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Lack of TP53 and FMS gene mutations in children with myelodysplastic syndrome. 2006
Biljana Jekic, and
Ivana Novakovic, and
Ljiljana Lukovic, and
Milos Kuzmanovic, and
Branka Popovic, and
Jelena Milasin, and
Gordana Bunjevacki, and
Tatjana Damnjanovic, and
Suzana Cvjeticanin, and
Vera Bunjevacki
Institute of Biology and Human Genetics, School of Medicine, 26 Visegradska Str., 11000 Belgrade, Serbia and Montenegro. biljanaj@verat.net
Myelodysplastic syndromes (MDS) are rare disorders in children. Molecular mechanisms underlying MDS in children are not yet completely understood. Considering the role of FMS and TP53 gene mutations in adult MDS patients, we analyzed mutations of these genes in a cohort of 35 children with MDS. Single-strand conformation polymorphism polymerase chain reaction analysis performed on FMS codon 969 and TP53 exons 5-9 showed no mutations in the analyzed sequences. Our results suggest that molecular mechanisms of MDS evolution in children are different from those in adults.
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