Advanced

Positional and functional mapping of a neuroblastoma differentiation gene on chromosome 11

De Preter, K; Vandesompele, J; Menten, B; Carr, P; Fiegler, H; Edsjö, Anders LU ; Carter, NP; Yigit, N; Waelput, W and Van Roy, N, et al. (2005) In BMC Genomics 6.
Abstract
Background: Loss of chromosome 11q defines a subset of high-stage aggressive neuroblastomas. Deletions are typically large and mapping efforts have thus far not lead to a well defined consensus region, which hampers the identification of positional candidate tumour suppressor genes. In a previous study, functional evidence for a neuroblastoma suppressor gene on chromosome 11 was obtained through microcell mediated chromosome transfer, indicated by differentiation of neuroblastoma cells with loss of distal 11q upon introduction of chromosome 11. Interestingly, some of these microcell hybrid clones were shown to harbour deletions in the transferred chromosome 11. We decided to further exploit this model system as a means to identify... (More)
Background: Loss of chromosome 11q defines a subset of high-stage aggressive neuroblastomas. Deletions are typically large and mapping efforts have thus far not lead to a well defined consensus region, which hampers the identification of positional candidate tumour suppressor genes. In a previous study, functional evidence for a neuroblastoma suppressor gene on chromosome 11 was obtained through microcell mediated chromosome transfer, indicated by differentiation of neuroblastoma cells with loss of distal 11q upon introduction of chromosome 11. Interestingly, some of these microcell hybrid clones were shown to harbour deletions in the transferred chromosome 11. We decided to further exploit this model system as a means to identify candidate tumour suppressor or differentiation genes located on chromosome 11. Results: In a first step, we performed high-resolution arrayCGH DNA copy-number analysis in order to evaluate the chromosome 11 status in the hybrids. Several deletions in both parental and transferred chromosomes in the investigated microcell hybrids were observed. Subsequent correlation of these deletion events with the observed morphological changes lead to the delineation of three putative regions on chromosome 11: 11q25, 11p13-> 11p15.1 and 11p15.3, that may harbour the responsible differentiation gene. Conclusion: Using an available model system, we were able to put forward some candidate regions that may be involved in neuroblastoma. Additional studies will be required to clarify the putative role of the genes located in these chromosomal segments in the observed differentiation phenotype specifically or in neuroblastoma pathogenesis in general. (Less)
Please use this url to cite or link to this publication:
author
, et al. (More)
(Less)
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
BMC Genomics
volume
6
publisher
BioMed Central
external identifiers
  • pmid:16000168
  • wos:000231175900001
  • scopus:25444509200
ISSN
1471-2164
DOI
10.1186/1471-2164-6-97
language
English
LU publication?
yes
id
2da7da59-35bd-418f-90d8-21fb4723d4d6 (old id 229805)
date added to LUP
2007-08-22 08:51:05
date last changed
2017-04-30 13:28:05
@article{2da7da59-35bd-418f-90d8-21fb4723d4d6,
  abstract     = {Background: Loss of chromosome 11q defines a subset of high-stage aggressive neuroblastomas. Deletions are typically large and mapping efforts have thus far not lead to a well defined consensus region, which hampers the identification of positional candidate tumour suppressor genes. In a previous study, functional evidence for a neuroblastoma suppressor gene on chromosome 11 was obtained through microcell mediated chromosome transfer, indicated by differentiation of neuroblastoma cells with loss of distal 11q upon introduction of chromosome 11. Interestingly, some of these microcell hybrid clones were shown to harbour deletions in the transferred chromosome 11. We decided to further exploit this model system as a means to identify candidate tumour suppressor or differentiation genes located on chromosome 11. Results: In a first step, we performed high-resolution arrayCGH DNA copy-number analysis in order to evaluate the chromosome 11 status in the hybrids. Several deletions in both parental and transferred chromosomes in the investigated microcell hybrids were observed. Subsequent correlation of these deletion events with the observed morphological changes lead to the delineation of three putative regions on chromosome 11: 11q25, 11p13-> 11p15.1 and 11p15.3, that may harbour the responsible differentiation gene. Conclusion: Using an available model system, we were able to put forward some candidate regions that may be involved in neuroblastoma. Additional studies will be required to clarify the putative role of the genes located in these chromosomal segments in the observed differentiation phenotype specifically or in neuroblastoma pathogenesis in general.},
  author       = {De Preter, K and Vandesompele, J and Menten, B and Carr, P and Fiegler, H and Edsjö, Anders and Carter, NP and Yigit, N and Waelput, W and Van Roy, N and Bader, S and Påhlman, Sven and Speleman, F},
  issn         = {1471-2164},
  language     = {eng},
  publisher    = {BioMed Central},
  series       = {BMC Genomics},
  title        = {Positional and functional mapping of a neuroblastoma differentiation gene on chromosome 11},
  url          = {http://dx.doi.org/10.1186/1471-2164-6-97},
  volume       = {6},
  year         = {2005},
}