Evidence map›Paper›PMID 39656401›Full record

ArticleInternational journal of clinical oncology2025

Characterization of PSA dynamics and oncological outcomes in patients with metastatic hormone-sensitive prostate cancer treated with androgen receptor signaling inhibitors.

Yasutaka Yamada, Kodai Sato, Shinichi Sakamoto, Takuya Tsujino, Sinpei Saito, Kazuki Nishimura, Tatsuo Fukushima, Ko Nakamura, Yuki Yoshikawa, Tomohisa Matsunaga and 16 more

Abstract read
In one paragraph

Article in International journal of clinical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
–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

2 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. 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

26 authors.

Yasutaka YamadaDepartment of Urology, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba-City, Chiba, 2608670, Japan.
Kodai SatoDepartment of Urology, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba-City, Chiba, 2608670, Japan.
Shinichi SakamotoDepartment of Urology, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba-City, Chiba, 2608670, Japan. rbatbat1@gmail.com.
Takuya TsujinoDepartment of Urology, Osaka Medical and Pharmaceutical University, Osaka, Japan.
Sinpei SaitoDepartment of Urology, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba-City, Chiba, 2608670, Japan.
Kazuki NishimuraDepartment of Urology, Osaka Medical and Pharmaceutical University, Osaka, Japan.
Tatsuo FukushimaDepartment of Urology, Osaka Medical and Pharmaceutical University, Osaka, Japan.
Ko NakamuraDepartment of Urology, Osaka Medical and Pharmaceutical University, Osaka, Japan.
Yuki YoshikawaDepartment of Urology, Osaka Medical and Pharmaceutical University, Osaka, Japan.
Tomohisa MatsunagaDepartment of Urology, Osaka Medical and Pharmaceutical University, Osaka, Japan.
Ryoichi MaenosonoDepartment of Urology, Osaka Medical and Pharmaceutical University, Osaka, Japan.
Manato KanesakaDepartment of Urology, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba-City, Chiba, 2608670, Japan.
Takayuki AraiDepartment of Urology, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba-City, Chiba, 2608670, Japan.
Tomokazu SazukaDepartment of Urology, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba-City, Chiba, 2608670, Japan.
Yusuke ImamuraDepartment of Urology, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba-City, Chiba, 2608670, Japan.
Kazumasa KomuraDepartment of Urology, Osaka Medical and Pharmaceutical University, Osaka, Japan.
Kazuo MikamiDepartment of Urology, Chibaken Saiseikai Narashino Hospital, Chiba, Japan.
Kazuyoshi NakamuraDepartment of Urology, Kimitsu Chuo Hospital, Chiba, Japan.
Satoshi FukasawaDepartment of Urology, Funabashi Municipal Medical Center, Chiba, Japan.
Kazuto ChibaDepartment of Urology, Fukaya Red Cross Hospital, Saitama, Japan.
Yukio NayaDepartment of Urology, Teikyo University Chiba Medical Center, Chiba, Japan.
Maki NagataDepartment of Urology, Yokohama Rosai Hospital, Kanagawa, Japan.
Atsushi KomaruProstate Center and Division of Urology, Chiba Cancer Center, Chiba, Japan.
Hiroomi NakatsuDepartment of Urology, Asahi General Hospital, Chiba, Japan.
Haruhito AzumaDepartment of Urology, Osaka Medical and Pharmaceutical University, Osaka, Japan.
Tomohiko IchikawaDepartment of Urology, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba-City, Chiba, 2608670, Japan.

Funding

Japan Society for the Promotion of Science London 24K02575Japan Society for the Promotion of Science London 24K19665
6 · The paper itself

Abstract

backgroundThis study investigated the characteristics of prostate-specific antigen (PSA) dynamics when androgen receptor signaling inhibitor (ARSI), or vintage agent (bicalutamide) was used for patients with metastatic hormone-sensitive prostate cancer (mHSPC). PATIENTS AND

methodsA total of 213 mHSPC patients from each of the ARSI and bicalutamide groups treated between 2015 and 2022 were selected from multiple institutions using propensity score-matched analysis to align backgrounds. PSA progression-free survival (PFS) and overall survival (OS) were assessed. PSA level at 3 months, PSA nadir level, and time to PSA nadir were examined to analyze of PSA kinetics.

resultsARSI treatment significantly improved PSA PFS compared to bicalutamide (P = 0.0063), although no significant difference in OS was seen (P = 0.3134). No significant differences were observed between treatment groups in median PSA levels at 3 months (1.47 vs 0.52 ng/ml, P = 0.3042) or PSA nadir levels (0.263 vs 0.1345 ng/ml, P = 0.1228). Bicalutamide treatment demonstrated longer time to nadir than ARSI in progression-free cases (median: 243 vs 213.5 days, P = 0.0003). Survival tree analysis found that PSA nadir ≤ 1.5 ng/ml and time to nadir ≥ 145 days were the optimal cut-offs for best stratifying OS with bicalutamide, while PSA nadir ≤ 0.45 ng/ml and time to nadir ≥ 70 days were optimal with ARSI.

conclusionNo significant differences in PSA response was seen between groups; however, distinct optimal cut-offs were demonstrated for PSA nadir and time to nadir. The present findings will be useful for optimal PSA monitoring for mHSPC patients and for early identification of poor-prognosis populations.

Indexed as

Androgen Receptor AntagonistsAnilidesNitrilesProstate-Specific AntigenProstatic NeoplasmsTosyl CompoundsAgedAged, 80 and overAndrogen AntagonistsHumansMaleMiddle AgedNeoplasm MetastasisProgression-Free SurvivalReceptors, AndrogenRetrospective StudiesAndrogen AntagonistsAndrogen Receptor AntagonistsAnilidesAR protein, humanbicalutamideNitrilesProstate-Specific AntigenReceptors, AndrogenTosyl CompoundsAndrogen receptor signaling inhibitorBicalutamideMetastatic hormone-sensitive prostate cancerPSA dynamicsPSA nadirTime to PSA nadir

Identifiers

PMID39656401
PMCPMC11842405

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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.