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Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/90033
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dc.contributor.authorParker, W.-
dc.contributor.authorPhillis, S.-
dc.contributor.authorYeung, D.-
dc.contributor.authorHughes, T.-
dc.contributor.authorScott, H.-
dc.contributor.authorBranford, S.-
dc.date.issued2014-
dc.identifier.citationBlood, 2014; 124(1):153-155-
dc.identifier.issn0006-4971-
dc.identifier.issn1528-0020-
dc.identifier.urihttp://hdl.handle.net/2440/90033-
dc.descriptionLetter to the editor-
dc.description.statementofresponsibilityWendy T. Parker, Stuart R. Phillis, David T. O. Yeung, Timothy P. Hughes, Hamish S. Scott, and Susan Branford-
dc.language.isoen-
dc.publisherAmerican Society of Hematology-
dc.rights© 2014 by The American Society of Hematology-
dc.source.urihttp://dx.doi.org/10.1182/blood-2014-05-573485-
dc.subjectFusion Proteins, bcr-abl-
dc.subjectPolymerase Chain Reaction-
dc.subjectMutation-
dc.subjectLeukemia, Myelogenous, Chronic, BCR-ABL Positive-
dc.subjectArtifacts-
dc.titleMany BCR-ABL1 compound mutations reported in chronic myeloid leukemia patients may actually be artifacts due to PCR-mediated recombination-
dc.typeJournal article-
dc.identifier.doi10.1182/blood-2014-05-573485-
pubs.publication-statusPublished-
dc.identifier.orcidYeung, D. [0000-0002-7558-9927]-
dc.identifier.orcidHughes, T. [0000-0002-0910-3730] [0000-0002-7990-4509]-
dc.identifier.orcidScott, H. [0000-0002-5813-631X]-
dc.identifier.orcidBranford, S. [0000-0002-1964-3626] [0000-0002-5095-7981]-
Appears in Collections:Aurora harvest 7
Medicine publications

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