Evidence map›Paper›PMID 27607576›Full record

ArticleCell death & disease2016

Atg5-dependent autophagy contributes to the development of acute myeloid leukemia in an MLL-AF9-driven mouse model.

Qiang Liu, Longgui Chen, Jennifer M Atkinson, David F Claxton, Hong-Gang Wang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

46 citing papers in PubMed, 61 citations in OpenAlex.

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  12. Autophagy and Its Lineage-Specific Roles in the Hematopoietic System.Oxidative medicine and cellular longevity · 2023
    Review
  13. Review
  14. Article
  15. Article
  16. The dual role of autophagy in acute myeloid leukemia.Journal of hematology & oncology · 2022
    Review
  17. Article
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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

5 authors at 1 institution in 1 country.

Qiang LiuDepartment of Pharmacology, Penn State College of Medicine, Hershey, PA, USA.
Longgui ChenDepartment of Pediatrics, Penn State College of Medicine, Hershey, PA, USA.
Jennifer M AtkinsonDepartment of Pediatrics, Penn State College of Medicine, Hershey, PA, USA.
David F ClaxtonPenn State Hershey Cancer Institute, Penn State College of Medicine, Hershey, PA, USA.
Hong-Gang WangDepartment of Pharmacology, Penn State College of Medicine, Hershey, PA, USA.
Penn State Milton S. Hershey Medical Center · US

Funding

Tissue Repository and Animal Models CoreP01CA171983 · NCI · UNIVERSITY OF VIRGINIA · PI LOUGHRAN, THOMAS P. · 2013 to 2024
$19.9M
NCI NIH HHS P01 CA171983
6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is a hierarchical hematopoietic malignancy originating from leukemic stem cells (LSCs). Autophagy is a lysosomal degradation pathway that is hypothesized to be important for the maintenance of AML as well as contribute to chemotherapy response. Here we employ a mouse model of AML expressing the fusion oncogene MLL-AF9 and explore the effects of Atg5 deletion, a key autophagy protein, on the malignant transformation and progression of AML. Consistent with a transient decrease in colony-forming potential in vitro, the in vivo deletion of Atg5 in MLL-AF9-transduced bone marrow cells during primary transplantation prolonged the survival of recipient mice, suggesting that autophagy has a role in MLL-AF9-driven leukemia initiation. In contrast, deletion of Atg5 in malignant AML cells during secondary transplantation did not influence the survival or chemotherapeutic response of leukemic mice. Interestingly, autophagy was found to be involved in the survival of differentiated myeloid cells originating from MLL-AF9-driven LSCs. Taken together, our data suggest that Atg5-dependent autophagy may contribute to the development but not chemotherapy sensitivity of murine AML induced by MLL-AF9.

Indexed as

Gene Expression Regulation, LeukemicAnimalsAutophagyAutophagy-Related Protein 5Bone Marrow CellsBone Marrow TransplantationCell Transformation, NeoplasticDisease Models, AnimalGene DeletionHumansLeukemia, Myeloid, AcuteLysosomesMiceMice, Inbred C57BLNeoplastic Stem CellsOncogene Proteins, FusionAtg5 protein, mouseAutophagy-Related Protein 5MLL-AF9 fusion protein, mouseOncogene Proteins, Fusion

Identifiers

PMID27607576
PMCPMC5059867
OpenAlexW2516345787

What OpenQuestion holds

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LicenceCC BY
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.