%0 Journal Article %1 Schulz.2000 %A Schulz, S. %A Becker, K. F. %A Braungart, E. %A Reichmuth, C. %A Klamt, B. %A Becker, I. %A Atkinson, M. %A Gessler, M. %A Hofler, H. %D 2000 %J J Pathol %K 16/*genetics Adolescent Adult Analysis;DNA Blotting;Northern Cadherins/*genetics Case-Control Chain Child Child;Preschool Chromosomes;Human;Pair Electrophoresis;Agar Expression Female Gel Gene Heterozygosity Humans Infant Infant;Newborn Kidney Loss Male Neoplasms/*genetics Polymerase Polymorphism;Genetic Profiling Reaction Reverse Sequence Silencing Studies Transcriptase Tumor/*genetics Wilms of %N 2 %P 162--169 %T Molecular analysis of E-cadherin and cadherin-11 in Wilms' tumours %V 191 %X Different studies of Wilms' tumours have demonstrated a loss of heterozygosity (LOH) of chromosome 16q ranging from 17 to 25\%. In order to search for a potential tumour suppressor gene on 16q, we chose the calcium-dependent cell adhesion molecules E-cadherin and cadherin-11 as candidate genes, which are both located on the long arm of chromosome 16. E-cadherin is known to be expressed in epithelial structures, whereas cadherin-11 is supposed to be expressed in mesenchymal structures and developing epithelium, including renal tubules. For the present study, fresh frozen tissue from 30 Wilms' tumours and corresponding non-tumour tissues were analysed. Single nucleotide polymorphisms of the E-cadherin and cadherin-11 genes were chosen and analysed for allelic inactivation by polymerase chain reaction (PCR) amplification and sequence analysis. Loss of expression of one E-cadherin allele was seen in 10\% (2/20) of the informative cases. Two out of 11 informative cases (18\%) showed loss of expression of one cadherin-11 allele. No length alterations of either the E-cadherin or the cadherin-11 messenger RNAs were identified using reverse transcription PCR and agarose gel electrophoresis in tumour tissue. Sequencing of the entire E-cadherin coding region in seven cases showed the wild-type sequence. These data imply that E-cadherin and cadherin-11 are not likely to play typical tumour suppressor roles in Wilms' tumour. Interestingly, the E-cadherin immunohistochemistry showed a deviation from the normal reaction pattern in 50\% of the cases, with 27\% (8/30) showing an apical or cytoplasmic reaction and 23\% (7/30) being completely negative. Northern blot analysis revealed that the overall expression of cadherin-11 is much stronger than that of E-cadherin. In several cases, the expression levels of the two genes were inversely correlated, suggesting the existence of a regulatory mechanism. Analysis of differential expression of the various cadherins and their subsequent signal transduction pathways might contribute to a better understanding of the complexity of Wilms' tumour formation.

@article{Schulz.2000, abstract = {Different studies of Wilms' tumours have demonstrated a loss of heterozygosity (LOH) of chromosome 16q ranging from 17 to 25{\%}. In order to search for a potential tumour suppressor gene on 16q, we chose the calcium-dependent cell adhesion molecules E-cadherin and cadherin-11 as candidate genes, which are both located on the long arm of chromosome 16. E-cadherin is known to be expressed in epithelial structures, whereas cadherin-11 is supposed to be expressed in mesenchymal structures and developing epithelium, including renal tubules. For the present study, fresh frozen tissue from 30 Wilms' tumours and corresponding non-tumour tissues were analysed. Single nucleotide polymorphisms of the E-cadherin and cadherin-11 genes were chosen and analysed for allelic inactivation by polymerase chain reaction (PCR) amplification and sequence analysis. Loss of expression of one E-cadherin allele was seen in 10{\%} (2/20) of the informative cases. Two out of 11 informative cases (18{\%}) showed loss of expression of one cadherin-11 allele. No length alterations of either the E-cadherin or the cadherin-11 messenger RNAs were identified using reverse transcription PCR and agarose gel electrophoresis in tumour tissue. Sequencing of the entire E-cadherin coding region in seven cases showed the wild-type sequence. These data imply that E-cadherin and cadherin-11 are not likely to play typical tumour suppressor roles in Wilms' tumour. Interestingly, the E-cadherin immunohistochemistry showed a deviation from the normal reaction pattern in 50{\%} of the cases, with 27{\%} (8/30) showing an apical or cytoplasmic reaction and 23{\%} (7/30) being completely negative. Northern blot analysis revealed that the overall expression of cadherin-11 is much stronger than that of E-cadherin. In several cases, the expression levels of the two genes were inversely correlated, suggesting the existence of a regulatory mechanism. Analysis of differential expression of the various cadherins and their subsequent signal transduction pathways might contribute to a better understanding of the complexity of Wilms' tumour formation.}, added-at = {2013-01-29T13:47:26.000+0100}, author = {Schulz, S. and Becker, K. F. and Braungart, E. and Reichmuth, C. and Klamt, B. and Becker, I. and Atkinson, M. and Gessler, M. and Hofler, H.}, biburl = {https://www.bibsonomy.org/bibtex/2cd86ece7d8f98b4e82574797b8a888c8/ebch}, interhash = {6f2fa78710f80a6328e9da63dbed065a}, intrahash = {cd86ece7d8f98b4e82574797b8a888c8}, journal = {J Pathol}, keywords = {16/*genetics Adolescent Adult Analysis;DNA Blotting;Northern Cadherins/*genetics Case-Control Chain Child Child;Preschool Chromosomes;Human;Pair Electrophoresis;Agar Expression Female Gel Gene Heterozygosity Humans Infant Infant;Newborn Kidney Loss Male Neoplasms/*genetics Polymerase Polymorphism;Genetic Profiling Reaction Reverse Sequence Silencing Studies Transcriptase Tumor/*genetics Wilms of}, number = 2, pages = {162--169}, timestamp = {2013-01-29T13:47:27.000+0100}, title = {Molecular analysis of E-cadherin and cadherin-11 in Wilms' tumours}, volume = 191, year = 2000 }