Mutation screening of the c-MYB negative regulatory domain in acute and chronic myeloid leukaemia

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dc.contributor.authorLutwyche, J.
dc.contributor.authorKeough, R.
dc.contributor.authorHughes, T.
dc.contributor.authorGonda, T.
dc.date.issued2001
dc.descriptionThe definitive version is available at www.blackwell-synergy.com
dc.description.abstractOver-expression of the c-myb gene and expression of activated forms of myb are known to transform haemopoietic cells, particularly cells of the myeloid lineage. Truncations or mutations that disrupt the negative regulatory domain (NRD) of the Myb protein confer an increased ability to transform cells. Although it has proved difficult to link mutations in c-MYB to human leukaemia, no studies investigating the presence of mutations within the c-MYB NRD have been reported. Therefore, we have performed mutational analysis of this region, using polymerase chain reaction±single-stranded conformation polymorphism and sequence analysis, in 26 patients with acute or chronic myeloid leukaemia. No mutations were detected, indicating that mutation of this region of the Myb protein is not common in the pathogenesis or progression of these diseases.
dc.description.statementofresponsibilityJodi K. Lutwyche, Rebecca A. Keough, Timothy P. Hughes and Thomas J. Gonda
dc.identifier.citationBritish Journal of Haematology, 2001; 114(3):632-634
dc.identifier.doi10.1046/j.1365-2141.2001.02966.x
dc.identifier.issn0007-1048
dc.identifier.issn1365-2141
dc.identifier.orcidHughes, T. [0000-0002-0910-3730] [0000-0002-7990-4509]
dc.identifier.orcidGonda, T. [0000-0002-8792-3021]
dc.identifier.urihttp://hdl.handle.net/2440/9327
dc.language.isoen
dc.publisherBlackwell Science Ltd
dc.source.urihttps://doi.org/10.1046/j.1365-2141.2001.02966.x
dc.subjectchronic myeloid leukaemia
dc.subjectacute myeloid leukaemia
dc.subjectproto-oncogene
dc.subjectc-Myb
dc.subjectsingle-stranded conformation polymorphism
dc.titleMutation screening of the c-MYB negative regulatory domain in acute and chronic myeloid leukaemia
dc.typeJournal article
pubs.publication-statusPublished

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