Evidence map›Paper›PMID 37848957›Full record

ArticleGenes and environment : the official journal of the Japanese Environmental Mutagen Society2023

Association of PSA variability with prostate cancer development using large-scale medical information data: a retrospective cohort study.

Ayako Maeda-Minami, Tomoki Nishikawa, Hideki Ishikawa, Michihiro Mutoh, Kazunori Akimoto, Yutaka Matsuyama, Yasunari Mano, Hiroji Uemura

Open access · goldAbstract read
In one paragraph

Article in Genes and environment : the official journal of the Japanese Environmental Mutagen Society, 2023. 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
1.8field-weighted citation impact, top 14% 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, 7 citations in OpenAlex.

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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 4 institutions in 1 country.

Ayako Maeda-MinamiFaculty of Pharmaceutical Sciences, Tokyo University of Science, Yamazaki, Noda, 2641, 278-8510, Chiba, Japan.
Tomoki NishikawaFaculty of Pharmaceutical Sciences, Tokyo University of Science, Yamazaki, Noda, 2641, 278-8510, Chiba, Japan.
Hideki IshikawaDepartment of Molecular-Targeting Prevention, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Michihiro MutohDepartment of Molecular-Targeting Prevention, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Kazunori AkimotoFaculty of Pharmaceutical Sciences, Tokyo University of Science, Yamazaki, Noda, 2641, 278-8510, Chiba, Japan.
Yutaka MatsuyamaDepartment of Biostatistics, School of Public Health, The University of Tokyo, Tokyo, Japan.
Yasunari ManoFaculty of Pharmaceutical Sciences, Tokyo University of Science, Yamazaki, Noda, 2641, 278-8510, Chiba, Japan. mano@rs.tus.ac.jp.ORCID http://orcid.org/0000-0002-2245-4260
Hiroji UemuraYokohama City University Medical Center, Yokohama, Japan.
Tokyo University of Science · JPKyoto Prefectural University of Medicine · JPThe University of Tokyo · JPYokohama City University Medical Center · JP

Funding

AMED AMED
6 · The paper itself

Abstract

backgroundProstate cancer is one of the most common cancers among men worldwide and the fourth most common cause of death. The number of prostate cancer cases and deaths is increasing every year because of population aging. This study aimed to clarify the risk of developing prostate cancer due to fluctuations in Prostate Specific Antigen (PSA) levels in patients without a history of prostate cancer using large medical information data.

resultsThis retrospective cohort included 1707 male patients aged 60 years or older who had a PSA level measurement date (2-PSA) within 3 months or more and 2 years from the first PSA level measurement date (1-PSA) in the database between 2008 and 2019. We subtracted 1-PSA from 2-PSA and designated patients with a higher 2-PSA than 1-PSA to the "up" group (n = 967) and patients with a lower 2-PSA than 1-PSA to the "down" group (n = 740). By using Cox proportional hazards model, a significant increase in prostate cancer risk was observed in the up group compared with the down group (adjusted hazard ratio [HR] = 1.82, 95% confidence interval [CI] = 1.21-2.72; adjusted for patient background factors). Subgroup analysis showed that patients with PSA levels < 4 ng/mL had a significantly increased risk of developing prostate cancer if the next PSA level increases by approximately 20% (adjusted HR = 2.94, 95% CI = 1.14-7.58), and patients with PSA levels of 4 ng/mL or higher if the next PSA level is decreased by approximately 20% had a significantly reduced risk of developing prostate cancer (adjusted HR = 0.36, 95% CI = 0.18-0.74), compared to that with no change.

conclusionsThis is the first study to clarify the association between PSA variability and risk of developing prostate cancer in patients without a history of prostate cancer. These results suggest that the suppression of elevated PSA levels may lead to the prevention of prostate cancer and that it would be better to perform a biopsy because the risk of developing prostate cancer may increase in the future if the PSA value increases above a certain level.

Indexed as

Claim databaseProstate cancerProstate specific AntigenReal-word dataRetrospective cohort study

Identifiers

PMID37848957
PMCPMC10580524
OpenAlexW4387695802

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.