Evidence map›Paper›PMID 34402095›Full record

ArticleThe Prostate2021

Phenotypic characterization of two novel cell line models of castration-resistant prostate cancer.

Michael C Haffner, Akshay Bhamidipati, Harrison K Tsai, David M Esopi, Ajay M Vaghasia, Jin-Yih Low, Radhika A Patel, Gunes Guner, Minh-Tam Pham, Nicole Castagna and 7 more

Open access · greenAbstract read
In one paragraph

Article in The Prostate, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. The Androgen Regulated lncRNANon-coding RNA · 2022
    Article
  6. Article
  7. Article
  8. Review
  9. 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

17 authors at 6 institutions in 4 countries.

Michael C HaffnerDivisions of Human Biology and Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.ORCID 0000-0003-0809-6425
Akshay BhamidipatiSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID 0000-0002-2345-3331
Harrison K TsaiSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
David M EsopiSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Ajay M VaghasiaSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Jin-Yih LowDivisions of Human Biology and Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.
Radhika A PatelDivisions of Human Biology and Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.
Gunes GunerDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Minh-Tam PhamSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Nicole CastagnaSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Jessica HicksDepartment of Pathology, University of Washington, Seattle, Washington, USA.
Nicolas WyhsSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Ruedi AebersoldDepartment of Biology, Institute of Molecular Systems Biology, ETH, Zürich, Switzerland.
Angelo M De MarzoDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
William G NelsonDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Tiannan GuoDepartment of Biology, Institute of Molecular Systems Biology, ETH, Zürich, Switzerland.
Srinivasan YegnasubramanianDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID 0000-0003-0744-6606
Johns Hopkins University · USFred Hutch Cancer Center · USBrigham and Women's Hospital · USUniversity of Washington · USUniversity of Zurich · CHWestlake University · CN

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI WILLIAM George NELSON · 1985 to 2026
$208.6M
TRANSCRIPTOME AND PROTEOME STRATIFICATION OF PROSTATE ADENOCARCINOMA PHENOTYPESP50CA097186 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI PETER S NELSON · 2002 to 2026
$58.1M
TRANSGENIC MODELS FOR PROSTATE CANCER AND AUTOIMMUNITYP50CA058236 · NCI · JOHNS HOPKINS UNIVERSITY · PI DENMEADE, SAMUEL R · 1992 to 2020
$43.9M
Multidiciplinary Integrative Genomic Approach to Distinguish Lethal from Indolent Prostate Cancer in Men of Europena and African AncestryU01CA196390 · NCI · JOHNS HOPKINS UNIVERSITY · PI DE MARZO, ANGELO MICHAEL, PIENTA, KENNETH J. · 2015 to 2020
$5.8M
Role of TOP2B in generating complex genomic rearrangements in human cancerR01CA183965 · NCI · JOHNS HOPKINS UNIVERSITY · PI WHEELAN, SARAH J, YEGNASUBRAMANIAN, SRINIVASAN · 2014 to 2018
$1.7M
NCI NIH HHS P30 CA006973NCI NIH HHS P50 CA058236NCI NIH HHS P50 CA097186NCI NIH HHS R01 CA183965NCI NIH HHS U01 CA196390
6 · The paper itself

Abstract

backgroundResistance to androgen deprivation therapies is a major driver of mortality in advanced prostate cancer. Therefore, there is a need to develop new preclinical models that allow the investigation of resistance mechanisms and the assessment of drugs for the treatment of castration-resistant prostate cancer.

methodsWe generated two novel cell line models (LAPC4-CR and VCaP-CR) which were derived by passaging LAPC4 and VCaP cells in vivo and in vitro under castrate conditions. We performed detailed transcriptomic (RNA-seq) and proteomic analyses (SWATH-MS) to delineate expression differences between castration-sensitive and castration-resistant cell lines. Furthermore, we characterized the in vivo and in vitro growth characteristics of these novel cell line models.

resultsThe two cell line derivatives LAPC4-CR and VCaP-CR showed castration-resistant growth in vitro and in vivo which was only minimally inhibited by AR antagonists, enzalutamide, and bicalutamide. High-dose androgen treatment resulted in significant growth arrest of VCaP-CR but not in LAPC4-CR cells. Both cell lines maintained AR expression, but exhibited distinct expression changes on the mRNA and protein level. Integrated analyses including data from LNCaP and the previously described castration-resistant LNCaP-abl cells revealed an expression signature of castration resistance.

conclusionsThe two novel cell line models LAPC4-CR and VCaP-CR and their comprehensive characterization on the RNA and protein level represent important resources to study the molecular mechanisms of castration resistance.

Indexed as

AnimalsCell Line, TumorCell ProliferationHumansMalePhenotypeProstatic Neoplasms, Castration-Resistantandrogen signalingcastration resistancecell line modelsxenograft

Identifiers

PMID34402095
PMCPMC8460612
OpenAlexW3193810245

What OpenQuestion holds

Textmetadata
LicenceTDM
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.