Reina Nagase

Shinagawa R&D Center, 1-2-5 Hiromachi, Shinagawa Ku
Hiromachi, 1400005, Japan

Last Updated: 09/26/2026

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Found 12 publications

A novel Menin-MLL1 inhibitor, DS-1594a, prevents the progression of acute leukemia with rearranged MLL1 or mutated NPM1.

A novel Menin-MLL1 inhibitor, DS-1594a, prevents the progression of acute leukemia with rearranged MLL1 or mutated NPM1.

Journal: Cancer cell international

Published: September 13, 2022

ASXL1 and SETBP1 mutations promote leukaemogenesis by repressing TGFβ pathway genes through histone deacetylation.

ASXL1 and SETBP1 mutations promote leukaemogenesis by repressing TGFβ pathway genes through histone deacetylation.

Journal: Scientific reports

Published: January 19, 2018

Expression of mutant Asxl1 perturbs hematopoiesis and promotes susceptibility to leukemic transformation.

Expression of mutant Asxl1 perturbs hematopoiesis and promotes susceptibility to leukemic transformation.

Journal: The Journal of experimental medicine

Published: June 27, 2017

A novel ASXL1-OGT axis plays roles in H3K4 methylation and tumor suppression in myeloid malignancies.

A novel ASXL1-OGT axis plays roles in H3K4 methylation and tumor suppression in myeloid malignancies.

Journal: Leukemia

Published: May 09, 2017

High expression of ABCG2 induced by EZH2 disruption has pivotal roles in MDS pathogenesis.

High expression of ABCG2 induced by EZH2 disruption has pivotal roles in MDS pathogenesis.

Journal: Leukemia

Published: December 31, 2016

Biological implications of somatic DDX41 p.R525H mutation in acute myeloid leukemia.

Biological implications of somatic DDX41 p.R525H mutation in acute myeloid leukemia.

Journal: Experimental hematology

Published: April 13, 2016

Truncation mutants of ASXL1 observed in myeloid malignancies are expressed at detectable protein levels.

Truncation mutants of ASXL1 observed in myeloid malignancies are expressed at detectable protein levels.

Journal: Experimental hematology

Published: November 10, 2015

Novel working hypothesis for pathogenesis of hematological malignancies: combination of mutations-induced cellular phenotypes determines the disease (cMIP-DD).

Novel working hypothesis for pathogenesis of hematological malignancies: combination of mutations-induced cellular phenotypes determines the disease (cMIP-DD).

Journal: Journal of biochemistry

Published: September 27, 2015

The molecular basis of myeloid malignancies.

The molecular basis of myeloid malignancies.

Journal: Proceedings of the Japan Academy. Series B, Physical and biological sciences

Published: December 16, 2014

Molecular basis of hematological malignancies

Molecular basis of hematological malignancies

Journal: [Rinsho ketsueki] The Japanese journal of clinical hematology

Published: October 10, 2014

SETBP1 mutations drive leukemic transformation in ASXL1-mutated MDS.

SETBP1 mutations drive leukemic transformation in ASXL1-mutated MDS.

Journal: Leukemia

Published: August 19, 2014

A C-terminal mutant of CCAAT-enhancer-binding protein α (C/EBPα-Cm) downregulates Csf1r, a potent accelerator in the progression of acute myeloid leukemia with C/EBPα-Cm.

A C-terminal mutant of CCAAT-enhancer-binding protein α (C/EBPα-Cm) downregulates Csf1r, a potent accelerator in the progression of acute myeloid leukemia with C/EBPα-Cm.

Journal: Experimental hematology

Published: July 17, 2014

Showing 1-12 of 12

Last Updated: 09/26/2026