Evidence map›Paper›PMID 31478278›Full record

ReviewGenes, chromosomes & cancer2019

Clonal evolution of acute myeloid leukemia from diagnosis to relapse.

Sebastian Vosberg, Philipp A Greif

Open access · hybridAbstract readReview
In one paragraph

Review in Genes, chromosomes & cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
7.9field-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

75 citing papers in PubMed, 120 citations in OpenAlex.

  1. Article
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  8. Synergistic adverse prognosis ofFrontiers in cell and developmental biology · 2026
    Article
  9. Review
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  11. Review
  12. A Relapsed AML Case Featuring MYC and MECOM Rearrangements.Diagnostics (Basel, Switzerland) · 2025
    Article
  13. Article
  14. Review
  15. Article
  16. Article
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  20. Article

15 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.

Sebastian VosbergDepartment of Medicine III, University Hospital, LMU Munich, Munich, Germany.ORCID 0000-0002-8464-1483
Philipp A GreifDepartment of Medicine III, University Hospital, LMU Munich, Munich, Germany.
German Cancer Research Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Based on the individual genetic profile, acute myeloid leukemia (AML) patients are classified into clinically meaningful molecular subtypes. However, the mutational profile within these groups is highly heterogeneous and multiple AML subclones may exist in a single patient in parallel. Distinct alterations of single cells may be key factors in providing the fitness to survive in this highly competitive environment. Although the majority of AML patients initially respond to induction chemotherapy and achieve a complete remission, most patients will eventually relapse. These points toward an evolutionary process transforming treatment-sensitive cells into treatment-resistant cells. As described by Charles Darwin, evolution by natural selection is the selection of individuals that are optimally adapted to their environment, based on the random acquisition of heritable changes. By changing their mutational profile, AML cell populations are able to adapt to the new environment defined by chemotherapy treatment, ultimately leading to cell survival and regrowth. In this review, we will summarize the current knowledge about clonal evolution in AML, describe different models of clonal evolution, and provide the methodological background that allows the detection of clonal evolution in individual AML patients. During the last years, numerous studies have focused on delineating the molecular patterns that are associated with AML relapse, each focusing on a particular genetic subgroup of AML. Finally, we will review the results of these studies in the light of Darwinian evolution and discuss open questions regarding the molecular background of relapse development.

Indexed as

Chronic DiseaseClonal EvolutionHumansLeukemia, Myeloid, AcuteRecurrenceRemission Inductionacute myeloid leukemiaclonal evolutionnext generation sequencingrelapsetherapy resistance

Identifiers

PMID31478278
PMCPMC6852285
OpenAlexW2971793138

What OpenQuestion holds

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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.