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

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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.
Keywords
COMPARATIVE GENOMIC HYBRIDIZATION, CLONING, INVITRO, MICROARRAYS, AMPLIFICATION, REARRANGEMENTS, PCR, TUMORS, CELLS, 11Q DELETION

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MLA
De Preter, Katleen et al. “Positional and Functional Mapping of a Neuroblastoma Differentiation Gene on Chromosome 11.” BMC GENOMICS 6 (2005): n. pag. Print.
APA
De Preter, K., Vandesompele, J., Menten, B., Carr, P., Fiegler, H., Edsjö, A., Carter, N. P., et al. (2005). Positional and functional mapping of a neuroblastoma differentiation gene on chromosome 11. BMC GENOMICS, 6.
Chicago author-date
De Preter, Katleen, Jo Vandesompele, Björn Menten, Philippa Carr, Heike Fiegler, Anders Edsjö, Nigel P Carter, et al. 2005. “Positional and Functional Mapping of a Neuroblastoma Differentiation Gene on Chromosome 11.” Bmc Genomics 6.
Chicago author-date (all authors)
De Preter, Katleen, Jo Vandesompele, Björn Menten, Philippa Carr, Heike Fiegler, Anders Edsjö, Nigel P Carter, Nurten Yigit, Wim Waelput, Nadine Van Roy, Scott Bader, Sven Påhlman, and Franki Speleman. 2005. “Positional and Functional Mapping of a Neuroblastoma Differentiation Gene on Chromosome 11.” Bmc Genomics 6.
Vancouver
1.
De Preter K, Vandesompele J, Menten B, Carr P, Fiegler H, Edsjö A, et al. Positional and functional mapping of a neuroblastoma differentiation gene on chromosome 11. BMC GENOMICS. 2005;6.
IEEE
[1]
K. De Preter et al., “Positional and functional mapping of a neuroblastoma differentiation gene on chromosome 11,” BMC GENOMICS, vol. 6, 2005.
@article{337297,
  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.},
  articleno    = {97},
  author       = {De Preter, Katleen and Vandesompele, Jo and Menten, Björn and Carr, Philippa and Fiegler, Heike and Edsjö, Anders and Carter, Nigel P and Yigit, Nurten and Waelput, Wim and Van Roy, Nadine and Bader, Scott and Påhlman, Sven and Speleman, Franki},
  issn         = {1471-2164},
  journal      = {BMC GENOMICS},
  keywords     = {COMPARATIVE GENOMIC HYBRIDIZATION,CLONING,INVITRO,MICROARRAYS,AMPLIFICATION,REARRANGEMENTS,PCR,TUMORS,CELLS,11Q DELETION},
  language     = {eng},
  pages        = {10},
  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},
}

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