Evidence map›Paper›PMID 33054115›Full record

ArticleHaematologica2021

Plasmacytoid dendritic cells proliferation associated with acute myeloid leukemia: phenotype profile and mutation landscape

Loria Zalmaï, Pierre-Julien Viailly, Sabeha Biichle, Meyling Cheok, Lou Soret, Fanny Angelot-Delettre, Tony Petrella, Marie-Agnès Collonge-Rame, Estelle Seilles, Sandrine Geffroy and 28 more

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

42 citing papers in PubMed, 73 citations in OpenAlex.

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  19. Case Report: A rareFrontiers in oncology · 2025
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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

38 authors at 19 institutions in 3 countries.

Loria ZalmaïService d'hématologie biologique, Hôpital Cochin, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris.
Pierre-Julien ViaillyINSERM U1245, Centre Henri Becquerel, Rouen.
Sabeha BiichleUniv. Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, Interactions Hôte-Greffon-Tumeur/Ingénierie Cellulaire et Génique, Besançon.
Meyling CheokINSERM U837, CHRU Lille, IRCL Laboratoire d'Hématologie, Centre de Biologie Pathologie, Lille.
Lou SoretUniv. Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, Interactions Hôte-Greffon-Tumeur/Ingénierie Cellulaire et Génique, Besançon.
Fanny Angelot-DelettreUniv. Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, Interactions Hôte-Greffon-Tumeur/Ingénierie Cellulaire et Génique, Besançon.
Tony PetrellaDepartment of Pathology, University of Montréal, Hôpital Maisonneuve-Rosemont, Montréal, QC.
Marie-Agnès Collonge-RameLaboratoire de Génétique biologie, CHU Besançon, Besançon.
Estelle SeillesUniv. Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, Interactions Hôte-Greffon-Tumeur/Ingénierie Cellulaire et Génique, Besançon.
Sandrine GeffroyINSERM U837, CHRU Lille, IRCL Laboratoire d'Hématologie, Centre de Biologie Pathologie, Lille, France; Laboratoire d'Hématologie A, Centre de Biologie Pathologie, Boulevard du Pr Leclercq, 59037 Lille.
Eric DeconinckService Hématologie, CHU Besançon, Besançon.
Etienne DaguindauService Hématologie, CHU Besançon, Besançon.
Sabrina BouyerService d'Hématologie biologique, CHU La Milétrie, Poitiers.
Elodie DindinaudService d'Hématologie biologique, CHU La Milétrie, Poitiers.
Victor BauninLaboratoire du Groupe Hospitalier de La Rochelle-Ré-Aunis, CH de La Rochelle, La Rochelle.
Magali Le Garff-TavernierLaboratoire d'Hématologie, Hôpital Pitié-Salpêtrière, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris.
Damien Roos-WeilService d'Hématologie Clinique, <sup></i></sup>Sorbonne Université, Hôpital Pitié-Salpêtrière, <i>Assistance Publique-Hôpitaux de Paris (AP-HP)</i>, Paris.
Orianne Wagner-BallonDépartement d'Hématologie biologique, Hôpitaux Universitaires Henri Mondor, Assistance Publique-Hôpitaux de Paris (AP-HP), Créteil.
Véronique SalaunLaboratoire d'Hématologie, CHU de Caen Normandie, Normandie Université, UNICAEN, Caen.
Jean FeuillardLaboratoire d'hématologie, CHU Dupuytren, avenue Martin Luther King, Limoges.
Sophie BrunLaboratoire d'Hématologie et Consultations d'Hématologie Biologique, Hôpital Universitaire Carémeau, Nîmes.
Bernard DrenouService d'Hématologie, Groupe Hospitalier de la région Mulhouse Sud Alsace, Mulhouse.
Caroline Mayeur-RousseLaboratoire d'Hématologie, CHRU Strasbourg, Hôpital de Hautepierre, 67098 Strasbourg.
Patricia OkambaLaboratoire d'hématologie et auto-immunité, Hôpital de Mercy, CHR de Metz-Thionville.
Véronique DorvauxService d'hématologie de l'hôpital de Mercy, CHR de Metz-Thionville.
Michel TichionniLaboratoire d'hématologie, Hôpital Pasteur, Nice.
Johann RoseLaboratoire d'hématologie, CH du Mans, Le Mans.
Marie Thérèse RubioService Hématologie, CNRS UMR7365, Biopôle Université de Lorraine, CHRU Nancy, Vandœuvre-lès-Nancy.
Marie Christine JacobLaboratoire d'immunologie, CHU Grenoble, La Tronche.
Victoria RaggueneauService de Biologie Médicale, Centre Hospitalier de Versailles A. Mignot, Le Chesnay.
Claude PreudhommeINSERM U837, CHRU Lille, IRCL Laboratoire d'Hématologie, Centre de Biologie Pathologie, Lille, France; Laboratoire d'Hématologie A, Centre de Biologie Pathologie, Boulevard du Pr Leclercq, 59037 Lille.
Philippe SaasUniv. Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, Interactions Hôte-Greffon-Tumeur/Ingénierie Cellulaire et Génique, Besançon.
Christophe FerrandUniv. Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, Interactions Hôte-Greffon-Tumeur/Ingénierie Cellulaire et Génique, Besançon.
Olivier AdoteviUniv. Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, Interactions Hôte-Greffon-Tumeur/Ingénierie Cellulaire et Génique, Besançon.
Christophe RoumierINSERM U837, CHRU Lille, IRCL Laboratoire d'Hématologie, Centre de Biologie Pathologie, Lille, France; Laboratoire d'Hématologie A, Centre de Biologie Pathologie, Boulevard du Pr Leclercq, 59037 Lille.
Fabrice JardinINSERM U1245, Centre Henri Becquerel, Rouen.
Francine Garnache-OttouUniv. Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, Interactions Hôte-Greffon-Tumeur/Ingénierie Cellulaire et Génique, Besançon. francine.garnache@efs.sante.fr.
Florian RenosiUniv. Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, Interactions Hôte-Greffon-Tumeur/Ingénierie Cellulaire et Génique, Besançon.
Université Bourgogne Franche-Comté · FRInserm · FRCentre Hospitalier Universitaire de Besançon · FRAssistance Publique – Hôpitaux de Paris · FRSisters of Mercy Health System · USCentre Hospitalier de La Rochelle · FRCentre Hospitalier de Versailles · FRCentre Hospitalier du Mans · FRCentre Hospitalier Universitaire de Grenoble · FRCentre Hospitalier Universitaire de Nîmes · FRGroupe Hospitalier de la Région de Mulhouse et Sud Alsace · FRHôpital Cochin · FRHôpital d'Hautepierre · FRHôpital Dupuytren · FRHôpital Maisonneuve-Rosemont · CAHôpital Pasteur · FRIngénierie Moléculaire et Physiopathologie Articulaire · FRNormandie Université · FRSorbonne Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neoplasms involving plasmacytoid Dendritic Cells (pDCs) include Blastic pDC Neoplasms (BPDCN) and other pDC proliferations, where pDCs are associated with myeloid malignancies: most frequently Chronic MyeloMonocytic Leukemia (CMML) but also Acute Myeloid Leukemia (AML), hereafter named pDC-AML. We aimed to determine the reactive or neoplastic origin of pDCs in pDC-AML, and their link with the CD34+ blasts, monocytes or conventional DCs (cDCs) associated in the same sample, by phenotypic and molecular analyses (targeted NGS, 70 genes). We compared 15 pDC-AML at diagnosis with 21 BPDCN and 11 normal pDCs from healthy donors. CD45low CD34+ blasts were found in all cases (10-80% of medullar cells), associated with pDCs (4-36%), monocytes in 14 cases (1-10%) and cDCs (2 cases, 4.8-19%). pDCs in pDC-AML harbor a clearly different phenotype from BPDCN: CD4+ CD56- in 100% of cases, most frequently CD303+, CD304+ and CD34+; lower expression of cTCL1 and CD123 with isolated lymphoid markers (CD22/CD7/CD5) in some cases, suggesting a pre-pDC stage. In all cases, pDCs, monocytes and cDC are neoplastic since they harbor the same mutations as CD34+ blasts. RUNX1 is the most commonly mutated gene: detected in all AML with minimal differentiation (M0-AML) but not in the other cases. Despite low number of cases, the systematic association between M0-AML, RUNX1 mutations and an excess of pDC is puzzling. Further evaluation in a larger cohort is required to confirm RUNX1 mutations in pDC-AML with minimal differentiation and to investigate whether it represents a proliferation of blasts with macrophage and DC progenitor potential.

Indexed as

Dendritic CellsLeukemia, Myeloid, AcuteCell ProliferationHumansMutationPhenotype

Identifiers

PMID33054115
PMCPMC8634182
OpenAlexW3093257661

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.