Evidence map›Paper›PMID 25919378›Full record

ArticleHuman gene therapy2015

Incorporation of Peptides Targeting EGFR and FGFR1 into the Adenoviral Fiber Knob Domain and Their Evaluation as Targeted Cancer Therapies.

Hanni Uusi-Kerttula, Mateusz Legut, James Davies, Rachel Jones, Emma Hudson, Louise Hanna, Richard J Stanton, John D Chester, Alan L Parker

Open access · hybridAbstract read
In one paragraph

Article in Human gene therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 48 citations in OpenAlex.

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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

9 authors at 3 institutions in 2 countries.

Hanni Uusi-Kerttula1Institutes of Cancer and Genetics, Cardiff University, Cardiff CF14 4XN, United Kingdom.
Mateusz Legut1Institutes of Cancer and Genetics, Cardiff University, Cardiff CF14 4XN, United Kingdom.
James Davies1Institutes of Cancer and Genetics, Cardiff University, Cardiff CF14 4XN, United Kingdom.
Rachel Jones3Velindre Cancer Centre, Cardiff CF14 2TL, United Kingdom.
Emma Hudson3Velindre Cancer Centre, Cardiff CF14 2TL, United Kingdom.
Louise Hanna3Velindre Cancer Centre, Cardiff CF14 2TL, United Kingdom.
Richard J Stanton2Institutes of Infection and Immunity, School of Medicine, Cardiff University, Cardiff CF14 4XN, United Kingdom.
John D Chester1Institutes of Cancer and Genetics, Cardiff University, Cardiff CF14 4XN, United Kingdom.
Alan L Parker1Institutes of Cancer and Genetics, Cardiff University, Cardiff CF14 4XN, United Kingdom.
Velindre Cancer Centre · GBCardiff University · GBInstitute of Infection and Immunity · CA

Funding

Cancer Research UK RX11705005HCRW_ HS-14-11Medical Research Council MR/L008734/1
6 · The paper itself

Abstract

Oncolytic virotherapies based on adenovirus 5 (Ad5) hold promise as adjunctive cancer therapies; however, their efficacy when delivered systemically is hampered by poor target cell specificity and preexisting anti-Ad5 immunity. Ovarian cancer represents a promising target for virotherapy, since the virus can be delivered locally into the peritoneal cavity. Both epidermal growth factor receptor (EGFR) and fibroblast growth factor receptor 1 (FGFR1) are overexpressed in the majority of human tumors, including ovarian cancer. To generate adenoviral vectors with improved tumor specificity, we generated a panel of Ad5 vectors with altered tropism for EGFR and FGFR, rather than the natural Ad5 receptor, hCAR. We have included mutations within AB loop of the viral fiber knob (KO1 mutation) to preclude interaction with hCAR, combined with insertions in the HI loop to incorporate peptides that bind either EGFR (peptide YHWYGYTPQNVI, GE11) or FGFR1 (peptides MQLPLAT, M*, and LSPPRYP, LS). Viruses were produced to high titers, and the integrity of the fiber protein was validated by Western blotting. The KO1 mutation efficiently ablated hCAR interactions, and significantly increased transduction was observed in hCAR(low)/EGFR(high) cell lines using Ad5.GE11, while transduction levels using Ad5.M* or Ad5.LS were not increased. In the presence of physiological concentrations of human blood clotting factor X (hFX), significantly increased levels of transduction via the hFX-mediated pathway were observed in cell lines, but not in primary tumor cells derived from epithelial ovarian cancer (EOC) ascites samples. Ad5-mediated transduction of EOC cells was completely abolished by the presence of 2.5% serum from patients, while, surprisingly, incorporation of the GE11 peptide resulted in significant evasion of neutralization in the same samples. We thus speculate that incorporation of the YHWYGYTPQNVI dodecapeptide within the fiber knob domain may provide a novel means of circumventing preexisting Ad5 immunity that warrants further investigation.

Indexed as

Recombinant Fusion ProteinsAdenoviridaeAnimalsAntibodies, NeutralizingCapsid ProteinsCell LineErbB ReceptorsFemaleGene ExpressionGenetic TherapyGenetic VectorsGene Transfer TechniquesHumansNeoplasmsNeutralization TestsOvarian Neoplasmsadenovirus receptorAntibodies, NeutralizingCapsid ProteinsErbB Receptorshexon capsid protein, AdenovirusPeptidesReceptor, Fibroblast Growth Factor, Type 1Receptors, VirusRecombinant Fusion Proteins

Identifiers

PMID25919378
PMCPMC4442602
OpenAlexW2012874922

What OpenQuestion 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 OpenQuestion graph.