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2014 Fiscal Year Final Research Report

Leukemogenesis between NUP98-HOX fusion genes and concomitant mutations

Research Project

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Project/Area Number 24591550
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Pediatrics
Research InstitutionShimane University

Principal Investigator

TAKETANI Takeshi  島根大学, 医学部, 講師 (30359880)

Project Period (FY) 2012-04-01 – 2015-03-31
KeywordsNUP98 / HOX / FLT3 / RAS / WT1
Outline of Final Research Achievements

To elucidate the pathogenesis of acute myeloid Leukemia with NUP98-HOX fusions, we examined the function of NUP98-HOXA9 fusion gene (NHA9) and the concomitant mutations, FLT3 internal tandem duplication (FLT3-ITD), NRAS G13V mutation (NRASMT), and WT1 R250W mutation (WT1MT). IL3-independent 32D cellular growth was significantly increased in the cells co-transfected with NHA9/FLT3-ITD, NHA9/RASMT and NHA9/WT1MT. Only cells transfected with NHA9/FLT3-ITD decreased differentiated markers, CD11b and Gr1. In all transfected cells, annexin V positive/propidium iodide negative apoptotic cells did not declined, and monodansylcadaverine used to reveal autophagic vacuoles after tamoxifen was not incorporated. Transfection of NHA9/FLT3-ITD and NHA9/NRASMT significantly increased the number of colony forming unit. These suggested that NHA9 with the simultaneous gene mutations obtained growth advantage because of augmentation of self-renewality, resulted in contribution to leukemogenesis.

Free Research Field

血液学、腫瘍学、再生医療学

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Published: 2016-06-03  

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