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No Genomic Aberrations in Langerhans Cell Histiocytosis as Assessed by Diverse Molecular Technologies

da Costa, Cristiana E. T. ; Szuhai, Karoly ; van Eijk, Ronald ; Hoogeboom, Manja ; Sciot, Raphael ; Mertens, Fredrik LU ; Bjorgvinsdottir, Helga ; Debiec-Rychter, Maria ; de Krijger, Ronald R. and Hogendoorn, Pancras C. W. , et al. (2009) In Genes, Chromosomes and Cancer 48(3). p.239-249
Abstract
The etiology of Langerhans cell histiocytosis (LCH), a disease characterized by uncontrolled proliferation of Langerhans cells, is unknown. Although some believe that LCH is reactive, others support a neoplastic origin. We tested the hypothesis that LCH is neoplastic by investigating potential consistent chromosomal aberrations in LCH cells. We used multiparameter DNA flow cytometry to analyze the DNA ploidy LCH cells in 20 cases, performed karyotype analysis in 31 cases, array-based comparative genomic hybridization (arrayCGH) and single nucleotide polymorphism (SNP) arrays with DNA from flow-sorted CD1a-positive and CD1a-negative cells in 19 cases. Ploidy analysis revealed diploid DNA content in all cases. The karyotype of all patients... (More)
The etiology of Langerhans cell histiocytosis (LCH), a disease characterized by uncontrolled proliferation of Langerhans cells, is unknown. Although some believe that LCH is reactive, others support a neoplastic origin. We tested the hypothesis that LCH is neoplastic by investigating potential consistent chromosomal aberrations in LCH cells. We used multiparameter DNA flow cytometry to analyze the DNA ploidy LCH cells in 20 cases, performed karyotype analysis in 31 cases, array-based comparative genomic hybridization (arrayCGH) and single nucleotide polymorphism (SNP) arrays with DNA from flow-sorted CD1a-positive and CD1a-negative cells in 19 cases. Ploidy analysis revealed diploid DNA content in all cases. The karyotype of all patients analyzed was normal, excluding the presence of balanced translocations. ArrayCGH and SNP arrays did not show genome abnormalities. Despite positive TP53 protein immunohistochemical staining, sequencing of exon 5 to 8 of p53 gene showed no alterations in 7 cases. This study strongly suggests that gross chromosomal abnormalities do not cause LCH. Although we cannot exclude cryptic point mutations in as yet unidentified genes, this study of 72 LCH cases shows that LCH may be the result of restricted oligoclonal stimulation rather than unlimited neoplastic proliferation. (c) 2008 Wiley-Liss, Inc. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Genes, Chromosomes and Cancer
volume
48
issue
3
pages
239 - 249
publisher
Wiley-Liss Inc.
external identifiers
  • wos:000262536700004
  • scopus:62449241914
  • pmid:19051326
ISSN
1045-2257
DOI
10.1002/gcc.20634
language
English
LU publication?
yes
id
edae5908-1656-4e51-a63c-4cb8275364e5 (old id 1312624)
date added to LUP
2016-04-01 12:37:16
date last changed
2025-04-04 15:14:09
@article{edae5908-1656-4e51-a63c-4cb8275364e5,
  abstract     = {{The etiology of Langerhans cell histiocytosis (LCH), a disease characterized by uncontrolled proliferation of Langerhans cells, is unknown. Although some believe that LCH is reactive, others support a neoplastic origin. We tested the hypothesis that LCH is neoplastic by investigating potential consistent chromosomal aberrations in LCH cells. We used multiparameter DNA flow cytometry to analyze the DNA ploidy LCH cells in 20 cases, performed karyotype analysis in 31 cases, array-based comparative genomic hybridization (arrayCGH) and single nucleotide polymorphism (SNP) arrays with DNA from flow-sorted CD1a-positive and CD1a-negative cells in 19 cases. Ploidy analysis revealed diploid DNA content in all cases. The karyotype of all patients analyzed was normal, excluding the presence of balanced translocations. ArrayCGH and SNP arrays did not show genome abnormalities. Despite positive TP53 protein immunohistochemical staining, sequencing of exon 5 to 8 of p53 gene showed no alterations in 7 cases. This study strongly suggests that gross chromosomal abnormalities do not cause LCH. Although we cannot exclude cryptic point mutations in as yet unidentified genes, this study of 72 LCH cases shows that LCH may be the result of restricted oligoclonal stimulation rather than unlimited neoplastic proliferation. (c) 2008 Wiley-Liss, Inc.}},
  author       = {{da Costa, Cristiana E. T. and Szuhai, Karoly and van Eijk, Ronald and Hoogeboom, Manja and Sciot, Raphael and Mertens, Fredrik and Bjorgvinsdottir, Helga and Debiec-Rychter, Maria and de Krijger, Ronald R. and Hogendoorn, Pancras C. W. and Egeler, R. Maarten and Annels, Nicola E.}},
  issn         = {{1045-2257}},
  language     = {{eng}},
  number       = {{3}},
  pages        = {{239--249}},
  publisher    = {{Wiley-Liss Inc.}},
  series       = {{Genes, Chromosomes and Cancer}},
  title        = {{No Genomic Aberrations in Langerhans Cell Histiocytosis as Assessed by Diverse Molecular Technologies}},
  url          = {{http://dx.doi.org/10.1002/gcc.20634}},
  doi          = {{10.1002/gcc.20634}},
  volume       = {{48}},
  year         = {{2009}},
}