Evidence map›Paper›PMID 31985806›Full record

ArticleBlood advances2020

Highly multiplexed proteomic assessment of human bone marrow in acute myeloid leukemia.

Haydar Çelik, Katherine E Lindblad, Bogdan Popescu, Gege Gui, Meghali Goswami, Janet Valdez, Christin DeStefano, Catherine Lai, Julie Thompson, Jack Y Ghannam and 10 more

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 5% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

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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

20 authors at 4 institutions in 1 country.

Haydar ÇelikLaboratory of Myeloid Malignancies, Hematology Branch, National Heart, Lung, and Blood Institute, and.
Katherine E LindbladLaboratory of Myeloid Malignancies, Hematology Branch, National Heart, Lung, and Blood Institute, and.
Bogdan PopescuLaboratory of Myeloid Malignancies, Hematology Branch, National Heart, Lung, and Blood Institute, and.
Gege GuiLaboratory of Myeloid Malignancies, Hematology Branch, National Heart, Lung, and Blood Institute, and.
Meghali GoswamiLaboratory of Myeloid Malignancies, Hematology Branch, National Heart, Lung, and Blood Institute, and.
Janet ValdezLaboratory of Myeloid Malignancies, Hematology Branch, National Heart, Lung, and Blood Institute, and.
Christin DeStefanoLaboratory of Myeloid Malignancies, Hematology Branch, National Heart, Lung, and Blood Institute, and.
Catherine LaiLaboratory of Myeloid Malignancies, Hematology Branch, National Heart, Lung, and Blood Institute, and.
Julie ThompsonLaboratory of Myeloid Malignancies, Hematology Branch, National Heart, Lung, and Blood Institute, and.
Jack Y GhannamLaboratory of Myeloid Malignancies, Hematology Branch, National Heart, Lung, and Blood Institute, and.
Giovanna FantoniCenter for Human Immunology, Autoimmunity and Inflammation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.
Angélique BiancottoCenter for Human Immunology, Autoimmunity and Inflammation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.
Julián CandiaCenter for Human Immunology, Autoimmunity and Inflammation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.
Foo CheungCenter for Human Immunology, Autoimmunity and Inflammation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.
Gauthaman SukumarCollaborative Health Initiative Research Program.
Clifton L DalgardCollaborative Health Initiative Research Program.
Richard H SmithLaboratory of Regenerative Therapies for Inherited Blood Disorders, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.
Andre LarochelleLaboratory of Regenerative Therapies for Inherited Blood Disorders, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.
Laura W DillonLaboratory of Myeloid Malignancies, Hematology Branch, National Heart, Lung, and Blood Institute, and.
Christopher S HouriganLaboratory of Myeloid Malignancies, Hematology Branch, National Heart, Lung, and Blood Institute, and.
National Heart Lung and Blood Institute · USNational Institutes of Health · USUniformed Services University of the Health Sciences · USWomen's Health Initiative · US

Funding

Center for Human Immunology ZICAI001226 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI CHERRY, JAMES · 2018 to 2025
$34.1M
Detection, prevention and treatment of acute myeloid leukemia (AML) relapse.ZIAHL006163 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI HOURIGAN, CHRISTOPHER · 2013 to 2023
$21.0M
Intramural NIH HHS ZIA HL006163
6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is a genetically heterogeneous disease that is characterized by abnormal clonal proliferation of myeloid progenitor cells found predominantly within the bone marrow (BM) and blood. Recent studies suggest that genetic and phenotypic alterations in the BM microenvironment support leukemogenesis and allow leukemic cells to survive and evade chemotherapy-induced death. However, despite substantial evidence indicating the role of tumor-host interactions in AML pathogenesis, little is known about the complex microenvironment of the BM. To address this, we performed novel proteomic profiling of the noncellular compartment of the BM microenvironment in patients with AML (n = 10) and age- and sex-matched healthy control subjects (n = 10) using an aptamer-based, highly multiplexed, affinity proteomics platform (SOMAscan). We show that proteomic assessment of blood or RNA-sequencing of BM are suboptimal alternate screening strategies to determine the true proteomic composition of the extracellular soluble compartment of AML patient BM. Proteomic analysis revealed that 168 proteins significantly differed in abundance, with 91 upregulated and 77 downregulated in leukemic BM. A highly connected signaling network of cytokines and chemokines, including IL-8, was found to be the most prominent proteomic signature associated with AML in the BM microenvironment. We report the first description of significantly elevated levels of the myelosuppressive chemokine CCL23 (myeloid progenitor inhibitory factor-1) in both AML and myelodysplastic syndrome patients and perform functional experiments supportive of a role in the suppression of normal hematopoiesis. This unique paired RNA-sequencing and proteomics data set provides innovative mechanistic insights into AML and healthy aging and should serve as a useful public resource.

Indexed as

Bone MarrowCase-Control StudiesCellular MicroenvironmentChemokinesChemokines, CCCytokinesGene Expression Regulation, LeukemicHumansInterleukin-8Leukemia, Myeloid, AcuteNeoplasm ProteinsProteomicsCCL23 protein, humanChemokinesChemokines, CCCXCL8 protein, humanCytokinesInterleukin-8Neoplasm Proteins

Identifiers

PMID31985806
PMCPMC6988405
OpenAlexW3002473427

What Socratic 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 Socratic graph.