Linked Life Data

2556071

Source:http://linkedlifedata.com/resource/pubmed/id/2556071

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1990-1-3
pubmed:abstractText
Wilms' tumour is an embryonal kidney tumour which exists in an hereditary and sporadic form. Apart from its obvious importance as a model for renal development and differentiation, the tumour has recently been exploited as an example of the action of tumour suppressor genes (or anti-oncogenes). The latter genes are characterised by a somatic loss of genetic information in tumour development, specifically from the short arm of human chromosome 11 in Wilms' tumour. To further study the developmental aspects of the tumour we have established in vitro cell cultures from tumour tissues, which, unlike the majority of Wilms' tumour cell lines, have been genotyped according to their chromosome 11 gene status and their antigen expression patterns, compared to the original normal kidney and tumour tissues. The cell cultures exist both as primary and secondary cultures, and their limited life span in culture has been extended by transfection of SV40 large T antigen. The mechanism of tumour suppression by the Wilms' locus has been explored by producing cell hybrids between the immortalised kidney cells, and an "indicator cell" (HeLa), whose chromosome 11 genotypes have been monitored in vivo and in vitro by restriction fragment length polymorphisms. Non-random patterns of inheritance of the mutant allele have also been investigated, both in tumour tissue and in syndromes, like the Beckwith-Wiedemann Syndrome, which pre-dispose to development of Wilms' tumour (and other embryonal tumours). It is also apparent that allele-specific methylation occurs in Wilms' tumour tissues, probably resulting in changes of gene expression patterns. Significant elevation of transcription of the N-myc oncogene was detected in the blastemal cells of the most malignant Wilms' tumours, whereas a marked decrease in the expression of HLA class I, at both RNA and protein levels was observed in the same cells. Wilm's tumour provides a clear illustration of the requirement for a combination of dominantly and recessively acting genes, in order to produce a malignant embryonal tumour.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0250-7005
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1417-26
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:articleTitle
Molecular and cellular biology of Wilms' tumour.
pubmed:affiliation
Department of Pathology, University of Bristol, Medical School, U.K.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't