Evidence map›Paper›PMID 26440282›Full record

ArticleCell stem cell2015

AMPK Protects Leukemia-Initiating Cells in Myeloid Leukemias from Metabolic Stress in the Bone Marrow.

Yusuke Saito, Richard H Chapple, Angelique Lin, Ayumi Kitano, Daisuke Nakada

Open access · bronzeAbstract read
In one paragraph

Article in Cell stem cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 165 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
165citing papers in PubMed, 1 pooled it
8.9field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

165 citing papers in PubMed, 1 synthesis or guideline pooled it, 272 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Oxidative Phosphorylation and Fatty Acid Oxidation Are Central to Mitochondrial Metabolism Rewiring in CML Stem/Progenitor Cell Survival.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Review
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  8. Article
  9. Review
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  17. Review
  18. BCAT1 contributes to the development of TKI-resistant CML.Cellular oncology (Dordrecht, Netherlands) · 2025
    Article
  19. Article
  20. Article

105 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Yusuke SaitoDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA.
Richard H ChappleDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA.
Angelique LinDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA.
Ayumi KitanoDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA.
Daisuke NakadaDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA. Electronic address: nakada@bcm.edu.
Baylor College of Medicine · US

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
Virology CoreP30AI036211 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI BUTEL, JANET S · 1994 to 2015
$21.7M
Statistics and Bioinformatics Core - WangU24DK097153 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BURANT, CHARLES F · 2012 to 2017
$10.1M
Hematology Training ProgramT32DK060445 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI GOODELL, MARGARET A. · 2002 to 2023
$8.3M
METABOLIC REGULATION IN LEUKEMIA-INITIATING CELLSR01CA193235 · NCI · BAYLOR COLLEGE OF MEDICINE · PI NAKADA, DAISUKE · 2015 to 2024
$4.6M
BD Biosciences Special Order LSRIIS10RR024574 · NCRR · BAYLOR COLLEGE OF MEDICINE · PI LUMPKIN, ELLEN A · 2009 to 2009
$430k
NCI NIH HHS NCIP30CA125123NCI NIH HHS P30 CA125123NCI NIH HHS R01 CA193235NCI NIH HHS R01CA193235NCRR NIH HHS S10 RR024574NCRR NIH HHS S10RR024574NIAID NIH HHS P30 AI036211NIDDK NIH HHS T32 DK060445NIDDK NIH HHS U24 DK097153
6 · The paper itself

Abstract

How cancer cells adapt to metabolically adverse conditions in patients and strive to proliferate is a fundamental question in cancer biology. Here we show that AMP-activated protein kinase (AMPK), a metabolic checkpoint kinase, confers metabolic stress resistance to leukemia-initiating cells (LICs) and promotes leukemogenesis. Upon dietary restriction, MLL-AF9-induced murine acute myeloid leukemia (AML) activated AMPK and maintained leukemogenic potential. AMPK deletion significantly delayed leukemogenesis and depleted LICs by reducing the expression of glucose transporter 1 (Glut1), compromising glucose flux, and increasing oxidative stress and DNA damage. LICs were particularly dependent on AMPK to suppress oxidative stress in the hypoglycemic bone marrow environment. Strikingly, AMPK inhibition synergized with physiological metabolic stress caused by dietary restriction and profoundly suppressed leukemogenesis. Our results indicate that AMPK protects LICs from metabolic stress and that combining AMPK inhibition with physiological metabolic stress potently suppresses AML by inducing oxidative stress and DNA damage.

Indexed as

Oxidative StressAMP-Activated Protein KinasesAnimalsBone MarrowDNA DamageLeukemia, Myeloid, AcuteMiceMice, Inbred C57BLMice, Inbred NODMice, KnockoutNeoplastic Stem CellsSpleenAMP-Activated Protein KinasesAMLAMPKdietary restrictionDNA damageglycolysisleukemia-initiating cellsmetabolic stressROS

Identifiers

PMID26440282
PMCPMC4597792
OpenAlexW2118519201

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.