Molecular Characterization of Congenital Pseudoarthrosis of the Tibia Associated with Neurofibromatosis / 대한정형외과학회잡지
The Journal of the Korean Orthopaedic Association
; : 825-832, 2000.
Artigo
em Coreano
| WPRIM (Pacífico Ocidental)
| ID: wpr-655824
Biblioteca responsável:
WPRO
ABSTRACT
PURPOSE:
Congenital pseudarthrosis of the tibia, which is recalcitrant to treatments and prone to recur, is frequently associated with neurofibromatosis. The causative gene for neurofibromatosis, NF1, has been identified, but the pathomechanism of congenital pseudarthrosis has not been elucidated. The purposes of this study were to establish primary cell culture from the fibrous hamartoma tissue of pseudoarthrosis, and to compare the gene expression patterns of the fibrous hamartoma and normal bone. MATERIALS ANDMETHODS:
Incubation of the enzymatically treated fibrous hamartoma tissue resulted in growth of the adherent fibroblast-like spindle cells. Expression of hundreds of genes including bone morphogenetic protein-2 and -4, and NF1 were screened by reverse transcription-polymerase chain reaction and cDNA array hydridization methods.RESULTS:
Bone morphogenetic protein-2 and -4, and, NF1 were found to express in normal bone, normal periosteum as well as fibrous hamartoma and adjacent hypotrophic bone. Twenty-four genes were found to express exclusively in the fibrous hamartoma, and fifty genes only in the normal bone.CONCLUSION:
These findings suggest that the causative gene of neurofibromatosis, NF1, may be associated with pathogenesis of the congenital pseudoarthrosis of the tibia in neurofibromatosis patients.
Texto completo:
Disponível
Base de dados:
WPRIM (Pacífico Ocidental)
Assunto principal:
Periósteo
/
Pseudoartrose
/
Tíbia
/
Expressão Gênica
/
Neurofibromatoses
/
Análise de Sequência com Séries de Oligonucleotídeos
/
Cultura Primária de Células
/
Hamartoma
Tipo de estudo:
Estudo prognóstico
Limite:
Humanos
Idioma:
Coreano
Revista:
The Journal of the Korean Orthopaedic Association
Ano de publicação:
2000
Tipo de documento:
Artigo