Evidence map›Paper›PMID 39768760›Full record

ReviewJournal of clinical medicine2024

Application of Original Prostate Cancer Progression Model Interacting with Fibroblasts in Preclinical Research.

Kenichiro Ishii, Kazuhiro Iguchi, Chise Matsuda, Yoshifumi Hirokawa, Yoshiki Sugimura, Masatoshi Watanabe

Abstract readReview
In one paragraph

Review in Journal of clinical medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

6 authors.

Kenichiro IshiiDepartment of Oncologic Pathology, Mie University Graduate School of Medicine, Tsu 514-8507, Japan.ORCID 0000-0001-9006-9148
Kazuhiro IguchiLaboratory of Community Pharmacy, Gifu Pharmaceutical University, Gifu 501-1196, Japan.
Chise MatsudaDepartment of Oncologic Pathology, Mie University Graduate School of Medicine, Tsu 514-8507, Japan.
Yoshifumi HirokawaDepartment of Oncologic Pathology, Mie University Graduate School of Medicine, Tsu 514-8507, Japan.
Yoshiki SugimuraDepartment of Urology, Murase Hospital, Suzuka 513-0801, Japan.
Masatoshi WatanabeDepartment of Oncologic Pathology, Mie University Graduate School of Medicine, Tsu 514-8507, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer (PCa) is a heterogeneous disease that exhibits androgen sensitivity and responsiveness to androgen deprivation therapy (ADT). However, ADT induces only temporary remission, and the majority of PCa cases eventually progress to castration-resistant PCa (CRPC). During the development and progression of CRPC, androgen sensitivity and androgen receptor (AR) dependency in PCa cells are often deceased or lost due to ADT or spontaneously arising AR variants even before starting ADT. To prevent CRPC, a clinical PCa model derived from an AR-positive cancer cell line with weak or no androgen sensitivity is required. The human prostate LNCaP cell line is a good model for PCa because of its androgen sensitivity and AR dependency in terms of cell growth and gene expression. Notably, LNCaP cells are heterogeneous cells comprising different clones with natural variations in androgen sensitivity and AR dependency resulting from spontaneously occurring changes. In our group, to obtain androgen-insensitive or weakly sensitive clones spontaneously derived from parental LNCaP cells, we performed a limiting dilution of parental LNCaP cells and obtained several sublines with varying levels of androgen sensitivity and AR dependency. In addition, we established an androgen-insensitive subline from parental LNCaP cells by continuous passage under hormone-depleted conditions. This article provides a unique perspective on our original PCa progression model interacting with fibroblasts and its application in preclinical research.

Indexed as

androgen receptor dependencyandrogen sensitivitycytokinesfibroblastsgrowth factorsLNCaP subline

Identifiers

PMID39768760
PMCPMC11678552

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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.