Evidence map›Paper›PMID 21138984›Full record

ArticleLupus2011

A systemic lupus erythematosus gene expression array in disease diagnosis and classification: a preliminary report.

Y-T Juang, C Peoples, R Kafri, V C Kyttaris, K Sunahori, K Kis-Toth, L Fitzgerald, S Ergin, M Finnell, G C Tsokos

Abstract read
In one paragraph

Article in Lupus, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Systemic lupus erythematosus diagnostics in the 'omics' era.International journal of clinical rheumatology · 2013
    Article
  7. Article
  8. 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

10 authors at 2 institutions in 1 country.

Y-T JuangDivision of Rheumatology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
C Peoples
R Kafri
V C Kyttaris
K Sunahori
K Kis-Toth
L Fitzgerald
S Ergin
M Finnell
G C Tsokos
Beth Israel Deaconess Medical Center · USHarvard University · US

Funding

Expanded Double Negative T cells in SLE.R01AI085567 · NIAID · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TSOKOS, GEORGE C · 2010 to 2025
$6.8M
LYMPHOCYTE SIGNALING DEFECTS IN PATIENTS WITH LUPUSR01AI042269 · NIAID · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI TSOKOS, GEORGE C · 1998 to 2017
$6.8M
Gene Transcription In SLER01AI049954 · NIAID · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI George C Tsokos · 2002 to 2026
$5.8M
Phosphatases in Human LupusR01AI068787 · NIAID · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TSOKOS, GEORGE C · 2007 to 2016
$4.1M
NFAT/AP-1 cooperation in SLE T cellsK23AR055672 · NIAMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KYTTARIS, VASILEIOS CHRISTOS · 2008 to 2012
$486k
NIAID NIH HHS R01 AI042269NIAID NIH HHS R01 AI049954NIAID NIH HHS R01 AI068787NIAID NIH HHS R01 AI085567NIAID NIH HHS R01AI42269NIAID NIH HHS R01AI49954NIAID NIH HHS R01AI68787NIAID NIH HHS R01AI85567NIAMS NIH HHS K23 AR055672NIAMS NIH HHS K23AR55672
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a clinically heterogeneous disease diagnosed on the presence of a constellation of clinical and laboratory findings. At the pathogenetic level, multiple factors using diverse biochemical and molecular pathways have been recognized. Succinct recognition and classification of clinical disease subsets, as well as the availability of disease biomarkers, remains largely unsolved. Based on information produced by the present authors' and other laboratories, a lupus gene expression array consisting of 30 genes, previously claimed to contribute to aberrant function of T cells, was developed. An additional eight genes were included as controls. Peripheral blood was obtained from 10 patients (19 samples) with SLE and six patients with rheumatoid arthritis (RA) as well as 19 healthy controls. T cell mRNA was subjected to reverse transcription and PCR, and the gene expression levels were measured. Conventional statistical analysis was performed along with principal component analysis (PCA) to capture the contribution of all genes to disease diagnosis and clinical parameters. The lupus gene expression array faithfully informed on the expression levels of genes. The recorded changes in expression reflect those reported in the literature by using a relatively small (5 ml) amount of peripheral blood. PCA of gene expression levels placed SLE samples apart from normal and RA samples regardless of disease activity. Individual principal components tended to define specific disease manifestations such as arthritis and proteinuria. Thus, a lupus gene expression array based on genes previously claimed to contribute to immune pathogenesis of SLE may define the disease, and principal components of the expression of 30 genes may define patients with specific disease manifestations.

Indexed as

AdultAgedArthritis, RheumatoidFemaleGene ExpressionGene Expression ProfilingHumansLupus Erythematosus, SystemicMaleMiddle AgedOligonucleotide Array Sequence Analysis

Identifiers

PMID21138984
PMCPMC3880791
OpenAlexW2046172155

What OpenQuestion holds

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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.