Detection of molecular cytogenetic aberrations in langerhans cell histiocytosis of bone

Langerhans cell histiocytosis (LCH) is a disorder of unknown etiology that gives rise to clonal expansion of Langerhans-like cells or their precursors. The molecular basis include aberrant expression of several adhesion molecules and elevated expression of p53, c-myc, and H-ras. To identify new loca...

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Bibliographic Details
Published in:Human pathology 2002-05, Vol.33 (5), p.555-560
Main Authors: Murakami, Ichiro, Gogusev, Jean, Fournet, Jean Christophe, Glorion, Christophe, Jaubert, Francis
Format: Article
Language:English
Subjects:
Adolescent
Biological and medical sciences
Bone Diseases - genetics
Bone Diseases - pathology
Child
Child, Preschool
comparative genomic hybridization
Diseases of the osteoarticular system
Dissection
DNA - analysis
Female
Hematologic and hematopoietic diseases
Histiocytosis, Langerhans-Cell - genetics
Histiocytosis, Langerhans-Cell - pathology
Humans
Langerhans cell histiocytosis
Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis
Loss of Heterozygosity
Male
Medical sciences
Micromanipulation
Nucleic Acid Hybridization
Polymerase Chain Reaction
Tumors of striated muscle and skeleton
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Summary:Langerhans cell histiocytosis (LCH) is a disorder of unknown etiology that gives rise to clonal expansion of Langerhans-like cells or their precursors. The molecular basis include aberrant expression of several adhesion molecules and elevated expression of p53, c-myc, and H-ras. To identify new locations of LCH-related oncogenes or tumor-suppressor genes, we performed comparative genomic hybridization (CGH) and loss of heterozygosity (LOH) analysis on a series of 7 bone LCH lesions. Recurrent abnormalities were found by the CGH in all cases representing losses of DNA sequences on chromosomes 1p, 5, 6, 7, 9, 16, 17, and 22q. Gain of DNA copy number was seen on chromosomes 2q, 4q, and 12. The CGH data were supplemented by LOH analysis by means of 85 polymorphic microsatellite markers distributed along chromosomes 1, 7, 9, and 22. The highest frequency of LOH was found on 1p region in 3 of 7 informative cases and on chromosome 7 in 4 cases. Allelic loss was also detected on chromosomes 9 in 2 of 7 informative cases and on 22q in 1 of 7 cases. These results indicate that the deleted chromosomal segments may contain genes important in LCH initiation and progression. HUM PATHOL 33:555-560. Copyright 2002, Elsevier Science (USA). All rights reserved.
ISSN:0046-8177
1532-8392
DOI:10.1053/hupa.2002.124035