Evidence map›Paper›PMID 23275297›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

ADAR1 promotes malignant progenitor reprogramming in chronic myeloid leukemia.

Qingfei Jiang, Leslie A Crews, Christian L Barrett, Hye-Jung Chun, Angela C Court, Jane M Isquith, Maria A Zipeto, Daniel J Goff, Mark Minden, Anil Sadarangani and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

121 citing papers in PubMed, 187 citations in OpenAlex.

  1. Article
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  4. Article
  5. Two codes of RNA editing by deamination in human diseases.Experimental & molecular medicine · 2026
    Review
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  17. Article
  18. Clinical and translational medicine · 2024
    Review
  19. Article
  20. Review

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

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors at 10 institutions in 4 countries.

Qingfei JiangStem Cell Program, Department of Medicine, Moores Cancer Center, University of California at San Diego, La Jolla, CA 92093, USA.
Leslie A Crews
Christian L Barrett
Hye-Jung Chun
Angela C Court
Jane M Isquith
Maria A Zipeto
Daniel J Goff
Mark Minden
Anil Sadarangani
Jessica M Rusert
Kim-Hien T Dao
Sheldon R Morris
Lawrence S B Goldstein
Marco A Marra
Kelly A Frazer
Catriona H M Jamieson
Stem Cell Institute · PASanford Consortium for Regenerative Medicine · USMoores Cancer CenterUniversity of California San Diego · USBC Cancer Agency · CAHoward Hughes Medical Institute · USHuman Genome Sciences (United States) · USOregon Health & Science University · USPrincess Margaret Cancer Centre · CAUniversity of British Columbia · CA

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007198 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHI, NEIL C, INSEL, PAUL A · 1985 to 2024
$29.3M
Biomarkers of Disease Progression in CLLR21CA152613 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FRAZER, KELLY A · 2010 to 2011
$367k
CIHR CSC-105367Howard Hughes Medical InstituteNCI NIH HHS R21 CA152613NIGMS NIH HHS T32 GM007198
6 · The paper itself

Abstract

The molecular etiology of human progenitor reprogramming into self-renewing leukemia stem cells (LSC) has remained elusive. Although DNA sequencing has uncovered spliceosome gene mutations that promote alternative splicing and portend leukemic transformation, isoform diversity also may be generated by RNA editing mediated by adenosine deaminase acting on RNA (ADAR) enzymes that regulate stem cell maintenance. In this study, whole-transcriptome sequencing of normal, chronic phase, and serially transplantable blast crisis chronic myeloid leukemia (CML) progenitors revealed increased IFN-γ pathway gene expression in concert with BCR-ABL amplification, enhanced expression of the IFN-responsive ADAR1 p150 isoform, and a propensity for increased adenosine-to-inosine RNA editing during CML progression. Lentiviral overexpression experiments demonstrate that ADAR1 p150 promotes expression of the myeloid transcription factor PU.1 and induces malignant reprogramming of myeloid progenitors. Moreover, enforced ADAR1 p150 expression was associated with production of a misspliced form of GSK3β implicated in LSC self-renewal. Finally, functional serial transplantation and shRNA studies demonstrate that ADAR1 knockdown impaired in vivo self-renewal capacity of blast crisis CML progenitors. Together these data provide a compelling rationale for developing ADAR1-based LSC detection and eradication strategies.

Indexed as

Adenosine DeaminaseAlternative SplicingAnimalsBlast CrisisCell Transformation, NeoplasticDisease ProgressionFusion Proteins, bcr-ablGene Knockdown TechniquesGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansInflammation MediatorsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveLeukemia, Myeloid, Chronic-PhaseMiceNeoplastic Stem CellsADARB1 protein, humanAdenosine DeaminaseFusion Proteins, bcr-ablGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, mouseInflammation MediatorsRNA-Binding Proteins

Identifiers

PMID23275297
PMCPMC3549099
OpenAlexW2016916936

What OpenQuestion holds

Textmetadata
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.