Evidence map›Paper›PMID 30052660›Full record

ArticlePloS one2018

Development of monoclonal anti-PDGF-CC antibodies as tools for investigating human tissue expression and for blocking PDGF-CC induced PDGFRα signalling in vivo.

Hong Li, Manuel Zeitelhofer, Ingrid Nilsson, Xicong Liu, Laura Allan, Benjamin Gloria, Angelo Perani, Carmel Murone, Bruno Catimel, A Munro Neville and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

5 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Angiogenic signaling pathways and anti-angiogenic therapy for cancer.Signal transduction and targeted therapy · 2023
    Review
  3. Review
  4. Article
  5. 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

13 authors at 4 institutions in 3 countries.

Hong LiDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Manuel ZeitelhoferDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Ingrid NilssonDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Xicong LiuDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Laura AllanLudwig institute for Cancer Research, Melbourne Austin Branch, Melbourne, Australia.
Benjamin GloriaLudwig institute for Cancer Research, Melbourne Austin Branch, Melbourne, Australia.
Angelo PeraniLudwig institute for Cancer Research, Melbourne Austin Branch, Melbourne, Australia.
Carmel MuroneLudwig institute for Cancer Research, Melbourne Austin Branch, Melbourne, Australia.
Bruno CatimelLudwig institute for Cancer Research, Melbourne Austin Branch, Melbourne, Australia.
A Munro NevilleLudwig Institute for Cancer Research, New York, New York, United States of America.
Fiona E ScottLudwig institute for Cancer Research, Melbourne Austin Branch, Melbourne, Australia.
Andrew M ScottLudwig institute for Cancer Research, Melbourne Austin Branch, Melbourne, Australia.
Ulf ErikssonDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0002-4439-3980
Karolinska Institutet · SELa Trobe University · AULudwig Cancer Research · AULudwig Cancer Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PDGF-CC is a member of the platelet-derived growth factor (PDGF) family that stimulates PDGFRα phosphorylation and thereby activates intracellular signalling events essential for development but also in cancer, fibrosis and neuropathologies involving blood-brain barrier (BBB) disruption. In order to elucidate the biological and pathological role(s) of PDGF-CC signalling, we have generated high affinity neutralizing monoclonal antibodies (mAbs) recognizing human PDGF-CC. We determined the complementarity determining regions (CDRs) of the selected clones, and mapped the binding epitope for clone 6B3. Using the monoclonal 6B3, we determined the expression pattern for PDGF-CC in different human primary tumours and control tissues, and explored its ability to neutralize PDGF-CC-induced phosphorylation of PDGFRα. In addition, we showed that PDGF-CC induced disruption of the blood-retinal barrier (BRB) was significantly reduced upon intraperitoneal administration of a chimeric anti-PDGF-CC antibody. In summary, we report on high affinity monoclonal antibodies against PDGF-CC that have therapeutic efficacy in vivo.

Indexed as

A549 CellsAnimalsAntibodies, MonoclonalBlood-Retinal BarrierCapillary PermeabilityGene ExpressionHumansImmunohistochemistryLymphokinesMice, Inbred C57BLMice, TransgenicNeoplasmsPlatelet-Derived Growth FactorReceptor, Platelet-Derived Growth Factor alphaRecombinant ProteinsSignal TransductionAntibodies, MonoclonalLymphokinesPlatelet-Derived Growth Factorplatelet-derived growth factor CReceptor, Platelet-Derived Growth Factor alphaRecombinant Proteins

Identifiers

PMID30052660
PMCPMC6063412
OpenAlexW2883466536

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.