Evidence map›Paper›PMID 31930191›Full record

ArticleJournal of translational autoimmunity2019

Angiotensin receptor autoantibodies as exposures that modify disease progression: Cross sectional, longitudinal and

Alka Jain, Haikoo Shah, Eleanor M Simonsick, E Jeffrey Metter, Leslie Mangold, Elizabeth Humphreys, Alan Partin, Neal S Fedarko

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational autoimmunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 29% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Article
  3. Autoimmunity in 2019.Clinical reviews in allergy & immunology · 2020
    Review
  4. 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

8 authors at 1 institution in 1 country.

Alka JainDepartment of Medicine, Johns Hopkins University, Baltimore, MD, 21224, USA.
Haikoo ShahDepartment of Medicine, Johns Hopkins University, Baltimore, MD, 21224, USA.
Eleanor M SimonsickIntramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21225, USA.
E Jeffrey MetterIntramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21225, USA.
Leslie MangoldDepartment of Urology, James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA.
Elizabeth HumphreysDepartment of Urology, James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA.
Alan PartinDepartment of Urology, James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA.
Neal S FedarkoDepartment of Medicine, Johns Hopkins University, Baltimore, MD, 21224, USA.
Johns Hopkins University · US

Funding

Small Integrin-binding Glycophosphoproteins as Biomarkers for Prostate CancerR01CA149273 · NCI · JOHNS HOPKINS UNIVERSITY · PI FEDARKO, NEAL S · 2011 to 2013
$896k
NCI NIH HHS R01 CA149273
6 · The paper itself

Abstract

Circulating angiotensin type I receptor (AT1R) agonistic autoantibodies (AT1RaAbs) that bind and chronically activate the receptor have been associated with a number of diseases suggesting that while the autoantibodies are not necessarily causative they may promote disease progression. The prostate has a local renin angiotensin system. The current study examines associations between AT1RaAbs and prostate cancer (PCA), disease-free survival (DFS), overall survival (OS) and AT1RaAb effects on PCA cell phenotype. In a cross-sectional set of serum obtained from 151 men diagnosed with PCA, nonmalignant prostate disease or no disease, higher serum AT1RaAb levels were associated with PCA and non-organ confined PCA. The odds ratio for PCA was 6.3 (95% confidence interval 2.2 to 18) for a positive 1:1600 titer and 18 (95% confidence interval 6.9 to 45) at AT1RaAb levels > 1.04 μg/ml, (p < 0.0001). In a longitudinal set of pre-diagnosis samples from 109 men, DFS hazard ratios of 2.2 (95% confidence interval 1.4 to 3.5) and 1.6 (95% confidence interval 1.0 to 2.5) for most proximal to diagnosis and most distal to diagnosis samples, respectively, were found for high versus low AT1RaAb groups. Hazard ratios for OS in most proximal and distal samples were 2.4 (95% confidence interval 1.6 to 3.6) and 1.8 (95% confidence interval 1.1 to 2.8), respectively. Accelerated failure modeling of survival indicated that a 1 μg/ml increase in AT1RaAb levels was associated with a reduction of DFS and OS by 20% at the most proximal time point and by 15% at the most distal time points. Adjusting for age, did not affect the association with DFS in proximal samples but changed distal time point DFS and OS to a 10% decrease for every 1 μg/ml increase in AT1RaAb. Additional adjustments for body mass index, systolic blood pressure and prostate-specific antigen did not appreciably alter these associations. AT1RaAb treatment of PC3, DU145, and LNCaP cells significantly increased the maximal growth rate approximately 2-fold and invasiveness approximately 3-fold.

Indexed as

Angiotensin type I receptorAutoantibodiesDisease-free survivalDisease progressionOverall survivalProstate cancerRisk stratification

Identifiers

PMID31930191
PMCPMC6953913
OpenAlexW2968620372

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.