Evidence map›Paper›PMID 31648319›Full record

ArticleBlood advances2019

The transcriptome of CMML monocytes is highly inflammatory and reflects leukemia-specific and age-related alterations.

Anca Franzini, Anthony D Pomicter, Dongqing Yan, Jamshid S Khorashad, Srinivas K Tantravahi, Hein Than, Jonathan M Ahmann, Thomas O'Hare, Michael W Deininger

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 53 citations in OpenAlex.

  1. Trial
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  5. The Role of Inflammation in CMML Pathobiology and Progression.Current hematologic malignancy reports · 2025
    Review
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  7. Article
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  12. Review
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  14. Clonal monocytosis of renal significance.Kidney international · 2024
    Review
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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

9 authors at 4 institutions in 3 countries.

Anca FranziniHuntsman Cancer Institute, University of Utah, Salt Lake City, UT.
Anthony D PomicterHuntsman Cancer Institute, University of Utah, Salt Lake City, UT.
Dongqing YanHuntsman Cancer Institute, University of Utah, Salt Lake City, UT.
Jamshid S KhorashadCentre for Haematology, Imperial College London, Hammersmith Hospital Campus, London, United Kingdom.
Srinivas K TantravahiHuntsman Cancer Institute, University of Utah, Salt Lake City, UT.
Hein ThanDepartment of Haematology, Singapore General Hospital, Singapore.
Jonathan M AhmannHuntsman Cancer Institute, University of Utah, Salt Lake City, UT.
Thomas O'HareHuntsman Cancer Institute, University of Utah, Salt Lake City, UT.
Michael W DeiningerHuntsman Cancer Institute, University of Utah, Salt Lake City, UT.
University of Utah · USHuntsman Cancer Institute · USHammersmith Hospital · GBSingapore General Hospital · SG

Funding

UTAH REGIONAL CANCER CENTERP30CA042014 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI KATHARINE S ULLMAN · 1986 to 2026
$72.6M
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
NCI NIH HHS P30 CA042014NCI NIH HHS R01 CA178397
6 · The paper itself

Abstract

Chronic myelomonocytic leukemia (CMML) is an aggressive myeloid neoplasm of older individuals characterized by persistent monocytosis. Somatic mutations in CMML are heterogeneous and only partially explain the variability in clinical outcomes. Recent data suggest that cardiovascular morbidity is increased in CMML and contributes to reduced survival. Clonal hematopoiesis of indeterminate potential (CHIP), the presence of mutated blood cells in hematologically normal individuals, is a precursor of age-related myeloid neoplasms and associated with increased cardiovascular risk. To isolate CMML-specific alterations from those related to aging, we performed RNA sequencing and DNA methylation profiling on purified monocytes from CMML patients and from age-matched (old) and young healthy controls. We found that the transcriptional signature of CMML monocytes is highly proinflammatory, with upregulation of multiple inflammatory pathways, including tumor necrosis factor and interleukin (IL)-6 and -17 signaling, whereas age per se does not significantly contribute to this pattern. We observed no consistent correlations between aberrant gene expression and CpG island methylation, suggesting that proinflammatory signaling in CMML monocytes is governed by multiple and complex regulatory mechanisms. We propose that proinflammatory monocytes contribute to cardiovascular morbidity in CMML patients and promote progression by selection of mutated cell clones. Our data raise questions of whether asymptomatic patients with CMML benefit from monocyte-depleting or anti-inflammatory therapies.

Indexed as

TranscriptomeAdultAgedAged, 80 and overAge FactorsBiomarkersCase-Control StudiesComputational BiologyDNA MethylationFemaleGene Expression ProfilingHumansInflammation MediatorsLeukemia, Myelomonocytic, ChronicMaleMiddle AgedBiomarkersInflammation Mediators

Identifiers

PMID31648319
PMCPMC6849944
OpenAlexW2980733946

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.