Evidence map›Paper›PMID 25422946›Full record

ArticlePloS one2014

Design of a highly effective therapeutic HPV16 E6/E7-specific DNA vaccine: optimization by different ways of sequence rearrangements (shuffling).

Fahad N Almajhdi, Tilo Senger, Haitham M Amer, Lutz Gissmann, Peter Öhlschläger

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Cancer DNA vaccines: current preclinical and clinical developments and future perspectives.Journal of experimental & clinical cancer research : CR · 2019
    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

5 authors at 4 institutions in 3 countries.

Fahad N AlmajhdiDepartment of Botany and Microbiology, College of Science, King Saud University, Riyadh, Saudi Arabia.
Tilo SengerGerman Cancer Research Center, Heidelberg, Germany.
Haitham M AmerDepartment of Botany and Microbiology, College of Science, King Saud University, Riyadh, Saudi Arabia; Virology Department, Faculty of Veterinary Medicine, Cairo University, Giza, Egypt.
Lutz GissmannDepartment of Botany and Microbiology, College of Science, King Saud University, Riyadh, Saudi Arabia; German Cancer Research Center, Heidelberg, Germany.
Peter ÖhlschlägerDepartment of Chemistry and Biotechnology, Aachen University of Applied Sciences, Jülich, Germany.
King Saud University · SAFH Aachen · DEGerman Cancer Research Center · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Persistent infection with the high-risk Human Papillomavirus type 16 (HPV 16) is the causative event for the development of cervical cancer and other malignant tumors of the anogenital tract and of the head and neck. Despite many attempts to develop therapeutic vaccines no candidate has entered late clinical trials. An interesting approach is a DNA based vaccine encompassing the nucleotide sequence of the E6 and E7 viral oncoproteins. Because both proteins are consistently expressed in HPV infected cells they represent excellent targets for immune therapy. Here we report the development of 8 DNA vaccine candidates consisting of differently rearranged HPV-16 E6 and E7 sequences within one molecule providing all naturally occurring epitopes but supposedly lacking transforming activity. The HPV sequences were fused to the J-domain and the SV40 enhancer in order to increase immune responses. We demonstrate that one out of the 8 vaccine candidates induces very strong cellular E6- and E7- specific cellular immune responses in mice and, as shown in regression experiments, efficiently controls growth of HPV 16 positive syngeneic tumors. This data demonstrates the potential of this vaccine candidate to control persistent HPV 16 infection that may lead to malignant disease. It also suggests that different sequence rearrangements influence the immunogenecity by an as yet unknown mechanism.

Indexed as

AlphapapillomavirusAnimalsAntibodies, ViralCell Line, TumorFemaleHuman Papillomavirus Recombinant Vaccine Quadrivalent, Types 6, 11, 16, 18HumansMiceMice, Inbred C57BLNeoplasms, ExperimentalOncogene Proteins, ViralPapillomavirus E7 ProteinsPapillomavirus VaccinesRepressor ProteinsVaccines, DNAAntibodies, ViralE6 protein, Human papillomavirus type 16Human Papillomavirus Recombinant Vaccine Quadrivalent, Types 6, 11, 16, 18oncogene protein E7, Human papillomavirus type 16Oncogene Proteins, ViralPapillomavirus E7 ProteinsPapillomavirus VaccinesRepressor ProteinsVaccines, DNA

Identifiers

PMID25422946
PMCPMC4244082
OpenAlexW2054385175

What OpenQuestion holds

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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.