Evidence map›Paper›PMID 19956425›Full record

ArticleAmerican journal of translational research2009

Disease evidence for IGFBP-2 as a key player in prostate cancer progression and development of osteosclerotic lesions.

David J Degraff, Adam A Aguiar, Robert A Sikes

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.8field-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

23 citing papers in PubMed, 40 citations in OpenAlex.

  1. Trial
  2. Trial
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  4. Gold Nanoparticles Disrupt the IGFBP2/mTOR/PTEN Axis to Inhibit Ovarian Cancer Growth.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022
    Article
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  10. Review
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  15. IGFBP-2 - taking the lead in growth, metabolism and cancer.Journal of cell communication and signaling · 2015
    Article
  16. Article
  17. Review
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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

3 authors at 1 institution in 1 country.

David J DegraffLaboratory for Cancer Ontogeny and Therapeutics, Center for Translational Cancer Research, Department of Biological Sciences, University of Delaware 19716.
Adam A Aguiar
Robert A Sikes
Center for Cancer Research · US

Funding

VOLUMETRIC BREAST DENSITY ESTIMATION USING BREAST SURFACE RECONSTRUCTEDP20RR016472 · NCRR · UNIVERSITY OF DELAWARE · PI STANHOPE, STEVEN J. · 2001 to 2011
$37.6M
NCRR NIH HHS P20 RR016472
6 · The paper itself

Abstract

Accumulating evidence indicates that alterations in the IGF axis contribute to the development of chemo- and radio-resistant, advanced-stage cancers. Additionally, they contribute to hormonal insensitivity in adenocarcinomas such as those derived from prostate and breast. The ligands, IGF-I and IGF-II, along with their receptors, IGF-IR and IGF-IIR, have been implicated in a wide range of disease. Activation and subsequent signal transduction through the receptors is attenuated, and/or potentiated, by the interactions of IGF axis ligands, IGF-I/II, with the high affinity IGF-binding proteins 1 to 6 (IGFBP1-6). New evidence indicates that the IGFBPs, irrespective of ligand interactions, correlate with the development and metastatic behavior of several cancers. Increased expression of insulin-like growth factor binding protein 2 (IGFBP-2) is found in advanced cancers of the ovary, breast, stomach, adrenal gland, bladder, CNS, and prostate. Further, IGFBP-2 seemingly has ligand-independent effects that participate in the development and dissemination of advanced cancer cells. As such, IGFBP-2 can assist in the development of the lethal phenotype for some cancers. While several reports have shown an important role for IGFBP-2 in the development of androgen insensitivity and the proliferation of AI PCa cells in vivo, these studies have not tested a role for IGFBP-2 in the metastatic spread of AI PCa cells. Additionally, the mechanism of IGFBP-2 action in these events has not been elucidated. The redundancy and abundance of the IGFBPs have precluded a clear understanding of the means by which IGFBP-2 signals. Components of these signaling pathways, particularly IGFBP-2, are being evaluated currently in clinical trials.

Indexed as

androgen insensitivity, AIandrogen sensitive, ASInsulin-like growth factor, IGFneoplasm, bone, metastasisprostate cancer, PCa

Identifiers

PMID19956425
PMCPMC2776314
OpenAlexW127913739

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.