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CREBBP inactivation sensitizes B cell acute lymphoblastic leukemia to ferroptotic cell death upon BCL2 inhibition

CREBBP mutations in B-cell acute lymphoblastic leukemia (B-ALL) are linked to poor prognosis and chemoresistance. Here, the authors show that genetic or pharmacological inactivation of CREBBP sensitizes B-ALL cells to the BCL2 inhibitor Venetoclax, inducing ferroptotic cell death and extending survival in B-ALL preclinical mouse models.

Alicia Garcia-Gimenez
Jonathan E. Ditcham
Simon E. Richardson
ResearchOpen Access20 May 2025
Nature Communications

Volume: 16, P: 1-21
Treatment of acute myeloid leukemia models by targeting a cell surface RNA-binding protein

An RNA-binding protein on leukemia cells provides an effective target in mouse models.

Benson M. George
Maria Eleftheriou
Konstantinos Tzelepis
ResearchOpen Access23 Apr 2025
Nature Biotechnology

P: 1-14
Mitochondrial metabolism sustains DNMT3A-R882-mutant clonal haematopoiesis

Metformin may serve as a non-toxic intervention to inhibit mitochondrial metabolism and slow DNMT3A-R882 clonal haematopoiesis expansion, thus delaying or averting progression to acute myeloid leukaemia.

Malgorzata Gozdecka
Monika Dudek
George S. Vassiliou
ResearchOpen Access16 Apr 2025
Nature

Volume: 642, P: 431-441
Mannose metabolism inhibition sensitizes acute myeloid leukaemia cells to therapy by driving ferroptotic cell death

Metabolic rewiring is involved in acute myeloid leukaemia (AML) maintenance. Here the authors show that the inhibition of mannose-6-phosphate isomerase in the mannose metabolism pathway sensitizes AML to FLT3-tyrosine kinase inhibitor and standard chemotherapy via enhancing lipid peroxidation and ferroptotic cell death.

Keith Woodley
Laura S. Dillingh
Paolo Gallipoli
ResearchOpen Access14 Apr 2023
Nature Communications

Volume: 14, P: 1-19
Dissecting the early steps of MLL induced leukaemogenic transformation using a mouse model of AML

The oncogene MLL is frequently translocated in leukemia, resulting in oncogenic fusion proteins. Here, the authors report a temporally controlled mouse model of MLL-ENL driven leukemia AND identify therapeutic targets associated with early MLL-ENL driven leukaemogenesis.

Silvia Basilico
Xiaonan Wang
Berthold Göttgens
ResearchOpen Access16 Mar 2020
Nature Communications

Volume: 11, P: 1-15
In vivo screening characterizes chromatin factor functions during normal and malignant hematopoiesis

Bulk ex vivo and single-cell in vivo CRISPR knockout screens are used to characterize 680 chromatin factors during mouse hematopoiesis, highlighting lineage-specific and normal and leukemia-specific functions.

David Lara-Astiaso
Ainhoa Goñi-Salaverri
Brian J. P. Huntly
ResearchOpen Access14 Aug 2023
Nature Genetics

Volume: 55, P: 1542-1554
Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leukaemia

Mark A. Dawson
Rab K. Prinjha
Tony Kouzarides
Research02 Oct 2011
Nature

Volume: 478, P: 529-533
Mutational synergy during leukemia induction remodels chromatin accessibility, histone modifications and three-dimensional DNA topology to alter gene expression

Mice bearing mutations in Flt3-ITD and Npm1c, which are commonly found in acute myeloid leukemia, are used to characterize the cooperative effects of these cancer drivers on the cellular epigenome and three-dimensional genome conformation during tumor development.

Haiyang Yun
Nisha Narayan
Brian J. P. Huntly
Research23 Sept 2021
Nature Genetics

Volume: 53, P: 1443-1455
Early loss of Crebbp confers malignant stem cell properties on lymphoid progenitors

Horton et al. show that early Crebbp loss in haematopoietic progenitors results in a defective p53-mediated DNA damage response, leading to the accumulation of epigenetic and genetic alterations, which promote the onset of lymphoid malignancies.

Sarah J. Horton
George Giotopoulos
Brian J. P. Huntly
Research21 Aug 2017
Nature Cell Biology

Volume: 19, P: 1093-1104
BET inhibitor resistance emerges from leukaemia stem cells

BET inhibitors that target bromodomain chromatin readers such as BRD4 are being explored as potential therapeutics in cancer; here, in a MLL–AF9 mouse leukaemia model, resistance to BET inhibitors is shown to emerge from leukaemia stem cells, and be partly due to increased Wnt/β-catenin signalling.

Chun Yew Fong
Omer Gilan
Mark A. Dawson
Research14 Sept 2015
Nature

Volume: 525, P: 538-542

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CREBBP inactivation sensitizes B cell acute lymphoblastic leukemia to ferroptotic cell death upon BCL2 inhibition

Treatment of acute myeloid leukemia models by targeting a cell surface RNA-binding protein

Mitochondrial metabolism sustains DNMT3A-R882-mutant clonal haematopoiesis

Mannose metabolism inhibition sensitizes acute myeloid leukaemia cells to therapy by driving ferroptotic cell death

Dissecting the early steps of MLL induced leukaemogenic transformation using a mouse model of AML

In vivo screening characterizes chromatin factor functions during normal and malignant hematopoiesis

Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leukaemia

Mutational synergy during leukemia induction remodels chromatin accessibility, histone modifications and three-dimensional DNA topology to alter gene expression

Early loss of Crebbp confers malignant stem cell properties on lymphoid progenitors

BET inhibitor resistance emerges from leukaemia stem cells

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