Evidence map›Paper›PMID 32655144›Full record

ArticleLeukemia2021

A transcriptomic continuum of differentiation arrest identifies myeloid interface acute leukemias with poor prognosis.

Jonathan Bond, Aleksandra Krzywon, Ludovic Lhermitte, Christophe Roumier, Anne Roggy, Mohamed Belhocine, Alexander Abdulkader Kheirallah, Patrick Villarese, Guillaume Hypolite, Francine Garnache-Ottou and 7 more

Open access · hybridAbstract read
In one paragraph

Article in Leukemia, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Frontiers in oncology · 2021
    Review
  6. 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

17 authors at 7 institutions in 4 countries.

Jonathan BondUniversité de Paris, Institut Necker Enfants Malades (INEM), Institut national de la santé et de la recherche médicale (INSERM UMR1151), 75743, Paris, France.
Aleksandra KrzywonDepartment of Haematology, University of Cambridge, Cambridge, United Kingdom.
Ludovic LhermitteUniversité de Paris, Institut Necker Enfants Malades (INEM), Institut national de la santé et de la recherche médicale (INSERM UMR1151), 75743, Paris, France.ORCID http://orcid.org/0000-0003-2498-0376
Christophe RoumierCancer Research Institute, INSERM Unité Mixte de Recherche (UMR)-S 1172, F-59000, Lille, France.
Anne RoggyUniversité de Paris, Institut Necker Enfants Malades (INEM), Institut national de la santé et de la recherche médicale (INSERM UMR1151), 75743, Paris, France.
Mohamed BelhocineUniversité de Paris, Institut Necker Enfants Malades (INEM), Institut national de la santé et de la recherche médicale (INSERM UMR1151), 75743, Paris, France.
Alexander Abdulkader KheirallahDepartment of Haematology, University of Cambridge, Cambridge, United Kingdom.
Patrick VillareseUniversité de Paris, Institut Necker Enfants Malades (INEM), Institut national de la santé et de la recherche médicale (INSERM UMR1151), 75743, Paris, France.
Guillaume HypoliteUniversité de Paris, Institut Necker Enfants Malades (INEM), Institut national de la santé et de la recherche médicale (INSERM UMR1151), 75743, Paris, France.
Francine Garnache-OttouUniv. Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, Interactions Hôte-Greffon-Tumeur/Ingénierie Cellulaire et Génique, F-25000, Besançon, France.
Sylvie CastaigneHematology/Oncology, Versailles Hospital and Versailles Saint Quentin University, Le Chesnay, France.
Nicolas BoisselUniversité Paris Diderot, Institut Universitaire d'Hématologie, EA-3518, AP-HP, University Hospital Saint-Louis, Paris, France.
Vahid AsnafiUniversité de Paris, Institut Necker Enfants Malades (INEM), Institut national de la santé et de la recherche médicale (INSERM UMR1151), 75743, Paris, France.
Claude PreudhommeCancer Research Institute, INSERM Unité Mixte de Recherche (UMR)-S 1172, F-59000, Lille, France.
Hervé DombretUniversité Paris Diderot, Institut Universitaire d'Hématologie, EA-3518, AP-HP, University Hospital Saint-Louis, Paris, France.
Elisa LaurentiDepartment of Haematology, University of Cambridge, Cambridge, United Kingdom. el422@cam.ac.uk.ORCID http://orcid.org/0000-0002-9917-9092
Elizabeth MacintyreUniversité de Paris, Institut Necker Enfants Malades (INEM), Institut national de la santé et de la recherche médicale (INSERM UMR1151), 75743, Paris, France. elizabeth.macintyre@aphp.fr.ORCID http://orcid.org/0000-0003-0520-0493
Hôpital Necker-Enfants Malades · FRInserm · FRDélégation Paris 7 · FRWellcome/MRC Cambridge Stem Cell Institute · GBCentre Hospitalier de Versailles · FRSilesian University of Technology · PLUniversity College Dublin · IE

Funding

Biotechnology and Biological Sciences Research CouncilMedical Research Council MC_PC_12009Medical Research Council MC_PC_17230Wellcome Trust 107630Wellcome Trust 107630/Z/15/ZWellcome Trust 203151Wellcome Trust 203151/Z/16/Z
6 · The paper itself

Abstract

Classification of acute lymphoblastic and myeloid leukemias (ALL and AML) remains heavily based on phenotypic resemblance to normal hematopoietic precursors. This framework can provide diagnostic challenges for immunophenotypically heterogeneous immature leukemias, and ignores recent advances in understanding of developmental multipotency of diverse normal hematopoietic progenitor populations that are identified by transcriptional signatures. We performed transcriptional analyses of a large series of acute myeloid and lymphoid leukemias and detected significant overlap in gene expression between cases in different diagnostic categories. Bioinformatic classification of leukemias along a continuum of hematopoietic differentiation identified leukemias at the myeloid/T-lymphoid interface, which shared gene expression programs with a series of multi or oligopotent hematopoietic progenitor populations, including the most immature CD34+CD1a-CD7- subset of early thymic precursors. Within these interface acute leukemias (IALs), transcriptional resemblance to early lymphoid progenitor populations and biphenotypic leukemias was more evident in cases originally diagnosed as AML, rather than T-ALL. Further prognostic analyses revealed that expression of IAL transcriptional programs significantly correlated with poor outcome in independent AML patient cohorts. Our results suggest that traditional binary approaches to acute leukemia categorization are reductive, and that identification of IALs could allow better treatment allocation and evaluation of therapeutic options.

Indexed as

Cell DifferentiationTranscriptomeBiomarkers, TumorComputational BiologyHumansLeukemia, Biphenotypic, AcuteLeukemia, Myeloid, AcutePrecursor Cell Lymphoblastic Leukemia-LymphomaPrognosisSurvival RateBiomarkers, Tumor

Identifiers

PMID32655144
PMCPMC7932917
OpenAlexW3041475419

What OpenQuestion holds

Textmetadata
LicenceTDM
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.