Evidence map›Paper›PMID 32430504›Full record

ReviewBlood2020

Genetics of progression from MDS to secondary leukemia.

Andrew J Menssen, Matthew J Walter

Open access · bronzeAbstract readReview
In one paragraph

Review in Blood, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed, 2 pooled it
10.4field-weighted citation impact, top 1% 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

103 citing papers in PubMed, 2 syntheses or guidelines pooled it, 160 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
  5. Review
  6. Article
  7. Article
  8. The Prognostic Value of the CD8Hematology reports · 2026
    Article
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  20. Targeting O-GlcNAcylated METTL3 impedes MDS/AML progression via diminishing SRSF1 mMolecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article

43 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

2 authors at 1 institution in 1 country.

Andrew J MenssenDivision of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO; and.
Matthew J WalterDivision of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO; and.
Washington University in St. Louis · US

Funding

Specimen Acquistition and Expression ProfilingP01CA101937 · NCI · WASHINGTON UNIVERSITY · PI LINK, DANIEL C · 2003 to 2023
$58.8M
TARGETED SINGLE-MOLECULE SEQUENCING ASSAY INCORPORATING MOLECULAR BARCODESR33CA217700 · NCI · WASHINGTON UNIVERSITY · PI DUNCAVAGE, ERIC J, WALTER, MATTHEW J · 2017 to 2019
$1.1M
NCI NIH HHS P01 CA101937NCI NIH HHS R33 CA217700
6 · The paper itself

Abstract

Our understanding of the genetics of acute myeloid leukemia (AML) development from myelodysplastic syndrome (MDS) has advanced significantly as a result of next-generation sequencing technology. Although differences in cell biology and maturation exist between MDS and AML secondary to MDS, these 2 diseases are genetically related. MDS and secondary AML cells harbor mutations in many of the same genes and functional categories, including chromatin modification, DNA methylation, RNA splicing, cohesin complex, transcription factors, cell signaling, and DNA damage, confirming that they are a disease continuum. Differences in the frequency of mutated genes in MDS and secondary AML indicate that the order of mutation acquisition is not random during progression. In almost every case, disease progression is associated with clonal evolution, typically defined by the expansion or emergence of a subclone with a unique set of mutations. Monitoring tumor burden and clonal evolution using sequencing provides advantages over using the blast count, which underestimates tumor burden, and could allow for early detection of disease progression prior to clinical deterioration. In this review, we outline advances in the study of MDS to secondary AML progression, with a focus on the genetics of progression, and discuss the advantages of incorporating molecular genetic data in the diagnosis, classification, and monitoring of MDS to secondary AML progression. Because sequencing is becoming routine in the clinic, ongoing research is needed to define the optimal assay to use in different clinical situations and how the data can be used to improve outcomes for patients with MDS and secondary AML.

Indexed as

Cell CountClonal EvolutionDisease ProgressionDNA MethylationDNA Mutational AnalysisEpigenesis, GeneticExome SequencingHematopoietic Stem CellsHumansLenalidomideLeukemia, Myeloid, AcuteMutationMyelodysplastic SyndromesMyelopoiesisNeoplastic Stem CellsPrognosisLenalidomide

Identifiers

PMID32430504
PMCPMC7332895
OpenAlexW3027124819

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.