Evidence map›Paper›PMID 30242112›Full record

ArticleCancer research2018

Downregulation of

Joshua W Russo, Ce Gao, Swati S Bhasin, Olga S Voznesensky, Carla Calagua, Seiji Arai, Peter S Nelson, Bruce Montgomery, Elahe A Mostaghel, Eva Corey and 4 more

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.5field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 61 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Increased ErbB2 Signaling Is an Early Adaptation to Androgen Signaling Inhibition and Persists in Castration-Resistant Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Integrative genomic analysis identifiesFrontiers in pharmacology · 2025
    Article
  11. Review
  12. Article
  13. A GATA2-CDC6 axis modulates androgen receptor blockade-induced senescence in prostate cancer.Journal of experimental & clinical cancer research : CR · 2023
    Article
  14. Article
  15. Assessment of Androgen Receptor Splice Variant-7 as a Biomarker of Clinical Response in Castration-Sensitive Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. 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

14 authors at 4 institutions in 2 countries.

Joshua W RussoDepartment of Medicine and Cancer Center, Hematology-Oncology Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts. sbalk@bidmc.harvard.edu jrusso1@bidmc.harvard.edu.
Ce GaoDepartment of Medicine, Bioinformatic and Systems Biology Unit, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
Swati S BhasinDepartment of Medicine, Bioinformatic and Systems Biology Unit, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
Olga S VoznesenskyDepartment of Medicine and Cancer Center, Hematology-Oncology Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
Carla CalaguaDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
Seiji AraiDepartment of Medicine and Cancer Center, Hematology-Oncology Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.ORCID 0000-0002-9514-735X
Peter S NelsonFred Hutchinson Cancer Research Center, Seattle, Washington.
Bruce MontgomeryUniversity of Washington School of Medicine, Seattle, Washington.
Elahe A MostaghelFred Hutchinson Cancer Research Center, Seattle, Washington.
Eva CoreyUniversity of Washington School of Medicine, Seattle, Washington.ORCID 0000-0002-9244-3807
Mary-Ellen TaplinDana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts.
Huihui YeDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
Manoj BhasinDepartment of Medicine, Bioinformatic and Systems Biology Unit, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
Steven P BalkDepartment of Medicine and Cancer Center, Hematology-Oncology Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts. sbalk@bidmc.harvard.edu jrusso1@bidmc.harvard.edu.
Beth Israel Deaconess Medical Center · USFred Hutch Cancer Center · USUniversity of Washington · USDana-Farber Cancer Institute · US

Funding

TRANSCRIPTOME AND PROTEOME STRATIFICATION OF PROSTATE ADENOCARCINOMA PHENOTYPESP50CA097186 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI PETER S NELSON · 2002 to 2026
$58.1M
Tumor and Circulating Markers as Links Between Obesity and Lethal Prostate CanceP50CA090381 · NCI · DANA-FARBER CANCER INSTITUTE · PI KANTOFF, PHILIP W · 2002 to 2017
$36.2M
Steroid Metabolism in Castration-Resistant Prostate CancerP01CA163227 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI PETER S NELSON · 2013 to 2026
$25.0M
NCI NIH HHS P01 CA163227NCI NIH HHS P50 CA090381NCI NIH HHS P50 CA097186
6 · The paper itself

Abstract

The standard treatment for metastatic prostate cancer, androgen deprivation therapy (ADT), is designed to suppress androgen receptor (AR) activity. However, men invariably progress to castration-resistant prostate cancer (CRPC), and AR reactivation contributes to progression in most cases. To identify mechanisms that may drive CRPC, we examined a VCaP prostate cancer xenograft model as tumors progressed from initial androgen sensitivity prior to castration to castration resistance and then on to relapse after combined therapy with further AR-targeted drugs (abiraterone plus enzalutamide). AR activity persisted in castration-resistant and abiraterone/enzalutamide-resistant xenografts and was associated with increased expression of the AR gene and the AR-V7 splice variant. We then assessed expression of individual AR-regulated genes to identify those that persisted, thereby contributing to tumor growth, versus those that decreased and may therefore exhibit tumor suppressor activities. The most significantly decreased AR target gene was dipeptidyl peptidase 4

Indexed as

Disease ProgressionDown-RegulationAlternative SplicingAndrogen AntagonistsAndrostenesAnimalsBenzamidesCell Line, TumorDipeptidyl Peptidase 4Drug Resistance, NeoplasmEpigenesis, GeneticGene Expression ProfilingHumansMaleMiceMice, SCIDabirateroneAndrogen AntagonistsAndrostenesAR protein, humanBenzamidesDipeptidyl Peptidase 4DPP4 protein, humanenzalutamideNitrilesPhenylthiohydantoinReceptors, AndrogenRNA, Small InterferingSitagliptin Phosphate

Identifiers

PMID30242112
PMCPMC6239953
OpenAlexW2891458328

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.