Evidence map›Paper›PMID 21512311›Full record

ReviewCell cycle (Georgetown, Tex.)2011

Autophagy in the pathogenesis of myelodysplastic syndrome and acute myeloid leukemia.

Alexander Scarth Watson, Monika Mortensen, Anna Katharina Simon

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.

  1. Vacuolated Marrow Cytopenias from Copper Deficiency toInternational journal of molecular sciences · 2025
    Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Immunologic Predictors for Clinical Responses during Immune Checkpoint Blockade in Patients with Myelodysplastic Syndromes.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Autophagy in acute myeloid leukemia: a paradoxical role in chemoresistance.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. [Role of lipophagy in the regulation of lipid metabolism and the molecular mechanism].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019
    Review
  16. Review
  17. Article
  18. Article
  19. GDC-0152-induced autophagy promotes apoptosis in HL-60 cells.Molecular and cellular biochemistry · 2018
    Article
  20. Targeting autophagy in lymphomas: a double-edged sword?International journal of hematology · 2018
    Review
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

3 authors at 2 institutions in 2 countries.

Alexander Scarth WatsonUniversity of Oxford, Oxford, UK.
Monika Mortensen
Anna Katharina Simon
Science Oxford · GBDanish Cancer Society · DK

Funding

Biotechnology and Biological Sciences Research Council BB/G021422/1Wellcome Trust
6 · The paper itself

Abstract

Autophagy is a conserved cellular pathway responsible for the sequestration of spent organelles and protein aggregates from the cytoplasm and their delivery into lysosomes for degradation. Autophagy plays an important role in adaptation to starvation, in cell survival, immunity, development and cancer. Recent evidence in mice suggests that autophagic defects in hematopoietic stem cells (HSCs) may be implicated in leukemia. Indeed, mice lacking Atg7 in HSCs develop an atypical myeloproliferation resembling human myelodysplastic syndrome (MDS) progressing to acute myeloid leukemia (AML). Studies suggest that accumulation of damaged mitochondria and reactive oxygen species result in cell death of the majority of progenitor cells and, possibly, concomitant transformation of some surviving ones. Interestingly, bone marrow cells from MDS patients are characterized by mitochondrial abnormalities and increased cell death. A role for autophagy in the transformation to cancer has been proposed in other cancer types. This review focuses on autophagy in human MDS development and progression to AML within the context of the role of mitochondria, apoptosis and reactive oxygen species (ROS) in its pathogenesis.

Indexed as

AutophagyBone Marrow CellsHumansLeukemia, Myeloid, AcuteMitochondriaMyelodysplastic SyndromesReactive Oxygen SpeciesReactive Oxygen Species

Identifiers

PMID21512311
PMCPMC3142456
OpenAlexW2025031829

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.