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dc.creatorJekić, B.
dc.creatorNovaković, I.
dc.creatorLuković, L
dc.creatorKuzmanović, M
dc.creatorPopović, Branka
dc.creatorMilašin, Jelena
dc.creatorBunjevacki, G
dc.creatorDamnjanović, Tatjana
dc.creatorCvjetičanin, S
dc.creatorBunjevački, Vera
dc.date.accessioned2020-07-02T12:12:36Z
dc.date.available2020-07-02T12:12:36Z
dc.date.issued2006
dc.identifier.issn0165-4608
dc.identifier.urihttps://smile.stomf.bg.ac.rs/handle/123456789/1314
dc.description.abstractMyelodysplastic syndromes (MDS) are rare disorders in children. Molecular mechanisims underlying MDS in children are not yet completely understood. Considering the role of FMS and TP53 gene mutations in adult MDS patients, we analyzed nnutations 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.en
dc.publisherElsevier Science Inc, New York
dc.rightsrestrictedAccess
dc.sourceCancer Genetics & Cytogenetics
dc.titleLack of TP53 and FMS gene mutations in children with myelodysplastic syndromeen
dc.typearticle
dc.rights.licenseARR
dcterms.abstractБуњевачки, Вера; Новаковић, И; Јекић, Б; Луковић, Л; Кузмановић, М; Цвјетичанин, С; Дамњановић, Татјана; Буњевацки, Г; Милашин, Јелена; Поповић, Бранка;
dc.citation.volume166
dc.citation.issue2
dc.citation.spage163
dc.citation.epage165
dc.citation.other166(2): 163-165
dc.citation.rankM23
dc.identifier.wos000237174400011
dc.identifier.doi10.1016/j.cancergencyto.2005.11.003
dc.identifier.pmid16631474
dc.identifier.scopus2-s2.0-33646073109
dc.type.versionpublishedVersion


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