Evidence map›Paper›PMID 34638371›Full record

ReviewCancers2021

Clonal Architecture and Evolutionary Dynamics in Acute Myeloid Leukemias.

Matthieu Duchmann, Lucie Laplane, Raphael Itzykson

Abstract readReview
In one paragraph

Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

  1. Trial
  2. Review
  3. Mutations and MRD: clinical implications of clonal ontogeny.Hematology. American Society of Hematology. Education Program · 2024
    Review
  4. Review
  5. Reuniting philosophy and science to advance cancer research.Biological reviews of the Cambridge Philosophical Society · 2023
    Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Role of TET dioxygenases in the regulation of both normal and pathological hematopoiesis.Journal of experimental & clinical cancer research : CR · 2022
    Review
  11. Article
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.

Matthieu DuchmannGénomes, Biologie Cellulaire et Thérapeutique U944, INSERM, CNRS, Université de Paris, 75010 Paris, France.ORCID 0000-0002-7299-4572
Lucie LaplaneInstitut d'Histoire et Philosophie des Sciences et des Techniques UMR 8590, CNRS, Université Paris 1 Panthéon-Sorbonne, 75010 Paris, France.
Raphael ItzyksonGénomes, Biologie Cellulaire et Thérapeutique U944, INSERM, CNRS, Université de Paris, 75010 Paris, France.ORCID 0000-0003-2139-6262

Funding

Agence Nationale de la Recherche ANR-19-CE27-0027-01Cancéropôle Ile de France 2021-1-EMERG-54-CNRSFondation ARC pour la Recherche sur le Cancer PGA1-RC20180206836Ligue Contre le Cancer RS21-7591Ligue Nationale Contre le Cancer F. Porteu U1287
6 · The paper itself

Abstract

Acute myeloid leukemias (AML) results from the accumulation of genetic and epigenetic alterations, often in the context of an aging hematopoietic environment. The development of high-throughput sequencing-and more recently, of single-cell technologies-has shed light on the intratumoral diversity of leukemic cells. Taking AML as a model disease, we review the multiple sources of genetic, epigenetic, and functional heterogeneity of leukemic cells and discuss the definition of a leukemic clone extending its definition beyond genetics. After introducing the two dimensions contributing to clonal diversity, namely, richness (number of leukemic clones) and evenness (distribution of clone sizes), we discuss the mechanisms at the origin of clonal emergence (mutation rate, number of generations, and effective size of the leukemic population) and the causes of clonal dynamics. We discuss the possible role of neutral drift, but also of cell-intrinsic and -extrinsic influences on clonal fitness. After reviewing available data on the prognostic role of genetic and epigenetic diversity of leukemic cells on patients' outcome, we discuss how a better understanding of AML as an evolutionary process could lead to the design of novel therapeutic strategies in this disease.

Indexed as

acute myeloid leukemiaclonal heterogeneitydrug resistanceevolutionary dynamicsprognosis

Identifiers

PMID34638371
PMCPMC8507870

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.