Please use this identifier to cite or link to this item: https://doi.org/10.1038/bcj.2017.74
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dc.titleOverexpression of SOX4 correlates with poor prognosis of acute myeloid leukemia and is leukemogenic in zebrafish
dc.contributor.authorLu, J.-W
dc.contributor.authorHsieh, M.-S
dc.contributor.authorHou, H.-A
dc.contributor.authorChen, C.-Y
dc.contributor.authorTien, H.-F
dc.contributor.authorLin, L.-I
dc.date.accessioned2020-10-26T02:43:14Z
dc.date.available2020-10-26T02:43:14Z
dc.date.issued2017
dc.identifier.citationLu, J.-W, Hsieh, M.-S, Hou, H.-A, Chen, C.-Y, Tien, H.-F, Lin, L.-I (2017). Overexpression of SOX4 correlates with poor prognosis of acute myeloid leukemia and is leukemogenic in zebrafish. Blood Cancer Journal 7 (8) : e593. ScholarBank@NUS Repository. https://doi.org/10.1038/bcj.2017.74
dc.identifier.issn2044-5385
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/179702
dc.description.abstractThe SOX4 transcription factor is a key regulator of embryonic development, cell-fate decision, cellular differentiation and oncogenesis. Abnormal expression of SOX4 is related to malignant tumor transformation and cancer metastasis. However, no reports are available regarding the clinical significance of SOX4 in acute myeloid leukemia (AML) and the role of SOX4 in leukemogenesis. In the current study, we found that AML patients with low bone marrow (BM) SOX4 expression had higher remission rates and longer overall survival than those with high SOX4 expression, regardless of age, white blood cell count at diagnosis, karyotype profile and NPM1/FLT3-ITD status. To elucidate the role of SOX4 in leukemogenesis, we generated a transgenic zebrafish model that overexpressed human SOX4 in the myeloid lineage Tg(spi1-SOX4-EGFP). These transgenic zebrafish showed, at 5 months of age, increased myelopoiesis with dedifferentiation in kidney marrow. At 9 months of age, their kidney structure was significantly effaced and distorted by increased infiltration of myeloid progenitor cells. These results suggest that SOX4 is not only an independent prognostic factor of AML, but also an important molecular factor in leukemogenesis. © 2017 The Author(s).
dc.publisherNature Publishing Group
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20201031
dc.subjectCD135 antigen
dc.subjectmessenger RNA
dc.subjectnucleophosmin
dc.subjecttranscription factor Sox4
dc.subjecttranscription factor Sox
dc.subjecttumor protein
dc.subjectzebrafish protein
dc.subjectacute myeloid leukemia
dc.subjectadult
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectbone marrow cell
dc.subjectcancer patient
dc.subjectcancer prognosis
dc.subjectcell dedifferentiation
dc.subjectcell infiltration
dc.subjectcontrolled study
dc.subjectde novo acute myeloid leukemia
dc.subjectdisease free survival
dc.subjectembryo
dc.subjectfollow up
dc.subjecthuman
dc.subjectimmunocytochemistry
dc.subjectin situ hybridization
dc.subjectinduction chemotherapy
dc.subjectkaryotype
dc.subjectkaryotyping
dc.subjectkidney structure
dc.subjectleukemogenesis
dc.subjectleukocyte count
dc.subjectmajor clinical study
dc.subjectmicroscopy
dc.subjectmyeloid progenitor cell
dc.subjectmyelopoiesis
dc.subjectnonhuman
dc.subjectoverall survival
dc.subjectpatient
dc.subjectpolymerase chain reaction
dc.subjectprotein expression
dc.subjectquantitative analysis
dc.subjectremission
dc.subjectreverse transcription polymerase chain reaction
dc.subjecttissue section
dc.subjectzebra fish
dc.subjectacute myeloid leukemia
dc.subjectanimal
dc.subjectbiosynthesis
dc.subjectgene expression regulation
dc.subjectgenetics
dc.subjectmetabolism
dc.subjectmyelopoiesis
dc.subjectpathology
dc.subjecttransgenic animal
dc.subjectAnimals
dc.subjectAnimals, Genetically Modified
dc.subjectGene Expression Regulation, Neoplastic
dc.subjectLeukemia, Myeloid, Acute
dc.subjectMyelopoiesis
dc.subjectNeoplasm Proteins
dc.subjectSOXC Transcription Factors
dc.subjectZebrafish
dc.subjectZebrafish Proteins
dc.typeArticle
dc.contributor.departmentBIOLOGICAL SCIENCES
dc.description.doi10.1038/bcj.2017.74
dc.description.sourcetitleBlood Cancer Journal
dc.description.volume7
dc.description.issue8
dc.description.pagee593
dc.published.statepublished
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