Evidence map›Paper›PMID 37305016›Full record

ReviewOncology research2022

The effect of Wnt/β-catenin signaling on PD-1/PDL-1 axis in HPV-related cervical cancer.

Parisa Shiri Aghbash, Nima Hemmat, Behzad Baradaran, Ahad Mokhtarzadeh, Vahdat Poortahmasebi, Mahin Ahangar Oskuee, Hossein Bannazadeh Baghi

Open access · hybridAbstract readReview
In one paragraph

Review in Oncology research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.7field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

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  15. NK cells in HPV-related tumorigenesis: mechanisms and clinical applications.Frontiers in cellular and infection microbiology · 2025
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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

7 authors at 1 institution in 1 country.

Parisa Shiri AghbashImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, 5165665931, Iran.
Nima HemmatImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, 5165665931, Iran.
Behzad BaradaranImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, 5165665931, Iran.
Ahad MokhtarzadehImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, 5165665931, Iran.
Vahdat PoortahmasebiInfectious and Tropical Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, 5165665931, Iran.
Mahin Ahangar OskueeInfectious and Tropical Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, 5165665931, Iran.
Hossein Bannazadeh BaghiImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, 5165665931, Iran.
Tabriz University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Infection with high-risk human papillomavirus (HPV), including HPV-16 and HPV-18, is the main cause of malignancies, such as cervical cancer. Viral oncoproteins encoded by HPV are expressed in HPV-positive cancers and associated with the early cancer stages and the transformation of normal cells. The signaling pathways involved in the transformation of normal cells to cancerous form and the subsequently expressed programmed cell death-ligand 1 (PD-L1) on the surface of the transformed cells lead to a disruption in recognition of tumor cells by the immune cell system, including T lymphocytes and dendritic cells which lead to the development of cervical cancer malignancy. These cells also produce modest levels of cytokines during exhaustion, tumor-infiltrating T CD4+ cells with high levels of PD-1 and CD39 release considerable quantities of cytokines. The Wnt/β-catenin signaling pathway, which controls the expression of genes involved in the tumor cells' markers, is demonstrated to be one of the most potent cancer stimulants. It leads to the evasion of the tumor cells from immune cell detection and ultimately avoids being recognized by dendritic cells or T-cells. PD-L1, as an inhibitory immune checkpoint, is essential for controlling immune system activity by inhibiting T-cells' inflammatory function. In the present review, we looked into how Wnt/β-catenin affects the expression of PD-L1 and related genes like c-MYC in cancer cells and its role in the development of HPV-induced malignancy. We hypothesized that blocking these pathways could be a potential immunotherapy and cancer prevention method.

Indexed as

Papillomavirus InfectionsUterine Cervical NeoplasmsB7-H1 Antigenbeta CateninBiomarkers, TumorCytokinesFemaleHumansProgrammed Cell Death 1 ReceptorWnt Signaling PathwayB7-H1 Antigenbeta CateninBiomarkers, TumorCytokinesProgrammed Cell Death 1 ReceptorCervical cancersHPV-related cancersPD-1PD-L1PD-L2Wnt/β-catenin pathway

Identifiers

PMID37305016
PMCPMC10208084
OpenAlexW4320152998

What OpenQuestion holds

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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.