Evidence map›Paper›PMID 24853186›Full record

ArticleBritish journal of cancer2014

Exogenous administration of protease-resistant, non-matrix-binding IGFBP-2 inhibits tumour growth in a murine model of breast cancer.

C-L Soh, K McNeil, C M Owczarek, M P Hardy, L J Fabri, M Pearse, C A Delaine, B E Forbes

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 24 citations in OpenAlex.

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  16. Role of insulin-like growth factor-binding proteins in the pathophysiology and tumorigenesis of gastroesophageal cancers.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

C-L SohSchool of Molecular and Biomedical Science, The University of Adelaide, Adelaide, South Australia 5005, Australia.
K McNeilSchool of Molecular and Biomedical Science, The University of Adelaide, Adelaide, South Australia 5005, Australia.
C M OwczarekCSL Limited, Parkville, Victoria, Australia.
M P HardyCSL Limited, Parkville, Victoria, Australia.
L J FabriCSL Limited, Parkville, Victoria, Australia.
M PearseCSL Limited, Parkville, Victoria, Australia.
C A Delaine1] School of Molecular and Biomedical Science, The University of Adelaide, Adelaide, South Australia 5005, Australia [2] School of Medicine, Flinders University of South Australia, Bedford Park, South Australia 5042, Australia.
B E Forbes1] School of Molecular and Biomedical Science, The University of Adelaide, Adelaide, South Australia 5005, Australia [2] School of Medicine, Flinders University of South Australia, Bedford Park, South Australia 5042, Australia.
CSL (Australia) · AUUniversity of Adelaide · AUFlinders University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInsulin-like growth factors (IGF-I and IGF-II) signal via the type 1 IGF receptor (IGF-1R) and IGF-II also activates the insulin receptor isoform A (IR-A). Signalling via both receptors promotes tumour growth, survival and metastasis. In some instances IGF-II action via the IR-A also promotes resistance to anti-IGF-1R inhibitors. This study assessed the efficacy of two novel modified IGF-binding protein-2 (IGFBP-2) proteins that were designed to sequester both IGFs. The two modified IGFBP-2 proteins were either protease resistant alone or also lacked the ability to bind extracellular matrix (ECM).

methodsThe modified IGFBP-2 proteins were tested in vitro for their abilities to inhibit cancer cell proliferation and in vivo to inhibit MCF-7 breast tumour xenograft growth.

resultsBoth mutants retained low nanomolar affinity for IGF-I and IGF-II (0.8-2.1-fold lower than IGFBP-2) and inhibited cancer cell proliferation in vitro. However, the combined protease resistant, non-matrix-binding mutant was more effective in inhibiting MCF-7 tumour xenograft growth and led to inhibition of angiogenesis.

conclusionsBy removing protease cleavage and matrix-binding sites, modified IGFBP-2 was effective in inhibiting tumour growth and reducing tumour angiogenesis.

Indexed as

Amino Acid SequenceAngiogenesis InhibitorsAnimalsBinding SitesCell ProliferationExtracellular MatrixFemaleHumansInsulin-Like Growth Factor Binding Protein 2Insulin-Like Growth Factor IInsulin-Like Growth Factor IIMammary Neoplasms, ExperimentalMCF-7 CellsMiceMice, Inbred BALB CMice, NudeAngiogenesis InhibitorsInsulin-Like Growth Factor Binding Protein 2Insulin-Like Growth Factor IInsulin-Like Growth Factor IIRecombinant Proteins

Identifiers

PMID24853186
PMCPMC4056053
OpenAlexW1973918010

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.