Evidence map›Paper›PMID 24990940›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2014

Clinically relevant doses of candesartan inhibit growth of prostate tumor xenografts in vivo through modulation of tumor angiogenesis.

Ahmed Alhusban, Ahmad Al-Azayzih, Anna Goc, Fei Gao, Susan C Fagan, Payaningal R Somanath

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 15% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
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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 4 institutions in 2 countries.

Ahmed AlhusbanProgram in Clinical and Experimental Therapeutics, University of Georgia College of Pharmacy and the Charlie Norwood VA Medical Center, Augusta, Georgia (A.A., A.A.-A., A.G., F.G., S.C.F., P.R.S.); Faculty of Pharmacy, Jordan University of Science and Technology, Irbid, Jordan (A.A.); and Departments of Neurology (S.C.F.), Medicine (P.R.S.), Cancer Center (P.R.S.), and Vascular Biology Center (P.R.S.), Georgia Regents University, Augusta, Georgia.
Ahmad Al-AzayzihProgram in Clinical and Experimental Therapeutics, University of Georgia College of Pharmacy and the Charlie Norwood VA Medical Center, Augusta, Georgia (A.A., A.A.-A., A.G., F.G., S.C.F., P.R.S.); Faculty of Pharmacy, Jordan University of Science and Technology, Irbid, Jordan (A.A.); and Departments of Neurology (S.C.F.), Medicine (P.R.S.), Cancer Center (P.R.S.), and Vascular Biology Center (P.R.S.), Georgia Regents University, Augusta, Georgia.
Anna GocProgram in Clinical and Experimental Therapeutics, University of Georgia College of Pharmacy and the Charlie Norwood VA Medical Center, Augusta, Georgia (A.A., A.A.-A., A.G., F.G., S.C.F., P.R.S.); Faculty of Pharmacy, Jordan University of Science and Technology, Irbid, Jordan (A.A.); and Departments of Neurology (S.C.F.), Medicine (P.R.S.), Cancer Center (P.R.S.), and Vascular Biology Center (P.R.S.), Georgia Regents University, Augusta, Georgia.
Fei GaoProgram in Clinical and Experimental Therapeutics, University of Georgia College of Pharmacy and the Charlie Norwood VA Medical Center, Augusta, Georgia (A.A., A.A.-A., A.G., F.G., S.C.F., P.R.S.); Faculty of Pharmacy, Jordan University of Science and Technology, Irbid, Jordan (A.A.); and Departments of Neurology (S.C.F.), Medicine (P.R.S.), Cancer Center (P.R.S.), and Vascular Biology Center (P.R.S.), Georgia Regents University, Augusta, Georgia.
Susan C FaganProgram in Clinical and Experimental Therapeutics, University of Georgia College of Pharmacy and the Charlie Norwood VA Medical Center, Augusta, Georgia (A.A., A.A.-A., A.G., F.G., S.C.F., P.R.S.); Faculty of Pharmacy, Jordan University of Science and Technology, Irbid, Jordan (A.A.); and Departments of Neurology (S.C.F.), Medicine (P.R.S.), Cancer Center (P.R.S.), and Vascular Biology Center (P.R.S.), Georgia Regents University, Augusta, Georgia.
Payaningal R SomanathProgram in Clinical and Experimental Therapeutics, University of Georgia College of Pharmacy and the Charlie Norwood VA Medical Center, Augusta, Georgia (A.A., A.A.-A., A.G., F.G., S.C.F., P.R.S.); Faculty of Pharmacy, Jordan University of Science and Technology, Irbid, Jordan (A.A.); and Departments of Neurology (S.C.F.), Medicine (P.R.S.), Cancer Center (P.R.S.), and Vascular Biology Center (P.R.S.), Georgia Regents University, Augusta, Georgia sshenoy@gru.edu.
Charlie Norwood VA Medical Center · USUniversity of Georgia · USGeorgia Regents Medical Center · USJordan University of Science and Technology · JO

Funding

Protein kinase B (Akt)-mediated pathway regulating endothelial-barrier functionR01HL103952 · NHLBI · UNIVERSITY OF GEORGIA · PI SHENOY, SOMANATH P RAMMOHAN · 2011 to 2015
$1.5M
NHLBI NIH HHS R01 HL103952NHLBI NIH HHS R01-HL103952
6 · The paper itself

Abstract

Angiotensin II receptor type 1 blockers (ARBs), widely used antihypertensive drugs, have also been investigated for their anticancer effects. The effect of ARBs on prostate cancer in experimental models compared with meta-analysis data from clinical trials is conflicting. Whereas this discrepancy might be due to the use of supratherapeutic doses of ARBs in cellular and animal models as compared with the clinical doses used in human trials, further investigation of the effects of clinical doses of ARBs on prostate cancer in experimental models is warranted. In the current study, we sought to determine the effects of candesartan on prostate cancer cellular function in vitro and tumor growth in vivo, and characterize the underlying mechanisms. Our analysis indicated that clinically relevant doses of candesartan significantly inhibited growth of PC3 cell tumor xenografts in mice. Interestingly, the same concentrations of candesartan actually promoted prostate cancer cellular function in vitro, through a modest but significant inhibition in apoptosis. Inhibition of tumor growth by candesartan was associated with a decrease in vascular endothelial growth factor (VEGF) expression in tumors and inhibition of tumor angiogenesis, but normalization of tumor vasculature. Although candesartan did not impair PC3 cell viability, it inhibited endothelial-barrier disruption by tumor-derived factors. Furthermore, candesartan significantly inhibited expression of VEGF in PC3 and DU145 cell lines independent of angiotensin II type 2 receptor, but potentially via angiotensin II type 1 receptor inhibition. Our findings clearly demonstrate the therapeutic potential of candesartan for prostate cancer and establish a link between ARBs, VEGF expression, and prostate tumor angiogenesis.

Indexed as

Xenograft Model Antitumor AssaysAngiogenesis InhibitorsAnimalsBenzimidazolesBiphenyl CompoundsCell Line, TumorCell MovementDose-Response Relationship, DrugHumansMaleMiceMice, NudeNeovascularization, PathologicProstatic NeoplasmsTetrazolesAngiogenesis InhibitorsBenzimidazolesBiphenyl CompoundscandesartanTetrazoles

Identifiers

PMID24990940
PMCPMC4152877
OpenAlexW2159005905

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.