Evidence map›Paper›PMID 22413953›Full record

ReviewExpert opinion on therapeutic targets2012

Targeting angiogenesis for the treatment of prostate cancer.

Emmanuel S Antonarakis, Michael A Carducci

Open access · greenAbstract readReview
In one paragraph

Review in Expert opinion on therapeutic targets, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

13 citing papers in PubMed, 32 citations in OpenAlex.

  1. Trial
  2. Membrane-derived particles shed by PSMA-positive cells function as pro-angiogenic stimuli in tumors.Journal of controlled release : official journal of the Controlled Release Society · 2023
    Article
  3. Article
  4. Different roles of myofibroblasts in the tumorigenesis of nonsmall cell lung cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  5. Article
  6. Adiponectin inhibits VEGF-A in prostate cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. 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

2 authors at 2 institutions in 1 country.

Emmanuel S AntonarakisSidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Prostate Cancer Research Program, Baltimore, MD 21231-1000, USA. eantona1@jhmi.edu
Michael A Carducci
Sidney Kimmel Comprehensive Cancer Center · USWeatherford College · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
NCI NIH HHS P30 CA006973
6 · The paper itself

Abstract

introductionWhile multiple therapies exist that prolong the lives of men with advanced prostate cancer, none are curative. This had led to a search to uncover novel targets for prostate cancer therapy, distinct from those of traditional hormonal approaches, chemotherapies, immunotherapies and bone-targeting approaches. The process of tumor angiogenesis is one target that is being exploited for therapeutic gain. AREAS COVERED: The most promising anti-angiogenic approaches for treatment of prostate cancer, focusing on clinical development of selected agents. These include VEGF-directed therapies, tyrosine kinase inhibitors, tumor-vascular disrupting agents, immunomodulatory drugs and miscellaneous anti-angiogenic agents. While none of these drugs have yet entered the market for the treatment of prostate cancer, several are now being tested in Phase III registrational trials. EXPERT OPINION: The development of anti-angiogenic agents for prostate cancer has met with several challenges. This includes discordance between traditional prostate-specific antigen responses and clinical responses, which have clouded clinical trial design and interpretation, potential inadequate exposure to anti-angiogenic therapies with premature discontinuation of study drugs and the development of resistance to anti-angiogenic monotherapies. These barriers will hopefully be overcome with the advent of more potent agents, the use of dual angiogenesis inhibition and the design of more informative clinical trials.

Indexed as

Angiogenesis InhibitorsAnimalsHumansImmunologic FactorsMaleNeovascularization, PathologicProstatic NeoplasmsProtein Kinase InhibitorsProtein-Tyrosine KinasesVascular Endothelial Growth Factor AAngiogenesis InhibitorsImmunologic FactorsProtein Kinase InhibitorsProtein-Tyrosine KinasesVascular Endothelial Growth Factor A

Identifiers

PMID22413953
PMCPMC4005337
OpenAlexW1979591854

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.