Evidence map›Paper›PMID 33499895›Full record

ArticleInfectious agents and cancer2021

Co-administration of 2'3'-cGAMP STING activator and CpG-C adjuvants with a mutated form of HPV 16 E7 protein leads to tumor growth inhibition in the mouse model.

Fariba Dorostkar, Arash Arashkia, Farzin Roohvand, Zabihollah Shoja, Mohsen Navari, Maryam Mashhadi Abolghasem Shirazi, Zahra Shahosseini, Mohammad Farahmand, Mohammad Sadegh Shams Nosrati, Somayeh Jalilvand

Open access · goldAbstract read
In one paragraph

Article in Infectious agents and cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 24 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

10 authors at 3 institutions in 1 country.

Fariba DorostkarDepartment of Virology, School of Public Health, Tehran University of Medical Sciences, 14155, Tehran, Iran.
Arash ArashkiaDepartment of Molecular Virology, Pasteur Institute of Iran, Tehran, Iran. arash.arashkia@gmail.com.
Farzin RoohvandDepartment of Molecular Virology, Pasteur Institute of Iran, Tehran, Iran.
Zabihollah ShojaDepartment of Molecular Virology, Pasteur Institute of Iran, Tehran, Iran.
Mohsen NavariDepartment of Medical Biotechnology, School of Paramedical Sciences, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran.
Maryam Mashhadi Abolghasem ShiraziDepartment of Molecular Virology, Pasteur Institute of Iran, Tehran, Iran.
Zahra ShahosseiniDepartment of Molecular Virology, Pasteur Institute of Iran, Tehran, Iran.
Mohammad FarahmandDepartment of Virology, School of Public Health, Tehran University of Medical Sciences, 14155, Tehran, Iran.
Mohammad Sadegh Shams NosratiDepartment of Molecular Virology, Pasteur Institute of Iran, Tehran, Iran.
Somayeh JalilvandDepartment of Virology, School of Public Health, Tehran University of Medical Sciences, 14155, Tehran, Iran. sjalilvand@tums.ac.ir.
Pasteur Institute of Iran · IRTehran University of Medical Sciences · IRTorbat Heydarieh University of Medical Sciences · IR

Funding

Tehran University of Medical Sciences and Health Services 240.293Tehran University of Medical Sciences and Health Services 34892
6 · The paper itself

Abstract

Persistent infection with high-risk genotypes of human papillomavirus (HPV) is the leading cause of cervical cancer. The HPV oncoprotein E7 is constitutively expressed in cervical cancer and considered as an essential target for tumor-specific immunity. The goal of this study was to develop a candidate therapeutic vaccine based on the mutated E7 protein that had possibly reduced transformation capacity while was able to elicit a robust immune response. Therefore, the mutant type of HPV 16 E7 (E7GRG) protein was recombinantly expressed in E. coli. The protein was then purified and formulated with 2'-3'cGAMP CDN and/or CpG-C ODN adjuvants and subcutaneously injected to female C57BL/6 mice. To evaluate the immunogenic response, lymphocyte proliferation, secretion levels of IFN-γ and IL-4 cytokines, granzyme B level, and total IgG and subclasses of IgG antibody were measured. The anti-tumor activity was evaluated in tumor-harboring C57BL/6 mice. The highest rate of cell proliferation, IFN-γ and granzyme B levels, and amount of IgG antibody were found in mice group that were injected by E7GRG + 2'-3'cGAMP + CpG-C. Therapeutic immunization with E7GRG + 2'-3'cGAMP + CpG-C also significantly suppressed TC-1 tumor growth in mice. In conclusion, the results demonstrated that E7GRG + 2'-3'cGAMP + CpG-C induced strong cell-mediated and humoral immune responses that resulted in inhibition of tumor in mouse model.

Indexed as

CpG ODN 2395Cyclic dinucleotide (CDN)E7 oncoproteinHPV vaccineHuman papillomavirusStimulator of interferon genesSTING

Identifiers

PMID33499895
PMCPMC7836183
OpenAlexW3122041590

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.