Evidence map›Paper›PMID 29464200›Full record

ArticleTransplantation direct2018

Polyomavirus BK Nephropathy-Associated Transcriptomic Signatures: A Critical Reevaluation.

Ling Pan, Zili Lyu, Benjamin Adam, Gang Zeng, Zijie Wang, Yuchen Huang, Zahidur Abedin, Parmjeet Randhawa

Abstract read
In one paragraph

Article in Transplantation direct, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. BK polyomavirus: latency, reactivation, diseases and tumorigenesis.Frontiers in cellular and infection microbiology · 2023
    Review
  5. Article
  6. Recent Advances on Biomarkers of Early and Late Kidney Graft Dysfunction.International journal of molecular sciences · 2020
    Review
  7. Article
  8. Article
  9. Cellular Immunity Against BK Polyomavirus in Kidney Transplant Recipients: A Comprehensive Review.Transplant infectious disease : an official journal of the Transplantation Society
    Review
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

8 authors.

Ling PanDepartment of Nephrology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.
Zili LyuDepartment of Pathology, The First Affiliated hospital of Guangxi Medical University, Nanning, Guangxi, China.
Benjamin AdamDivision of Anatomical Pathology, Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, Alberta, Canada.
Gang ZengDepartment of Pathology, University of Pittsburgh Medical Center, Pittsburgh, PA.
Zijie WangDepartment of Pathology, University of Pittsburgh Medical Center, Pittsburgh, PA.
Yuchen HuangDepartment of Pathology, University of Pittsburgh Medical Center, Pittsburgh, PA.
Zahidur AbedinPrimBio Research Institute LLC, Exton, PA.
Parmjeet RandhawaDepartment of Pathology, University of Pittsburgh Medical Center, Pittsburgh, PA.

Funding

T-cell clonotypes in BK virus infection complicated by acute rejectionR21AI117644 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI RANDHAWA, PARMJEET S · 2016 to 2017
$423k
NIAID NIH HHS R21 AI117644
6 · The paper itself

Abstract

backgroundRecent work using DNA microarrays has suggested that genes related to DNA replication, RNA polymerase assembly, and pathogen recognition receptors can serve as surrogate tissue biomarkers for polyomavirus BK nephropathy (BKPyVN).

methodsWe have examined this premise by looking for differential regulation of these genes using a different technology platform (RNA-seq) and an independent set 25 biopsies covering a wide spectrum of diagnoses.

resultsRNA-seq could discriminate T cell-mediated rejection from other common lesions seen in formalin fixed biopsy material. However, overlapping RNA-seq signatures were found among all disease processes investigated. Specifically, genes previously reported as being specific for the diagnosis of BKPyVN were found to be significantly upregulated in T cell-mediated rejection, inflamed areas of fibrosis/tubular atrophy, as well as acute tubular injury.

conclusionsIn conclusion, the search for virus specific molecular signatures is confounded by substantial overlap in pathogenetic mechanisms between BKPyVN and nonviral forms of allograft injury. Clinical heterogeneity, overlapping exposures, and different morphologic patterns and stage of disease are a source of substantial variability in "Omics" experiments. These variables should be better controlled in future biomarker studies on BKPyVN, T cell-mediated rejection, and other forms of allograft injury, before widespread implementation of these tests in the transplant clinic.

Identifiers

PMID29464200
PMCPMC5811268

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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.