Evidence map›Paper›PMID 31052459›Full record

ArticleJournal of clinical medicine2019

Consecutive Prostate Cancer Specimens Revealed Increased Aldo⁻Keto Reductase Family 1 Member C3 Expression with Progression to Castration-Resistant Prostate Cancer.

Yu Miyazaki, Yuki Teramoto, Shinsuke Shibuya, Takayuki Goto, Kosuke Okasho, Kei Mizuno, Masayuki Uegaki, Takeshi Yoshikawa, Shusuke Akamatsu, Takashi Kobayashi and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Intracrine androgen biosynthesis and drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2020
    Review
  8. 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

12 authors at 2 institutions in 1 country.

Yu MiyazakiDepartment of Urology, Kyoto University Graduate School of Medicine, Kyoto 606-8507, Japan. urozaki@kuhp.kyoto-u.ac.jp.
Yuki TeramotoDepartment of Diagnostic Pathology, Kyoto University Hospital, Kyoto 606-8507, Japan. tera1980@kuhp.kyoto-u.ac.jp.
Shinsuke ShibuyaDepartment of Diagnostic Pathology, Kyoto University Hospital, Kyoto 606-8507, Japan. sshibuya@kuhp.kyoto-u.ac.jp.
Takayuki GotoDepartment of Urology, Kyoto University Graduate School of Medicine, Kyoto 606-8507, Japan. goto@kuhp.kyoto-u.ac.jp.
Kosuke OkashoDepartment of Urology, Kyoto University Graduate School of Medicine, Kyoto 606-8507, Japan. k_okasho@kuhp.kyoto-u.ac.jp.
Kei MizunoDepartment of Urology, Kyoto University Graduate School of Medicine, Kyoto 606-8507, Japan. km1207@kuhp.kyoto-u.ac.jp.
Masayuki UegakiDepartment of Urology, Kyoto University Graduate School of Medicine, Kyoto 606-8507, Japan. uegaki57@kuhp.kyoto-u.ac.jp.
Takeshi YoshikawaDepartment of Urology, Kyoto University Graduate School of Medicine, Kyoto 606-8507, Japan. urotake9@kuhp.kyoto-u.ac.jp.
Shusuke AkamatsuDepartment of Urology, Kyoto University Graduate School of Medicine, Kyoto 606-8507, Japan. akamats@kuhp.kyoto-u.ac.jp.
Takashi KobayashiDepartment of Urology, Kyoto University Graduate School of Medicine, Kyoto 606-8507, Japan. selecao@kuhp.kyoto-u.ac.jp.ORCID 0000-0003-1069-2816
Osamu OgawaDepartment of Urology, Kyoto University Graduate School of Medicine, Kyoto 606-8507, Japan. ogawao@kuhp.kyoto-u.ac.jp.
Takahiro InoueDepartment of Urology, Kyoto University Graduate School of Medicine, Kyoto 606-8507, Japan. takahi@kuhp.kyoto-u.ac.jp.
Kyoto University · JPKyoto University Hospital · JP

Funding

Japan Society for the Promotion of Science 15K10587 & 18H02936
6 · The paper itself

Abstract

Aldo-keto reductase family 1 member C3 (AKR1C3) is an enzyme in the steroidogenesis pathway, especially in formation of testosterone and dihydrotestosterone, and is believed to have a key role in promoting prostate cancer (PCa) progression, particularly in castration-resistant prostate cancer (CRPC). This study aims to compare the expression level of AKR1C3 between benign prostatic epithelium and cancer cells, and among hormone-naïve prostate cancer (HNPC) and CRPC from the same patients, to understand the role of AKR1C3 in PCa progression. Correlation of AKR1C3 immunohistochemical expression between benign and cancerous epithelia in 134 patient specimens was analyzed. Additionally, correlation between AKR1C3 expression and prostate-specific antigen (PSA) progression-free survival (PFS) after radical prostatectomy was analyzed. Furthermore, we evaluated the consecutive prostate samples derived from 11 patients both in the hormone-naïve and castration-resistant states. AKR1C3 immunostaining of cancer epithelium was significantly stronger than that of the benign epithelia in patients with localized HNPC (

Indexed as

AKR1C3castration-resistant prostate cancerhormone-naïve prostate cancerimmunohistochemistrytissue microarray

Identifiers

PMID31052459
PMCPMC6571723
OpenAlexW2943208181

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.