2) mutation of the von Hippel-Lindau tumor-suppressor gene at 3p25. This study further evaluates the role of the von Hippel-Lindau gene in the etiology and pathogenesis of t(3;8)-associated renal carcinomas.
|
pubmed:commentsCorrections |
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:issn |
1081-4442
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
1
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
191-5
|
pubmed:meshHeading |
pubmed-meshheading:9166475-Carcinoma, Renal Cell,
pubmed-meshheading:9166475-Chromosomes, Human, Pair 3,
pubmed-meshheading:9166475-Chromosomes, Human, Pair 8,
pubmed-meshheading:9166475-DNA Methylation,
pubmed-meshheading:9166475-Female,
pubmed-meshheading:9166475-Humans,
pubmed-meshheading:9166475-Kidney Neoplasms,
pubmed-meshheading:9166475-Male,
pubmed-meshheading:9166475-Mutation, Missense,
pubmed-meshheading:9166475-Pedigree,
pubmed-meshheading:9166475-Polymorphism, Single-Stranded Conformational,
pubmed-meshheading:9166475-Translocation, Genetic,
pubmed-meshheading:9166475-Von Hippel-Lindau Tumor Suppressor Protein
|
pubmed:articleTitle |
Mechanism of tumorigenesis of renal carcinomas associated with the constitutional chromosome 3;8 translocation.
|
pubmed:affiliation |
Biological Carcinogenesis and Development Program, Program Resources, Inc./DynCorp, USA.
|
pubmed:publicationType |
Journal Article
|