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MIR29B regulates expression of MLLT11 (AF1Q), an MLL fusion partner, and low MIR29B expression associates with adverse cytogenetics and poor overall survival in AML
Author(s) -
Xiong Yin,
Li Zejuan,
Ji Min,
Tan AikChoon,
Bemis Judson,
Tse JoveVictor,
Huang Gang,
Park Jino,
Ji Chunyan,
Chen Jianjun,
Bemis Lynne T.,
Bunting Kevin D.,
Tse William
Publication year - 2011
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2011.08662.x
Subject(s) - cytogenetics , biomarker , haematopoiesis , oncology , myeloid leukemia , myelodysplastic syndromes , medicine , npm1 , fusion gene , cancer research , myeloid , biology , stem cell , karyotype , bone marrow , gene , chromosome , genetics
Summary MLLT11 , an MLL fusion partner, is a poor prognostic biomarker for paediatric acute myeloid leukaemia (AML), adult normal cytogenetics AML, and adult myelodysplastic syndrome. MLLT11 is highly regulated during haematopoietic progenitor differentiation and development but its regulatory mechanisms have not been defined. In this study, we demonstrate by transfection experiments that MIR29B directly regulates MLLT11 expression in vitro . MIR29B expression level was also inversely related to MLLT11 expression in a cohort of 56 AML patients ( P < 0·05). AML patients with low MIR29B /elevated MLLT11 expression had poor overall survival ( P = 0·038). Therefore, MIR29B may be a potential prognostic biomarker for AML patients.