Evidence map›Paper›PMID 30590461›Full record

SynthesisCarcinogenesis2019

Modeling human prostate cancer progression in vitro.

Teresa T Liu, Jonathan A Ewald, Emily A Ricke, Robert Bell, Colin Collins, William A Ricke

Open access · bronzeAbstract readMeta-Analysis
In one paragraph

Synthesis in Carcinogenesis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

10 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. RNA-binding protein DDX3 mediates posttranscriptional regulation of androgen receptor: A mechanism of castration resistance.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  9. Article
  10. 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 at 3 institutions in 2 countries.

Teresa T LiuDepartment of Urology, University of Wisconsin-Madison, Madison, WI, USA.
Jonathan A EwaldDepartment of Urology, University of Wisconsin-Madison, Madison, WI, USA.
Emily A RickeDepartment of Urology, University of Wisconsin-Madison, Madison, WI, USA.
Robert BellVancouver Prostate Center, Vancouver Coastal Health Research Institute, Vancouver, British Columbia, Canada.
Colin CollinsVancouver Prostate Center, Vancouver Coastal Health Research Institute, Vancouver, British Columbia, Canada.
William A RickeDepartment of Urology, University of Wisconsin-Madison, Madison, WI, USA.
University of Wisconsin–Madison · USVancouver Coastal Health Research Institute · CAUniversity of Wisconsin Carbone Cancer Center · US

Funding

Role of Beta-Catenin in Urinary DysfunctionU54DK104310 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI MACOSKA, JILL A., MARKER, PAUL C · 2014 to 2023
$12.8M
Wisconsin Multidisciplinary K12 Urologic Research Career Development ProgramK12DK100022 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI CHAD M. VEZINA · 2013 to 2026
$8.6M
NIDDK NIH HHS K12 DK100022NIDDK NIH HHS U54 DK104310
6 · The paper itself

Abstract

Detailed mechanisms involved in prostate cancer (CaP) development and progression are not well understood. Current experimental models used to study CaP are not well suited to address this issue. Previously, we have described the hormonal progression of non-tumorigenic human prostate epithelial cells (BPH1) into malignant cells via tissue recombination. Here, we describe a method to derive human cell lines from distinct stages of CaP that parallel cellular, genetic and epigenetic changes found in patients with cancers. This BPH1-derived Cancer Progression (BCaP) model represents different stages of cancer. Using diverse analytical strategies, we show that the BCaP model reproduces molecular characteristics of CaP in human patients. Furthermore, we demonstrate that BCaP cells have altered gene expression of shared pathways with human and transgenic mouse CaP data, as well as, increasing genomic instability with TMPRSS2-ERG fusion in advanced tumor cells. Together, these cell lines represent a unique model of human CaP progression providing a novel tool that will allow the discovery and experimental validation of mechanisms regulating human CaP development and progression. This BPH1-derived Cancer Progression (BCaP) model represents different stages of cancer. The BCaP model reproduces molecular characteristics of prostate cancer. The cells have altered gene expression with TMPRSS2-ERG fusion representing a unique model for prostate cancer progression.

Indexed as

AnimalsCarcinogenesisCell LineDatasets as TopicDisease ProgressionDNA MethylationEpithelial CellsGene Expression Regulation, NeoplasticGenomic InstabilityHumansMaleMiceMice, TransgenicNeoplasm StagingOncogene Proteins, FusionPromoter Regions, GeneticOncogene Proteins, FusionTMPRSS2-ERG fusion protein, human

Identifiers

PMID30590461
PMCPMC6642366
OpenAlexW2906643453

What OpenQuestion holds

Textmetadata
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.