Evidence map›Paper›PMID 33690800›Full record

ArticleBlood2021

Cytokine-like protein 1-induced survival of monocytes suggests a combined strategy targeting MCL1 and MAPK in CMML.

Margaux Sevin, Franck Debeurme, Lucie Laplane, Séverine Badel, Margot Morabito, Hanna L Newman, Miguel Torres-Martin, Qin Yang, Bouchra Badaoui, Orianne Wagner-Ballon and 17 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

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  11. Mouse Models of CMML.International journal of molecular sciences · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

27 authors at 13 institutions in 4 countries.

Margaux SevinINSERM U1287, Gustave Roussy Cancer Campus, Villejuif, France.
Franck DebeurmeINSERM U1287, Gustave Roussy Cancer Campus, Villejuif, France.
Lucie LaplaneCentre National de la Recherche Scientifique (CNRS), Unité Mixte de Recherche (UMR) 8590, Université Paris I, Paris, France.ORCID 0000-0003-0185-3323
Séverine BadelINSERM U1287, Gustave Roussy Cancer Campus, Villejuif, France.
Margot MorabitoINSERM U1287, Gustave Roussy Cancer Campus, Villejuif, France.
Hanna L NewmanMalignant Hematology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL.
Miguel Torres-MartinDivision of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, NY.ORCID 0000-0003-1589-8936
Qin YangHuman Genetics, University of Miami Miller School of Medicine, Miami, FL.
Bouchra BadaouiDépartement d'Hématologie et Immunologie Biologiques, Assistance Publique-Hôpitaux de Paris (AP-HP), Hôpitaux Universitaires Henri-Mondor, Créteil, France.ORCID 0000-0002-2096-2229
Orianne Wagner-BallonDépartement d'Hématologie et Immunologie Biologiques, Assistance Publique-Hôpitaux de Paris (AP-HP), Hôpitaux Universitaires Henri-Mondor, Créteil, France.ORCID 0000-0001-9071-6683
Véronique SaadaDepartment of Biopathology, Gustave Roussy Cancer Campus, Villejuif, France.
Dorothée Sélimoglu-BuetINSERM U1287, Gustave Roussy Cancer Campus, Villejuif, France.ORCID 0000-0002-3565-2709
Laurence Kraus-BerthierInstitut de Recherches Internationales Servier Oncology R&D Unit, Suresnes, France.
Sébastien BanquetInstitut de Recherches Internationales Servier Oncology R&D Unit, Suresnes, France.
Alix DerrealInstitut de Recherches Internationales Servier Oncology R&D Unit, Suresnes, France.
Pierre FenauxSenior Hematology Department and.
Raphael ItzyksonDepartment of Hematology, Hôpital Saint Louis, Université Paris Diderot, Paris, France.ORCID 0000-0003-2139-6262
Thorsten BraunDepartment of Hematology, Hôpital Avicenne, Université Paris XIII, Bobigny, France.
Gabriel EtienneDepartment of Medical Oncology, Institut Bergonie, Bordeaux, France.ORCID 0000-0001-7600-4954
Celine BerthonDepartment of Hematology, Centre Hospitalier Universitaire Claude Huriez, Lille, France.ORCID 0000-0002-3474-2577
Sylvain ThépotMaladies du Sang, Centre Hospitalier Universitaire, Angers, France.ORCID 0000-0003-3492-2778
Oliver KeppMetabolomics and Cell Biology Platforms, Institut Gustave Roussy, Villejuif, France.ORCID 0000-0002-6081-9558
Guido KroemerMetabolomics and Cell Biology Platforms, Institut Gustave Roussy, Villejuif, France.
Eric PadronMalignant Hematology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL.
Maria E FigueroaHuman Genetics, University of Miami Miller School of Medicine, Miami, FL.
Nathalie DroinINSERM U1287, Gustave Roussy Cancer Campus, Villejuif, France.ORCID 0000-0002-6099-5324
Eric SolaryINSERM U1287, Gustave Roussy Cancer Campus, Villejuif, France.ORCID 0000-0002-8629-1341
Inserm · FRServier (France) · FRCentre National de la Recherche Scientifique · FRMoffitt Cancer Center · USUniversity of Miami · USAssistance Publique – Hôpitaux de Paris · FRCentre Hospitalier Universitaire d'Angers · FRDélégation Paris 7 · FRIcahn School of Medicine at Mount Sinai · USInstitut Bergonié · FRInstitut Gustave Roussy · FRKarolinska University Hospital · SEUniversité Sorbonne Paris Nord · FR

Funding

Developing and credentialing patient-derived xenograft models to advance therapeutic approaches for chronic myelomonocytic leukemiaR37CA234021 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI PADRON, ERIC · 2019 to 2025
$3.4M
NCI NIH HHS R37 CA234021
6 · The paper itself

Abstract

Mouse models of chronic myeloid malignancies suggest that targeting mature cells of the malignant clone disrupts feedback loops that promote disease expansion. Here, we show that in chronic myelomonocytic leukemia (CMML), monocytes that accumulate in the peripheral blood show a decreased propensity to die by apoptosis. BH3 profiling demonstrates their addiction to myeloid cell leukemia-1 (MCL1), which can be targeted with the small molecule inhibitor S63845. RNA sequencing and DNA methylation pattern analysis both point to the implication of the mitogen-activated protein kinase (MAPK) pathway in the resistance of CMML monocytes to death and reveal an autocrine pathway in which the secreted cytokine-like protein 1 (CYTL1) promotes extracellular signal-regulated kinase (ERK) activation through C-C chemokine receptor type 2 (CCR2). Combined MAPK and MCL1 inhibition restores apoptosis of monocytes from patients with CMML and reduces the expansion of patient-derived xenografts in mice. These results show that the combined inhibition of MCL1 and MAPK is a promising approach to slow down CMML progression by inducing leukemic monocyte apoptosis.

Indexed as

Leukemia, Myelomonocytic, ChronicMonocytesAdultAgedAged, 80 and overBlood ProteinsCell SurvivalCytokinesExtracellular Signal-Regulated MAP KinasesFemaleHumansMaleMAP Kinase Signaling SystemMiddle AgedMyeloid Cell Leukemia Sequence 1 ProteinProtein Kinase InhibitorsBlood ProteinsCYTL1 protein, humanCytokinesExtracellular Signal-Regulated MAP KinasesMCL1 protein, humanMyeloid Cell Leukemia Sequence 1 ProteinProtein Kinase Inhibitors

Identifiers

PMID33690800
PMCPMC8233685
OpenAlexW3135409633

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.