Evidence map›Paper›PMID 28355571›Full record

ArticleCell reports2017

Identification of Interleukin-1 by Functional Screening as a Key Mediator of Cellular Expansion and Disease Progression in Acute Myeloid Leukemia.

Alyssa Carey, David K Edwards, Christopher A Eide, Laura Newell, Elie Traer, Bruno C Medeiros, Daniel A Pollyea, Michael W Deininger, Robert H Collins, Jeffrey W Tyner and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 183 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
183citing papers in PubMed, 1 pooled it
13.6field-weighted citation impact, top 1% 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

183 citing papers in PubMed, 1 synthesis or guideline pooled it, 265 citations in OpenAlex.

  1. Pooled it
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  9. Immune interplay between sepsis and haematological malignancies.Intensive care medicine experimental · 2026
    Review
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123 more citing papers are in PubMed but not listed here.

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

14 authors at 6 institutions in 1 country.

Alyssa CareyDivision of Hematology and Medical Oncology, Knight Cancer Institute, Oregon Health & Science University, Portland, OR 97239, USA.
David K EdwardsDepartment of Cell, Developmental and Cancer Biology, Knight Cancer Institute, Oregon Health & Science University, Portland, OR 97239, USA.
Christopher A EideDivision of Hematology and Medical Oncology, Knight Cancer Institute, Oregon Health & Science University, Portland, OR 97239, USA; Howard Hughes Medical Institute, Portland, OR 97239, USA.
Laura NewellDivision of Hematology and Medical Oncology, Knight Cancer Institute, Oregon Health & Science University, Portland, OR 97239, USA.
Elie TraerDivision of Hematology and Medical Oncology, Knight Cancer Institute, Oregon Health & Science University, Portland, OR 97239, USA.
Bruno C MedeirosStanford University School of Medicine, Stanford, CA 94305, USA.
Daniel A PollyeaUniversity of Colorado School of Medicine, Aurora, CO 80045, USA.
Michael W DeiningerUniversity of Utah Huntsman Cancer Institute, Salt Lake City, UT 84112, USA.
Robert H CollinsUniversity of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Jeffrey W TynerDepartment of Cell, Developmental and Cancer Biology, Knight Cancer Institute, Oregon Health & Science University, Portland, OR 97239, USA.
Brian J DrukerDivision of Hematology and Medical Oncology, Knight Cancer Institute, Oregon Health & Science University, Portland, OR 97239, USA; Howard Hughes Medical Institute, Portland, OR 97239, USA.
Grover C BagbyDivision of Hematology and Medical Oncology, Knight Cancer Institute, Oregon Health & Science University, Portland, OR 97239, USA.
Shannon K McWeeneyDivision of Bioinformatics and Computational Biology, Department of Medical Informatics & Clinical Epidemiology, Knight Cancer Institute, Oregon Health & Science University, Portland, OR 97239, USA.
Anupriya AgarwalDivision of Hematology and Medical Oncology, Knight Cancer Institute, Oregon Health & Science University, Portland, OR 97239, USA; Department of Molecular and Medical Genetics, Oregon Health & Science University, Portland, OR 97239, USA. Electronic address: agarwala@ohsu.edu.
Oregon Health & Science University · USHoward Hughes Medical Institute · USStanford University · USThe University of Texas Southwestern Medical Center · USUniversity of Colorado Denver · USUniversity of Utah · US

Funding

CHRONIC MYELOGENOUS LEUKEMIA AND BCR-ABL SUBSTRATESR01CA065823 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI DRUKER, BRIAN J · 1995 to 2021
$4.7M
Mechanisms of resistance to ponatinib therapy in chronic myeloid leukemiaR01CA178397 · NCI · UNIVERSITY OF UTAH · PI DEININGER, MICHAEL W., O'HARE, THOMAS J. · 2014 to 2018
$2.6M
Pathogenetic Mechanism and Clinical Targeting of CSF3R-Driven CancerR01CA183974 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI TYNER, JEFFREY WALLACE · 2014 to 2018
$1.6M
Role of p27 in chronic myeloid leukemia and its potential as a therapeutic targetR00CA151670 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI AGARWAL, ANUPRIYA · 2014 to 2016
$738k
Howard Hughes Medical InstituteNCI NIH HHS R00 CA151670NCI NIH HHS R01 CA065823NCI NIH HHS R01 CA178397NCI NIH HHS R01 CA183974
6 · The paper itself

Abstract

Secreted proteins in the bone marrow microenvironment play critical roles in acute myeloid leukemia (AML). Through an ex vivo functional screen of 94 cytokines, we identified that the pro-inflammatory cytokine interleukin-1 (IL-1) elicited profound expansion of myeloid progenitors in ∼67% of AML patients while suppressing the growth of normal progenitors. Levels of IL-1β and IL-1 receptors were increased in AML patients, and silencing of the IL-1 receptor led to significant suppression of clonogenicity and in vivo disease progression. IL-1 promoted AML cell growth by enhancing p38MAPK phosphorylation and promoting secretion of various other growth factors and inflammatory cytokines. Treatment with p38MAPK inhibitors reversed these effects and recovered normal CD34

Indexed as

Disease ProgressionBone MarrowCell ProliferationCell SurvivalHumansInflammation MediatorsIntercellular Signaling Peptides and ProteinsInterleukin-1Interleukin-1betaLeukemia, Myeloid, AcuteModels, BiologicalMonocytesp38 Mitogen-Activated Protein KinasesPhosphorylationReceptors, Interleukin-1Signal TransductionInflammation MediatorsIntercellular Signaling Peptides and ProteinsInterleukin-1Interleukin-1betap38 Mitogen-Activated Protein KinasesReceptors, Interleukin-1AMLbone marrow microenvironmentfunctional screeningIL1R1interleukin-1p38MAPK

Identifiers

PMID28355571
PMCPMC5437102
OpenAlexW2597865830

What OpenQuestion holds

Textmetadata
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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.