Evidence map›Paper›PMID 37904125›Full record

ArticleBMC pulmonary medicine2023

Prevalence and significance of clonal hematopoiesis of indeterminate potential in lung transplant recipients.

Aparna C Swaminathan, Richard Barfield, Mengqi Zhang, Gundula Povysil, Cliburn Chen, Courtney Frankel, Francine Kelly, Matthew McKinney, Jamie L Todd, Andrew Allen and 1 more

Open access · goldAbstract read
In one paragraph

Article in BMC pulmonary medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 28% 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

3 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Review
  3. Solid Organ Transplant Recipients Exhibit More TET2-Mutant Clonal Hematopoiesis of Indeterminate Potential Not Driven by Increased Transplantation Risk.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Article
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

11 authors at 4 institutions in 1 country.

Aparna C SwaminathanDuke Clinical Research Institute, Durham, NC, USA. aparna.swaminathan@dm.duke.edu.
Richard BarfieldDepartment of Biostatistics and Bioinformatics, Duke University Medical Center, Durham, USA.
Mengqi ZhangDepartment of Biostatistics and Bioinformatics, Duke University Medical Center, Durham, USA.
Gundula PovysilInstitute for Genomic Medicine, Columbia University Medical Center, New York, NY, USA.
Cliburn ChenDepartment of Biostatistics and Bioinformatics, Duke University Medical Center, Durham, USA.
Courtney FrankelDepartment of Medicine, Duke University Medical Center, Durham, NC, USA.
Francine KellyDepartment of Medicine, Duke University Medical Center, Durham, NC, USA.
Matthew McKinneyDepartment of Medicine, Duke University Medical Center, Durham, NC, USA.
Jamie L ToddDuke Clinical Research Institute, Durham, NC, USA.
Andrew AllenDepartment of Biostatistics and Bioinformatics, Duke University Medical Center, Durham, USA.
Scott M PalmerDuke Clinical Research Institute, Durham, NC, USA.
Duke University · USDuke Medical Center · USClinical Research Institute · USColumbia University Irving Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundClonal hematopoiesis of indeterminate potential (CHIP), the age-related acquisition of somatic mutations that leads to an expanded blood cell clone, has been associated with development of a pro-inflammatory state. An enhanced or dysregulated inflammatory response may contribute to rejection after lung transplantation, however the prevalence of CHIP in lung recipients and influence of CHIP on allograft outcomes is unknown.

methodsWe analyzed whole-exome sequencing data in 279 lung recipients to detect CHIP, defined by pre-specified somatic mutations in 74 genes known to promote clonal expansion of hematopoietic stem cells. We compared the burden of acute rejection (AR) over the first post-transplant year in lung recipients with vs. without CHIP using multivariable ordinal regression. Multivariate Cox proportional hazards models were used to assess the association between CHIP and CLAD-free survival. An exploratory analysis evaluated the association between the number of CHIP-associated variants and chronic lung allograft dysfunction (CLAD)-free survival.

resultsWe detected 64 CHIP-associated mutations in 45 individuals (15.7%), most commonly in TET2 (10.8%), DNMT3A (9.2%), and U2AF1 (9.2%). Patients with CHIP tended to be older but did not significantly differ from patients without CHIP in terms of race or native lung disease. Patients with CHIP did not have a higher incidence of AR over the first post-transplant year (p = 0.45) or a significantly increased risk of death or CLAD (adjusted HR 1.25, 95% CI 0.88-1.78). We did observe a significant association between the number of CHIP variants and CLAD-free survival, specifically patients with 2 or more CHIP-associated variants had an increased risk for death or CLAD (adjusted HR 3.79, 95% CI 1.98-7.27).

conclusionsLung recipients have a higher prevalence of CHIP and a larger variety of genes with CHIP-associated mutations compared with previous reports for the general population. CHIP did not increase the risk of AR, CLAD, or death in lung recipients.

Indexed as

Clonal HematopoiesisLung TransplantationHumansLungPrevalenceTransplant Recipients

Identifiers

PMID37904125
PMCPMC10614406
OpenAlexW4388034558

What OpenQuestion holds

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LicenceCC BY
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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.