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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
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
Retraction Note: The NAD-dependent deacetylase SIRT2 is required for programmed necrosis

Nisha Narayan
In Hye Lee
Toren Finkel
Amendments and Corrections26 Feb 2014
Nature

Volume: 506, P: 516
The NAD-dependent deacetylase SIRT2 is required for programmed necrosis

Here it is shown that the NAD-dependent deacetylase SIRT2 is an essential component of necrosis, and that mouse hearts that do not contain SIRT2 or that are treated with a pharmacological inhibitor of SIRT2 are largely protected from ischaemic injury.

Nisha Narayan
In Hye Lee
Toren Finkel
Research28 Nov 2012
Nature

Volume: 492, P: 199-204
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
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
Predicting opioid consumption after surgical discharge: a multinational derivation and validation study using a foundation model

Chris Varghese
Luke Peters
Caroline Reinke
ResearchOpen Access26 Aug 2025
npj Digital Medicine

Volume: 8, P: 1-16
Hemopoietic Cell Kinase amplification with Protein Tyrosine Phosphatase Receptor T depletion leads to polycythemia, aberrant marrow erythoid maturation, and splenomegaly

Matthew Ku
Ruth N. MacKinnon
Harshal Nandurkar
ResearchOpen Access07 May 2019
Scientific Reports

Volume: 9, P: 1-11
Letting the breaks off MYCN

Giovanni Perini
Giorgio Milazzo
Paul G Ekert
News14 Oct 2016
Cell Death & Differentiation

Volume: 23, P: 1904-1905

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

Mitochondrial metabolism sustains DNMT3A-R882-mutant clonal haematopoiesis

Retraction Note: The NAD-dependent deacetylase SIRT2 is required for programmed necrosis

The NAD-dependent deacetylase SIRT2 is required for programmed necrosis

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

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

Predicting opioid consumption after surgical discharge: a multinational derivation and validation study using a foundation model

Hemopoietic Cell Kinase amplification with Protein Tyrosine Phosphatase Receptor T depletion leads to polycythemia, aberrant marrow erythoid maturation, and splenomegaly

Letting the breaks off MYCN

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