Evidence map›Paper›PMID 27431530›Full record

ArticleEuropean journal of epidemiology2017

Prostate-specific antigen testing for prostate cancer: Depleting a limited pool of susceptible individuals?

Morten Valberg, Tom Grotmol, Steinar Tretli, Marit B Veierød, Tron A Moger, Susan S Devesa, Odd O Aalen

Abstract read
In one paragraph

Article in European journal of epidemiology, 2017. 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
–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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Prostate cancer incidence as an iceberg.European journal of epidemiology · 2017
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Morten ValbergDepartment of Biostatistics, Oslo Centre for Biostatistics and Epidemiology, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway. morten.valberg@medisin.uio.no.
Tom GrotmolCancer Registry of Norway, Institute of Population-Based Cancer Research, Oslo, Norway.
Steinar TretliCancer Registry of Norway, Institute of Population-Based Cancer Research, Oslo, Norway.
Marit B VeierødDepartment of Biostatistics, Oslo Centre for Biostatistics and Epidemiology, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Tron A MogerDepartment of Biostatistics, Oslo Centre for Biostatistics and Epidemiology, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Susan S DevesaDivision of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD, USA.
Odd O AalenDepartment of Biostatistics, Oslo Centre for Biostatistics and Epidemiology, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.

Funding

Intramural NIH HHS Z99 CA999999Kreftforeningen 4493570
6 · The paper itself

Abstract

After the introduction of the prostate specific antigen (PSA) test in the 1980s, a sharp increase in the incidence rate of prostate cancer was seen in the United States. The age-specific incidence patterns exhibited remarkable shifts to younger ages, and declining rates were observed at old ages. Similar trends were seen in Norway. We investigate whether these features could, in combination with PSA testing, be explained by a varying degree of susceptibility to prostate cancer in the populations. We analyzed incidence data from the United States' Surveillance, Epidemiology, and End Results program for 1973-2010, comprising 511,027 prostate cancers in men ≥40 years old, and Norwegian national incidence data for 1953-2011, comprising 113,837 prostate cancers in men ≥50 years old. We developed a frailty model where only a proportion of the population could develop prostate cancer, and where the increased risk of diagnosis due to the massive use of PSA testing was modelled by encompassing this heterogeneity in risk. The frailty model fits the observed data well, and captures the changing age-specific incidence patterns across birth cohorts. The susceptible proportion of men is [Formula: see text] in the United States and [Formula: see text] in Norway. Cumulative incidence rates at old age are unchanged across birth cohort exposed to PSA testing at younger and younger ages. The peaking cohort-specific age-incidence curves of prostate cancer may be explained by the underlying heterogeneity in prostate cancer risk. The introduction of the PSA test has led to a larger number of diagnosed men. However, no more cases are being diagnosed in total in birth cohorts exposed to the PSA era at younger and younger ages, even though they are diagnosed at younger ages. Together with the earlier peak in the age-incidence curves for younger cohorts, and the strong familial association of the cancer, this constitutes convincing evidence that the PSA test has led to a higher proportion, and an earlier timing, of diagnoses in a limited pool of susceptible individuals.

Indexed as

AdultAgedAged, 80 and overAge DistributionCross-Cultural ComparisonDisease SusceptibilityHumansIncidenceMaleMass ScreeningMiddle AgedNorwayPopulation SurveillanceProportional Hazards ModelsProstate-Specific AntigenProstatic NeoplasmsProstate-Specific AntigenFrailtyProstate cancerPSA testSusceptibility

Identifiers

PMID27431530
PMCPMC5468491

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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.