Evidence map›Paper›PMID 31125365›Full record

ArticlePloS one2019

Interaction between leukocyte aldo-keto reductase 1C3 activity, genotypes, biological, lifestyle and clinical features in a prostate cancer cohort from New Zealand.

Nishi Karunasinghe, Eva Symes, Amy Gamage, Alice Wang, Pam Murray, Shuotun Zhu, Megan Goudie, Jonathan Masters, Lynnette R Ferguson

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. 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
0.7field-weighted citation impact, top 34% 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, 8 citations in OpenAlex.

  1. Trial
  2. Review
  3. 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

9 authors at 2 institutions in 1 country.

Nishi KarunasingheAuckland Cancer Society Research Centre (ACSRC), Faculty of Medical and Health Sciences (FM&HS), The University of Auckland, Auckland, New Zealand.ORCID 0000-0002-6383-4163
Eva SymesAuckland Cancer Society Research Centre (ACSRC), Faculty of Medical and Health Sciences (FM&HS), The University of Auckland, Auckland, New Zealand.
Amy GamageAuckland Cancer Society Research Centre (ACSRC), Faculty of Medical and Health Sciences (FM&HS), The University of Auckland, Auckland, New Zealand.
Alice WangAuckland Cancer Society Research Centre (ACSRC), Faculty of Medical and Health Sciences (FM&HS), The University of Auckland, Auckland, New Zealand.
Pam MurrayAuckland Cancer Society Research Centre (ACSRC), Faculty of Medical and Health Sciences (FM&HS), The University of Auckland, Auckland, New Zealand.
Shuotun ZhuAuckland Cancer Society Research Centre (ACSRC), Faculty of Medical and Health Sciences (FM&HS), The University of Auckland, Auckland, New Zealand.
Megan GoudieUrology Department, Auckland City Hospital, Auckland, New Zealand.
Jonathan MastersUrology Department, Auckland City Hospital, Auckland, New Zealand.
Lynnette R FergusonEmeritus Professor, FM&HS, The University of Auckland, Auckland, New Zealand.
University of Auckland · NZAuckland City Hospital · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAldo-keto reductase 1C3 (AKR1C3) is known for multiple functions including its catalytic activity towards producing extra-testicular androgen. The present study is towards understanding interaction between biological, lifestyle and genetic impacts of AKR1C3 and their influence on clinical factors in a prostate cancer (PC) cohort from New Zealand (NZ).

methodCharacteristics of 516 PC patients were collected from the Auckland Regional Urology Facility, NZ. These men were genotyped for the AKR1C3 rs12529 single nucleotide polymorphism (SNP). The leukocyte AKR1C3 activity was measured in a sub-cohort. Variability of leukocyte AKR1C3 activity between biological, lifestyle and clinical features as well as correlation between biological and clinical features were assessed with and without genetic stratification.

resultsThe leukocyte AKR1C3 activity was associated with age at diagnosis (0.51 vs 0.34 μM coumberol units for >69y vs ≤69y, P = 0.03); and with anatomic stage/prognostic grouping among the AKR1C3 rs12529 CC genotype carriers (0.50 vs 28 μM coumberol units among low- and high-risk groups respectively, P = 0.02). Significant correlation between leukocyte AKR1C3 activity and age at PC diagnosis was also observed (correlation coefficient 0.20 and P = 0.02). Ever- smoking impacted both age and PSA at PC diagnosis among AKR1C3 rs12529 GG and CG genotype carriers respectively. Age at diagnosis significantly correlated with PSA at diagnosis in the main (correlation coefficient 0.29, and P<0.001) and sub-cohorts (correlation coefficient 0.24, and P = 0.01); and those carrying the AKR1C3 rs12529 CG and GG genotypes in both the main (correlation coefficient 0.30, and P<0.001 and correlation coefficient 0.35, and P<0.001 respectively) and sub-cohorts (correlation coefficient 0.43, and P<0.001 and correlation coefficient 0.39, and P = 0.06 respectively); but not with those carrying the CC genotype.

conclusionsAge dependent PSA thresholds in PC screening could have been valid only in men carrying the AKR1C3 rs12529 CG and GG genotypes in this NZ cohort.

Indexed as

AgedAged, 80 and overAldo-Keto Reductase Family 1 Member C3Body Mass IndexCohort StudiesGenotypeHumansKallikreinsLeukocytesLife StyleMaleMiddle AgedNeoplasm GradingNew ZealandPolymorphism, Single NucleotideProstate-Specific AntigenAKR1C3 protein, humanAldo-Keto Reductase Family 1 Member C3KallikreinsKLK3 protein, humanProstate-Specific Antigen

Identifiers

PMID31125365
PMCPMC6534310
OpenAlexW2946445902

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.