TY - JOUR
T1 - MiR-424 and miR-155 deregulated expression in cytogenetically normal acute myeloid leukaemia
T2 - Correlation with NPM1 and FLT3 mutation status
AU - Faraoni, Isabella
AU - Laterza, Serena
AU - Ardiri, Davide
AU - Ciardi, Claudia
AU - Fazi, Francesco
AU - Lo-Coco, Francesco
PY - 2012
Y1 - 2012
N2 - Background: MicroRNA have a central role in normal haematopoiesis and are deregulated in acute myeloid leukaemia (AML). The purpose of the study was to investigate by qRT-PCR the expression of miRNAs involved in myeloid differentiation (miR-424, miR-155, miR-223, miR-17-5p) in 48 patients with cytogenetically normal AML well characterized for NPM1 and/or FLT3 mutations. Three types of normalization were used for the data validation. Findings: We found that miR-424 was down-modulated in AMLs with NPM1mutA regardless of FLT3 status. On the contrary, miR-155 showed up-regulation in patients with FLT3 internal tandem duplications (ITD) with or without NPM1 mutations. No significant associations were found by analyzing miR-223 and miR-17-5p in relation to FLT3 and NPM1 status. Conclusions: This study supports the view that major genetic subsets of CN-AML are associated with distinct miRNA signatures and suggests that miR-424 and miR-155 deregulation is involved in the pathogenesis of CN-AML with NPM1 and FLT3-ITD mutations, respectively.
AB - Background: MicroRNA have a central role in normal haematopoiesis and are deregulated in acute myeloid leukaemia (AML). The purpose of the study was to investigate by qRT-PCR the expression of miRNAs involved in myeloid differentiation (miR-424, miR-155, miR-223, miR-17-5p) in 48 patients with cytogenetically normal AML well characterized for NPM1 and/or FLT3 mutations. Three types of normalization were used for the data validation. Findings: We found that miR-424 was down-modulated in AMLs with NPM1mutA regardless of FLT3 status. On the contrary, miR-155 showed up-regulation in patients with FLT3 internal tandem duplications (ITD) with or without NPM1 mutations. No significant associations were found by analyzing miR-223 and miR-17-5p in relation to FLT3 and NPM1 status. Conclusions: This study supports the view that major genetic subsets of CN-AML are associated with distinct miRNA signatures and suggests that miR-424 and miR-155 deregulation is involved in the pathogenesis of CN-AML with NPM1 and FLT3-ITD mutations, respectively.
KW - Cytogenetically normal AML
KW - FLT3-ITD
KW - MiR-155
KW - MiR-424
KW - NPM1
UR - http://www.scopus.com/inward/record.url?scp=84861947624&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84861947624&partnerID=8YFLogxK
U2 - 10.1186/1756-8722-5-26
DO - 10.1186/1756-8722-5-26
M3 - Article
C2 - 22681934
AN - SCOPUS:84861947624
VL - 5
JO - Journal of Hematology and Oncology
JF - Journal of Hematology and Oncology
SN - 1756-8722
M1 - 26
ER -