Evidence map›Paper›PMID 28976133›Full record

ArticleJournal of experimental therapeutics & oncology2017

Angiotensin receptor signaling and prostate tumor growth in mice.

Jem Scott-Emuakpor, Emma Allot, Stacy A Johnson, Lauren E Howard, Everardo Macias, Stephen J Freedland, Susan B Gurley

Open access · greenAbstract read
In one paragraph

Article in Journal of experimental therapeutics & oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

7 authors at 1 institution in 1 country.

Jem Scott-EmuakporDepartment of Research and Development, Durham VA Medical Center, USA.
Emma AllotDepartment of Surgery, Durham VA Medical Center, USA.
Stacy A JohnsonDepartment of Research and Development, Durham VA Medical Center, USA.
Lauren E HowardDepartment of Biostatistics and Bioinformatics, Duke University School of Medicine, Duke University, USA.
Everardo MaciasDuke Prostate Center, Division of Urology, Department of Surgery, Duke University, USA.
Stephen J FreedlandDepartment of Research and Development, Durham VA Medical Center, USA.
Susan B GurleyDepartment of Research and Development, Durham VA Medical Center, USA.
Duke University · US

Funding

Renal Genomics CoreP30DK096493 · NIDDK · DUKE UNIVERSITY · PI FOSTER, MARY H., SVETKEY, LAURA P · 2012 to 2016
$5.9M
Gene expression programs of lactic acidosis in human cancersR01CA125618 · NCI · DUKE UNIVERSITY · PI CHI, JEN-TSAN ASHLEY · 2007 to 2016
$3.3M
Midcareer Investigator AwardK24CA160653 · NCI · DUKE UNIVERSITY · PI FREEDLAND, STEPHEN JAY · 2012 to 2016
$877k
NCI NIH HHS K24 CA160653NCI NIH HHS R01 CA125618NIDDK NIH HHS P30 DK096493
6 · The paper itself

Abstract

objectiveThe renin-angiotensin system, through its type 1 and type 2 angiotensin receptors (AT1R and AT2R, respectively) may have a role in prostate cancer. The objective of this pilot study was to explore that potential role by determining whether the AT1R blocker, losartan, would reduce the growth of LAPC-4 prostate cancer xenografts in nude mice. We also evaluated the tumor growth effects of using angiotensin II to activate both AT1R and AT2R simultaneously. Our data showed that losartan decreased tumor volumes by 56% versus control. This decrease reached statistical significance at day 54 (p = 0.0014). By day 54, Ki67 was also reduced in the losartan group, though not significantly so (p = 0.077). Losartan had no significant effect on AT1R or AT2R expression. Despite significant increases in both AT1R and AT2R at day 29 (p = 0.043 and 0.038, respectively), the administration of angiotensin II did not result in any significant differences in tumor volumes or ki67 at any time point. These data suggest that selective activation and induction of AT2R coupled with blockade of AT1R may slow prostate cancer growth. Future larger studies are needed to confirm these results.

Indexed as

Angiotensin IIAngiotensin II Type 1 Receptor BlockersAnimalsCell Line, TumorLosartanMaleMiceNeoplasm TransplantationProstatic NeoplasmsReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2RNA, MessengerSignal TransductionTranscriptomeTumor BurdenVasoconstrictor AgentsAngiotensin IIAngiotensin II Type 1 Receptor BlockersLosartanReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2RNA, MessengerVasoconstrictor AgentsangiotensinAT1RAT2RcancermouseprostateRAStumor

Identifiers

PMID28976133
PMCPMC6311706
OpenAlexW2791873561

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.