Evidence map›Paper›PMID 33896829›Full record

ArticleCancer biomarkers : section A of Disease markers2021

Targeting IL-17alpha to promote anti-PD-1 therapy effect by screening the tumor immune microenvironment in a mouse oral carcinogenesis model.

Shan Wang, Xiaorong Yu, Fang Li, Haixia Fan, Eryang Zhao, Zheng Hu

Abstract read
In one paragraph

Article in Cancer biomarkers : section A of Disease markers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 32% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Review
  3. The IL-17 family in diseases: from bench to bedside.Signal transduction and targeted therapy · 2023
    Review
  4. The Role of IL-17 in the Pathogenesis of Oral Squamous Cell Carcinoma.International journal of molecular sciences · 2023
    Review
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

6 authors at 5 institutions in 1 country.

Shan WangDepartment of Oral Pathology, Hospital of Stomatology, the First Affiliated Hospital, Harbin Medical University, Harbin, Heilongjiang, China.
Xiaorong YuCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, Heilongjiang, China.
Fang LiDepartment of Stomatology, Women's and Children's Medical Center, Haikou, Hainan, China.
Haixia FanDepartment of Oral Medicine, Jining Medical College, Jining, Shandong, China.
Eryang ZhaoDepartment of Oral Pathology, Hospital of Stomatology, the First Affiliated Hospital, Harbin Medical University, Harbin, Heilongjiang, China.
Zheng HuLaboratory of Sono- and Photo-Theranostic Technologies, Harbin Institute of Technology, Harbin, Heilongjiang, China.
Harbin Medical University · CNHainan Modern Women and Children's Hospital · CNHarbin Institute of Technology · CNHeilongjiang Academy of Sciences · CNJining Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundResistance to PD-1 blocking agents is not uncommon, limiting their wide clinical success. Certain tumor-infiltrating immune cells (e.g., TILs/CTLs) have emerged as biomarkers of response, and absence of such immune cells contributes to resistance.

objectiveWe deconvoluted the dynamic immune microenvironment in a mouse model of oral carcinogenesis for augmenting the resistance to PD-1 blocking agents by combination.

methodsBioinformatics methods and routine biological experiments were adopted such as morphological analysis and ELISA in the 4NQO-treated mice model.

resultsOur findings revealed that dysplastic tongue tissues from 4NQO-treated mice were characterized by an immunosuppressive tumor microenvironment. Tongue tissues from mice treated with 4NQO for 12 weeks had higher levels of Th2 cells and Tregs compared to tissues taken from control mice or mice treated with 4NQO for 28 weeks; these results suggested a potential therapeutic benefit of anti-PD-1 in the oral cancer. The IL-17 pathway was significantly upregulated during progression from normal mucosa to hyperplasia and tumor formation in mice. Inhibition of IL-17α combined with PD-1 blockade delayed the development of 4NQO-induced precancerous and cancerous lesions and prolonged the survival of 4NQO-treated mice.

conclusionsOur data suggested a strong rationale of IL-17α blockade as a potential approach to augment the tumor-eliminating effects of anti-PD-1 therapy.

Indexed as

AnimalsCarcinogenesisDisease Models, AnimalFemaleImmune Checkpoint InhibitorsImmunotherapyInterleukin-17MiceMice, Inbred BALB CMice, Inbred C57BLMolecular Targeted TherapyMouth NeoplasmsProgrammed Cell Death 1 ReceptorTumor MicroenvironmentIl17a protein, mouseImmune Checkpoint InhibitorsInterleukin-17Pdcd1 protein, mouseProgrammed Cell Death 1 ReceptorIL-17alphaImmunotherapypre-cancerous lesionsprogrammed death receptor 1resistancesquamous cell carcinomas

Identifiers

PMID33896829
PMCPMC12500027
OpenAlexW3155248021

What OpenQuestion holds

Textmetadata
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.